In women's reproductive years, their brains are exposed to high levels of sex hormones, and their neurons may come to depend on those hormones to function optimally. But leading up to and after menopause, the ovaries produce far less estrogen and progesterone, raising concerns that this drop in hormones may contribute to women's dementia risk.

"We think that the loss of those hormones at menopause renders those neurons more vulnerable to age-related cellular decline and pathologies like Alzheimer's," said Karyn Frick, a neuroscientist and professor of psychological and brain sciences at the University of Wisconsin-Milwaukee.

So, if falling hormone levels are a risk factor for dementia, could replacing those hormones help stave off the disease?

While the idea sounds logical on its face, studies that have looked at hormone replacement therapy (HRT) for dementia prevention have had mixed results. There are early hints that restoring estrogen during early menopause may protect brain health, but ultimately, more gold-standard clinical trials are needed to know for sure, experts told Live Science.

Support for estrogen protecting the brain

The idea that estrogen could help ward off dementia is plausible. Women are more likely to develop Alzheimer's disease than men are, and scientists think the loss of estrogen during menopause may be partly to blame, said Jennifer Bruno, an instructor of psychiatry and behavioral sciences at Stanford University.

Lab and animal studies buttress the idea that estrogen could protect brain health.

In the brain, estrogens act as neuromodulators, or chemical messengers that alter how neurons behave. Estrogen also helps neurons keep their shape. Estrogen loss in female mice triggers a drop in the number of dendritic spines ‪—‬ the small, bud-like bumps on neurons that receive chemical messages.

Researchers think that estrogen may help prevent the formation of the abnormal proteins — including one called amyloid beta — that accumulate, disrupt communication between neurons and ultimately kill cells in Alzheimer's disease. Amyloid beta is produced when a larger protein is cut the "wrong" way by an enzyme, Frick explained. Estrogen promotes the "normal" cutting of this protein, thus reducing amyloid beta, studies in lab mice show.

And estrogen may limit the buildup of a second Alzheimer's-related protein, called tau, by preventing the chemical processes that cause the tau proteins to clump together. This helps prevent the formation of tau tangles, a hallmark of Alzheimer's disease.

The hormone may also support brain health indirectly by improving sleep quality.

"It's well documented that menopausal women have difficulty sleeping, whether it's due to hot flashes or insomnia," Frick said. Estrogen can ease those nighttime hot flashes, thus helping menopausal women get more, less-fragmented sleep. Deep rest may help the brain clean out toxic proteins, while research shows sleep deficiency is linked to Alzheimer's disease.

Mixed results with estrogen-only HRT

HRT for menopause comes in two main forms: treatments that include only estrogen, and combined therapies with both estrogen and progesterone. The treatment has a complicated history.

HRT was popular in the 1990s but fell out of favor after results from the Women's Health Initiative study were published in 2002. That study identified various risks tied to both estrogen-only and combined HRT options, some of which have since been overturned by newer data.

That said, the Women's Health Initiative study found that estrogen-only HRT came with an increased risk of endometrial cancers, and later analyses have backed up this idea. That's why today, clinical guidelines recommend that women who have not gotten a hysterectomy take combined HRT, while estrogen-only options are reserved for those who have had their uterus removed. (The added progesterone counteracts estrogen's thickening effect on the uterine lining.)

For the subset of women who take estrogen-only HRT, observational data published in August showed that this form of the treatment was linked to a reduced risk of dementia. The study, published in the journal Neurology, found that women who took estrogen-only HRT were less likely to show Alzheimer's-related changes in the brain than women who didn't take any HRT.

Estrogen-only HRT was also tied to better clinical outcomes: Treated women were less likely to be diagnosed with dementia, were less likely to show clinical and functional cognitive decline, and had better scores on memory tests, on average, compared with untreated women. These findings drew on two large, separate groups of older women, reporting data from 21,400 people in total, but they didn't include data on when each woman started HRT.

Whereas earlier studies of HRT and dementia risk relied on doctors' ratings of patients' symptoms, the Neurology study measured levels of Alzheimer's-related proteins in the brain after death. That's a more "definitive" marker of disease, said Bruno, a co-author of the study. However, the research was observational, so it can't say whether estrogen-only HRT directly causes the better brain outcomes the team observed, she stressed.

Although the Neurology study's findings are promising, they don't necessarily match the results of other studies of estrogen-only HRT and dementia. For example, a slightly larger observational study, published in 2023, found that estrogen-only HRT was associated with an increased dementia rate.

In that research, most of the women took a type of estrogen called estradiol, while Bruno's study included a greater variety of estrogens. That may have been the difference in the two studies' results, but teasing that out would require further study. Meanwhile, the conflicting findings muddy the waters of what estrogen-only HRT can do for brain health.

Does timing matter?

One big finding from the Women's Health Initiative study was that starting HRT — either estrogen-only or combined — after age 65 was associated with worse cognitive function and increased dementia risk, said Yuko Hara, director of aging and Alzheimer's prevention at the Alzheimer's Drug Discovery Foundation.

The same may not be true for people who start HRT earlier. For context, menopause starts around age 51 to 52, on average, and it's preceded by perimenopause, a transitional period when hormone levels begin to drop, typically around the mid-40s.

An observational study published in August in the journal Alzheimer's & Dementia found that starting HRT between ages 46 and 56 was linked to a reduced risk of dementia. That study did not differentiate between estrogen-only and combined treatment; it lumped all of the data together.

The protective link was especially strong in three groups: women with "surgical menopause," triggered by the removal of one or both ovaries; carriers of a certain variant of a gene called APOE that raises Alzheimer's risk; and women who had a relatively short time between their first period and menopause.

A 2024 meta-analysis of randomized controlled trials also found that HRT had a cognitive benefit for women with surgical menopause; that finding was tied mostly to estrogen-only therapies.

However, outside of that specific group, the idea of early HRT protecting brain health is far from settled.

Who might benefit, if anyone?

When it comes to using hormone replacement to protect brain health, the evidence isn't yet strong enough to recommend any kind of HRT as a way to protect the brain in all women, Hara said. Women who had one or both of their ovaries surgically removed are the exception to this rule.

"This is a distinct clinical population because the procedure can cause an abrupt, early loss of estrogen, rather than the gradual hormonal decline that occurs with natural menopause," Hara said.

For most women who have gone through natural menopause, "there is not enough evidence to recommend [HRT] specifically for preventing cognitive decline or dementia," she said.

HRT is not currently prescribed to prevent dementia — it is prescribed to ease menopause symptoms, such as hot flashes, night sweats and sleep disturbances. To settle the science on HRT and the brain, what's really needed is a well-designed clinical trial that follows women from perimenopause to postmenopause, Bruno said. That would reveal the effects of HRT on brain health and dementia risk more reliably than the studies done so far.

This article is for informational purposes only and is not meant to offer medical advice.

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Artificial intelligence (AI) algorithms that hunt for cancer may do a better job when they approach the analysis as if they were a human pathologist, a new study suggests.

Many AI systems analyze preselected regions of a tissue sample, or they split a whole pathology slide into patches of a fixed size. By contrast, a pathologist searches more dynamically, panning across the tissue, zooming in and out, and pausing over areas that raise red flags. A whole slide can contain billions of pixels, while the evidence of cancer may occupy only a tiny patch.

Study co-author Zhi Huang, an assistant professor of pathology and laboratory medicine at the University of Pennsylvania, compared the process to a search-and-rescue helicopter. "You don't start by inspecting one square meter of ground," Huang told Live Science. You scan the landscape first and then swoop in for a closer look.

In the new study, published in July in the journal Nature, Huang and colleagues demonstrated that cancer-detecting AI might work better when it takes this humanized approach.

Training AI to hunt for cancer

AI algorithms called vision language models (VLMs) struggle with the first step that Huang described — that initial, cursory scan. That's in part because many pathology AI systems learn from what pathologists leave behind at the end of that search: a labeled image pointing out where the cancer is or an official diagnosis.

Instead, the researchers trained their new AI on pathologists' search behavior. They called this approach to training "Pathology-CoT," short for "chain of thought." It turns observable actions, including where pathologists move around and zoom in on an image, into training data.

To collect the data, the team created a tool that recorded how pathologists moved around a slide and changed magnification. The raw logs, gathered from eight pathologists, were messy, as a given pathologist might drift across a slide, overshoot their intended region of focus or fiddle with magnification to adjust it to their liking.

To clean up the data, the researchers filtered out those incidental movements, focusing on moments that appeared to represent deliberate attention, such as lingering over one view or making a sustained pan. Then, they compared those regions with eye-tracking data to check that the software was capturing where pathologists were actually looking.

For each region a pathologist inspected, the VLM also drafted a short rationale explaining why the region was worth examining and what features were visible; human pathologists could then accept, edit, or reject the rationale, creating additional training data for the AI. In one example, the AI flagged a portion of a slide as potentially metastatic and suggested zooming in to look for atypical cells. Other inspected regions were flagged as healthy tissue.

Ultimately, the researchers used this training method to build a new tool called Pathology-o3. It scans a slide at low resolution, uses a model trained on pathologists' behavior to choose regions worth a closer look, then sends higher-resolution views of those regions to a VLM for analysis.

Putting it to the test

Huang said the goal of the new study was not to show that Pathology-o3 worked better than specialized AI models that are specifically built to detect specific types of cancer; those models are often trained disease by disease. Rather, the researchers wanted to see whether their new training approach could help a general-purpose AI navigate a pathology slide more effectively.

They compared Pathology-o3 to other general-use AI systems, such as OpenAI's o3, and asked the algorithms to examine slides containing lymph node tissue. These slides were collected from colorectal cancer cases and some contained metastatic cancer, which human pathologists had already labeled.

The algorithm correctly identified slides that were positive for cancer 100% of the time. However, of the slides it identified as positive, 15.5% were actually negative. By comparison, OpenAI o3 correctly identified slides that were positive for cancer 87.5% of the time. Of the slides it identified as positive, 53.3% were actually negative.

The researchers designed Pathology-o3 to err on the side of flagging something for another look, rather than potentially missing cancer. That might help to explain the rate of false positives, Huang said.

Whether that rate of false alarms is acceptable depends on how Pathology-o3 is used, said Mohammad Asadi, a data scientist at Stanford University who was not involved in the research. It's not precise enough for the AI to diagnose patients on its own, but it could still be useful for a system to point a human toward regions of a slide that are worth double-checking. It may be an advantage that the approach shows the pathologist a specific region to inspect rather than declaring an entire slide suspicious, he said.

The researchers tried repeating the test on an independent dataset that the algorithms hadn't seen before to see how well it worked on unfamiliar slides. Pathology-o3 correctly identified slides that were positive for cancer 97.6% of the time. Of the slides it identified as positive, 37.1% were actually negative. The finding is an example of how AI performance can change when the data source changes, even when the medical task stays the same.

Asadi explained this result suggests the system can still work with slides from a different source. But that result does not yet show that using this tool would make pathologists more accurate or efficient in practice.

Can it help pathologists?

The researchers applied their training approach to several existing VLMs, finding that the models' performance consistently improved after the training. That suggests that the navigation data from pathologists was useful across settings, Asadi said.

For Huang, that is the most important result. "The takeaway isn't our system," he said. "It's that the missing ingredient has been sitting in hospitals this whole time."

The study did not compare Pathology-o3 directly with human pathologists, but the researchers said that wasn't their aim.

"The right question isn't whether it beats a pathologist," Huang said. "It's whether a pathologist working with it catches more [cancer cases] and works faster." The current study did not address the latter question, either, but the team's next experiment is designed to test pathologists on the same cases with and without Pathology-o3, measuring what they catch and how long they take to do so.

The system's most plausible use is as a prescreening tool, Asadi said, but he stressed that the research has not yet shown that doctors who use it become faster or more accurate. Asadi wants an even tougher test: trials conducted across multiple hospitals that measure not just accuracy and speed but also pathologists' workloads. He wants the trails to assess the burden of false alarms from the AI algorithms and whether doctors recognize when the AI is wrong.

Importantly, cancer diagnoses can require information from multiple slides, stains and a patient's medical history, while the current system just reads one slide at a time. "I wouldn't claim it should diagnose on its own," Huang said.

This article is for informational purposes only and is not meant to offer medical advice.

Yellow fever is appearing in regions that haven't seen cases of the disease in years, largely as a result of climate change.

Historically, the virus ravaged cities across the Americas, Europe and Africa, until a vaccine was introduced in 1937 and its range shrunk significantly. But now, as climate change creates favorable conditions for virus-carrying mosquitoes, scientists are seeing outbreaks in unexpected areas.

"Yellow fever is a highly deadly disease," Dr. Joelle Ivy Rosser, an infectious-disease researcher at Stanford University, told Live Science, "so any environmental pressures that increase the likelihood of future yellow fever virus outbreaks … is highly concerning."

How is climate change contributing to this pattern, and could it get worse in the future?

How rising temperatures impact yellow fever

Yellow fever is a mosquito-borne disease caused by the Orthoflavivirus flavi virus, better known as yellow fever virus (YFV). The infection causes fever, muscle aches, headaches and vomiting. About 15% of cases become severe, with patients showing jaundiced skin and eyes, bleeding from the mouth, eyes, nose and stomach, or organ failure.

Devastating yellow fever epidemics spread in the 17th to 19th centuries, before the development of a vaccine. Nowadays, an estimated 31,000 to 82,000 yellow fever deaths occur each year; severe cases have an estimated fatality rate of 20% to 50%.

Most yellow fever infections are a result of spillover from nonhuman primates; mosquitoes bite monkeys that carry the virus, such as howler monkeys, and then the infected mosquitoes bite humans. Several types of mosquitoes carry the virus, but the species Aedes aegypti is the main vector for yellow fever in cities, where high population density can make outbreaks especially severe.

Although there is an effective vaccine for yellow fever, cases have been on the rise in the past three decades. This led the World Health Organization (WHO) to set out a strategy in 2017 for eliminating yellow fever epidemics by 2026 through outbreak prevention and containment.

Climate-change-driven warming and extreme weather events may have heightened yellow fever risk over the past few decades, experts say. Rising temperatures make mosquitoes bite more because heat makes their metabolisms more active, said Dr. Seth Judson, an infectious-disease physician-scientist at UCLA. Warming also cuts down the virus's extrinsic incubation period, meaning the time it takes for the virus to replicate in a newly infected mosquito and then get passed on to another person, he told Live Science.

Weather patterns and deforestation

Changing weather patterns play a role, too. In 2017-2018, Brazil saw its first yellow fever outbreak in a city in almost a century. That outbreak, primarily in Belo Horizonte and São Paulo, was likely a result of drought, according to one study.

While heavy rainfall creates a breeding ground for mosquitoes, in this case, drought pushed forest-based mosquitoes — as well as YFV carriers like marmosets and howler monkeys — closer to cities as the animals searched for water. Drier conditions can also prompt dehydrated mosquitoes to bite more as they search for fluids, study co-author Jamie Caldwell, a disease ecologist at Princeton University, told Live Science.

"Extremes of weather in either direction" — very wet or very dry — "can exacerbate mosquito-borne disease transmission," Rosser said.

Parts of Africa and South America that were considered low-risk for yellow fever have already been seeing new outbreaks, Judson said, so maps of yellow-fever-affected areas have had to be updated. In research that's been released as a preprint but not peer-reviewed yet, Judson found that yellow fever is reemerging in an area of the Colombian Andes where it hadn't been reported since 1940.

Experts are paying particular attention to the edges of cities, where urban centers meet the forest. The risk of yellow fever transmission from monkeys to humans via mosquitoes is rising at these edges due to both climate change and deforestation.

"Humans are expanding the agricultural frontier and encroaching on forests where yellow fever mosquitoes … are found," Gabriel Parra-Henao, a biologist with the WHO, told Live Science in an email. "[This] results in more people being exposed to their bites."

Similar patterns have been seen with other mosquito-borne infections, such as malaria.

Could yellow fever return to the U.S.?

Climate change is expected to bring yellow fever to new areas. One study predicts that, under the most severe climate change scenario, nearly a billion people could face their first exposure to the mosquitoes that can carry YFV in the next century. While that worst-case scenario may not be the most likely, the mosquitoes' ranges are still expected to expand under less-severe conditions.

Europe is predicted to face the largest increase in exposure to Ae. aegypti mosquitoes compared to the rest of the world, and the U.S. and Canada are predicted to see increases too. In the U.S., the mosquito species already lives in a number of states, including Florida, Mississippi, Arizona and New Mexico. However, warming would increase the chances of mosquitoes surviving in locations further north, such as Philadelphia and New York, which suffered major yellow fever outbreaks in the past. One model predicts Ae. aegypti could spread as far north as Chicago by 2050.

Although the mosquito lives in the U.S. already, yellow fever cases are exceedingly rare within the country because the virus is not present in local populations. That's because of an international campaign that the U.S. spearheaded in the 20th century, which involved researching YFV, eradicating mosquito breeding grounds, and vaccinating people widely.

"If yellow fever virus reestablished itself in our local Aedes aegypti population, then that would be very concerning," Rosser said.

One way yellow fever could return to the U.S. would be via people carrying the virus home with them after traveling to regions where the disease regularly circulates. Local mosquitoes could then catch the virus by biting those infected people, and then pass it on to others.

For local transmission to take hold, "there needs to be significant numbers of infections [passed to locals], and infections among travelers," Judson said. "But … it's in the realm of possibility."

With climate change driving resurgences of yellow fever in more places, and more regions of the U.S. becoming hospitable to the mosquitoes, that reintroduction scenario may become more likely. But some scientists think that even if North American cities saw yellow fever outbreaks, the outcome would likely not be devastating. Infrastructure in wealthier cities could be the difference between a disaster and a manageable health concern.

"There's access to medicines and vaccines; we pipe water to our homes, so we don't have standing water around," Caldwell said. "So it is a concern, but it's never going to be the next COVID."

Other experts noted that diligent surveillance of yellow fever infections can help public health officials prepare. In places where yellow fever is circulating in forest primates, forest conservation can limit contact among humans, wildlife and the mosquitoes that spread diseases among them. It's also crucial to make vaccines widely accessible to people who live in the virus's endemic regions and to travelers who visit those regions.

The WHO's yellow fever campaign is set to conclude at the end of this year, and its next steps are unclear. There's ongoing discussion of what comes next, Judson said, with questions about whether the control of yellow fever outbreaks will rely more on national strategies than on international coordination via the WHO.

Whatever happens, this is a time for heightened awareness of the virus, Judson said.

"We think of yellow fever as this historic disease," he said. "I think many people don't realize that we're still seeing significant yellow fever outbreaks. … It's really important to be aware of the risks and think about how we prepare for that."

This article is for informational purposes only and is not meant to offer medical advice.

Editor's note: This is a developing story and may be updated.

Michigan has reported two deaths in its ongoing Cyclospora outbreak, a wave of parasitic infections that has affected over 11,000 people in the state.

Since early May, 193 people in Michigan have been hospitalized with cases of Cyclospora cayetanensis infection, called cyclosporiasis. The parasite can enter the body when someone consumes food or water contaminated with the organism, and the cases in Michigan have been linked to iceberg lettuce sourced from central Mexico.

These two deaths are the first reported in the Michigan outbreak, as well as the first deaths documented in any of the ongoing Cyclospora outbreaks in the United States.

Multiple outbreaks have been detected in the country in recent months, but not all have been linked to a specific source of exposure, such as lettuce. Since May, the Centers for Disease Control and Prevention has confirmed over 6,700 cases of cyclosporiasis acquired within the U.S. (In some states, case counts are typical of what's usually seen this time of year, while in others, case counts are higher than normal.)

Regarding the deaths in Michigan, "according to medical records, both individuals had significant underlying health conditions that may have been impacted by cyclosporiasis and dehydration," the state's Department of Health and Human Services (HHS) said in a statement. "No additional information will be provided on these two cases."

Cases of cyclosporiasis range from mild to severe, with severe cases being more likely in young children, older adults, and people with weakened immune systems. Symptoms include loss of appetite, fatigue, low-grade fever, vomiting and diarrhea. The infection is treated with antibiotics, which block the parasite's ability to multiply.

In mild cases, the infection can sometimes resolve on its own, but without treatment, the symptoms can linger for over a month. Severe and prolonged infections can raise the risk of dehydration due to vomiting and diarrhea. Severe dehydration can then cause various complications, such as electrolyte imbalances and hypovolemia (severe fluid loss).

While these complications can be dangerous — causing kidney failure or shock, for instance — cyclosporiasis is not usually life-threatening. For instance, over 2,200 cases were reported in the U.S. between 2011 and 2015, but there were no associated deaths.

"Death resulting from cyclosporiasis is uncommon in the United States," Michigan HHS representatives noted in the statement.

This article is for informational purposes only and is not meant to offer medical advice.

LONDON — In the packed halls of the recent Alzheimer's Association International Conference in mid-July, over 10,000 experts in brain research discussed strategies to beat dementia. But in one room, attendees gathered to watch a video from a nonscientist named Isabel Beltre, whose life was transformed by a recent trial.

Beltre was one of 1,200 participants ages 60 to 77 who took part in the Latin American Initiative for Lifestyle Intervention to Prevent Cognitive Decline (LatAm-FINGERS), the first trial to test a culturally adapted lifestyle intervention to prevent cognitive decline in Latin America. Rather than attempting to treat dementia after it has developed, the trial tackled risk factors that raise the likelihood of the condition, like smoking and a sedentary lifestyle.

In her native Spanish, Beltre thanked both God and the project for its impact on her life. There was a celebratory air in the conference room as the trial's results were released. The lifestyle interventions, which included exercise programs and brain training, had statistically improved participants' thinking skills, compared with a control group who received only bare-bones support, like general health advice.

Trials like LatAm-FINGERS — including a related U.S.-based trial called the POINTER study — ultimately aim to cut rates of dementia around the world. The LatAm trial is the most successful of these trials to date, raising hopes that this approach could help to prevent dementia en masse.

Whether that promise pans out remains to be seen, though, experts told Live Science.

The lifestyle factors that increase dementia risk

When it comes to dementia prevention, few guidelines are as influential as those written by the Lancet Commission, an expert-led review of the available evidence on dementia. Three editions of this review have provided comprehensive overviews of risk factors; the most recent, published in 2024, identified 14 factors, including smoking, infrequent social contact, and a lack of physical activity.

The commission estimated that, together, the identified risk factors contribute to 45% of dementia cases at a population level.

Long before the 2024 report, Dr. Miia Kivipelto, a professor of clinical geriatrics at the Karolinska Institute in Sweden, wanted to tackle these risk factors at the individual and population level in her work as a medical doctor and epidemiologist.

"I felt that I wanted to move on to interventions to really show that if you do something, you can change the risk," Kivipelto told Live Science.

The many contributing factors that lead to cognitive decline, and ultimately dementia, couldn't be tackled in isolation, Kivipelto realized. She designed a trial in her native Finland, called the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) study, that would aim to tackle many risks simultaneously.

The two-year project recruited 1,260 participants ages 60 to 77 and divided them into two groups. The first group received general health advice, such as tips on healthy eating and exercise, at the start of the study and then again after six and 12 months.

The other group additionally received a multipart intervention consisting of meetings with nutritionists to discuss personalized meal plans, brain training, exercise programs, social activities, and metabolic and vascular tests. These programs lasted throughout the study period, with the brain training alone including 144 sessions over 12 months of the study.

At the end, the two groups' cognitive skills, such as thinking speed and memory, were tested; the trial did not track dementia rates, only overall cognition. In both groups, these skills improved by the end of the study. But the headline finding was that in the group given the comprehensive intervention, overall brain function was judged to be 25% stronger than in the control group.

What did that difference mean in concrete terms? It turns out, the improvement was relatively small.

It was calculated in terms of a statistical measure called a z-score, which represented the extent of the improvement in brain-function test scores in each group. In the end, the difference in z-scores between the two groups was just 0.04 points, which a 2021 review defined as "small."

However, Kivipelto maintained that the improvement is significant. "It's as big as anti-amyloid treatments," she said.

Several drugs approved by the U.S Food and Drug Administration for the treatment of Alzheimer's disease target amyloid, a protein that forms unruly tangles in the brain. These drugs have been reported to marginally slow the disease's progression, but statistically, their overall effect is small.

Targeting those most at risk of dementia

Despite criticism of the trial's moderate effects, Kivipelto's FINGER intervention has since been repeated all over the world, including by the U.S.-based POINTER study, and, most recently, LatAm-FINGERS.

Dr. Gill Livingston, a psychiatrist at University College London who led the 2024 Lancet Commission report, told Live Science that the data from these trials shows that dementia interventions need to be tailored to the risks the participants actually face.

In the POINTER study, 70% of the participants had a college degree, compared with roughly 43% of the wider U.S. population. "People who are usually in randomized controlled trials are usually highly educated people who are very interested in health," Livingston noted. "And that means they're at less risk of developing dementia, and therefore, less can be done to help them" through lifestyle interventions.

The difference between the test group and the control group in the POINTER study was even smaller than in the original FINGER trial — just 0.029 points.

LatAm-FINGERS tried to maximize flexibility in its approach by better tailoring its interventions to its study participants, said study first author Dr. Lucía Crivelli, a neuropsychologist at the neurology center FLENI in Argentina. Dietary advice reflected the produce available in each region. Exercise programs considered local environmental factors; for example, sessions were held outside, avoiding hot gyms during the sweltering summers in Ecuador and Mexico.

The trial recruited volunteers across Argentina, Brazil, Bolivia, Chile, Colombia, Costa Rica, Ecuador, Mexico, Peru, Puerto Rico, the Dominican Republic and Uruguay. The participants were less highly educated than the POINTER cohort had been; 37% had no education beyond a high school diploma, compared to just 5% in the POINTER study. That likely made the study participants more representative of people who might benefit from the trial's interventions.

When Crivelli announced the results of the trial at the conference, a large cheer filled the room. The intervention had achieved a difference of 0.11 points between the test and control groups' z-scores — more than twice the difference seen in the FINGER trial.

That difference corresponded to a relative 55% improvement in overall brain function in the test group compared to the control group at the end of the study.

What made the difference?

Crivelli, Kivipelto and Livingston all pointed to one key factor in explaining the project's relative success. "In Latin America, there are more modifiable risk factors," Kivipelto summarized.

The study participants had lower academic attainment and higher cardiometabolic risk factors, such as high BMI, than the participants in previous studies. The trial had reaped the rewards of delivering the intervention to people who needed it most, experts concluded.

But the approach wasn't perfect. said Dr. Claudia Suemoto, a neuroscientist at the University of São Paulo who presented a detailed breakdown of the trial's results. They found that the intervention didn't improve men's overall cognitive ability, compared with the control group. Only women benefited.

The difference may be that men simply didn't engage in the trial as much as women did, Suemoto's data suggested. Livingston pointed to the trials' exercise classes as an example of an activity that men may not be as likely to participate in, although that's an assumption rather than being based on the trial data.

Can we really prevent dementia?

The LatAm-FINGERS results show that addressing the dementia risk factors that people face is the most effective way to prevent dementia, Livingston said.

And Livingston is leaning into the idea. She's planning a dementia prevention trial in the U.K. that will ask participants about their risk factors and then give them tailored interventions based on the risks they can realistically avoid.

"We ask them to choose which ones they want," Livingston said. "If somebody doesn't want to stop drinking or smoking, then they're not going to."

While LatAm-FINGERS has been the most successful of the FINGER trials to date, it's still unclear whether such projects actually reduce dementia rates.

Only two previous prevention trials have attempted to measure dementia incidence, and neither saw a notable change in their test group. That said, neither trial included cognitive training interventions like FINGER did; they instead focused on cardiovascular risk factors, such as low exercise rates and high body weight.

Measuring changes in dementia rates requires trials much longer than two years, and they also need massive recruitment. Implementing an intensive study like LatAM-FINGERS in the wider community "is not practical," Crivelli said. Instead, she said the study's interventions would need to be distilled into their essential parts so that they could be implemented at scale.

Kivipelto is optimistic that advances in Alzheimer's screening, including new blood-based tests, could provide an early biological measure to show that FINGERS-style interventions can help stave off dementia. This would be an indirect measure but wouldn't require as long a trial as tracking dementia rates.

Some of the risk factors the Lancet Commission identified, like air pollution, can't be modified at an individual level, Livingston noted. A combination of personal and governmental change could address this, she said, as it has in the realm of infectious-disease prevention.

While the scientific field still has uncertainty about the scale of change that trials like FINGERS can bring about, Beltre has little doubt about the trial's impact.

While she previously relied on help from family members like her grandson to complete everyday activities, she said, "I do everything myself now."

This article is for informational purposes only and is not meant to offer medical advice.

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LONDON ‪—‬ New blood tests for Alzheimer's disease aim to catch the condition in its earliest stages. Scientists hope that, someday, by spotting very early signs of dementia and enabling earlier treatments, these tests could significantly improve patients' prognoses.

But how well do current blood tests work for that purpose?

At the Alzheimer's Association International Conference in London on July 12-15, Live Science spoke with researchers and clinicians who study and use blood tests for Alzheimer's disease. Here's their take on the current state of these tests and their practicality for real-world use

Scientists' big hopes for the tests

People diagnosed with Alzheimer's disease face an incurable condition, but their outlook is marginally more hopeful than it was 10 years ago. That's because the first "disease-modifying" drugs for Alzheimer's, which target the disease's causes rather than its symptoms, have been approved in recent years.

These drugs, which include the lab-made antibodies lecanemab and donanemab, only slow, rather than stop, the progression of the disease. However, researchers hope these medicines could be the precursors to more effective treatments.

Alzheimer's disease researchers hotly debate the exact causes of the condition, but they are united on the idea that early intervention is likely to produce the best possible outcome for patients. The aim is to remove disease-linked proteins before they can damage the brain.

That's why new blood tests for Alzheimer's disease, some of which have been approved in the past year, are exciting so many scientists. These tests, which measure chemical signals of the disease circulating through the bloodstream, are currently paired with other clinical exams to provide an accurate Alzheimer's diagnosis for patients with early symptoms, such as subtle changes to memory or personality.

The hope is that if these patients could be identified at this stage, they could access clinical trials and treatments when they might be the most helpful.

What do Alzheimer's blood tests measure?

The U.S. Food and Drug Administration (FDA) has approved two blood tests for Alzheimer's disease: Roche's Elecsys pTau181 assay and Fujirebio's Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio test.

An additional test from Roche (the Elecsys pTau217 test) has received a basic safety certification in the European Union and U.K., which allows it to be sold but is not equivalent to FDA approval. This test is not approved in the U.S. yet. A second test from Fujirebio (the Lumipulse G pTau 217 Plasma assay) is in the same boat.

Plus, there are a host of other tests made in specific clinical laboratories; these are not FDA-approved but they are available in certain specialist clinics.

All of these tests in varying stages of approval measure "a core part of the pathology of Alzheimer's disease in the brain," said Dr. Sebastian Palmqvist, a clinical neurologist at Lund University in Sweden. These include two proteins that build up in the brains of Alzheimer's patients: tau and amyloid.

The Elecsys tests and the FDA-approved Lumipulse test measure levels of tau in the blood, while the other Lumipulse test measures the ratio of tau to amyloid. Both measurements can be used to indirectly assess the presence of amyloid plaques, sticky deposits in the brain that are associated with the disease's progression.

It's important to note that the blood tests alone aren't diagnostics for Alzheimer's disease, said Dr. Jemma Hazan, an old-age psychiatrist at University College London. Instead, "the test is telling you whether you have certain abnormal proteins in your brain." This, she said, makes it important to use the test in a setting where patients can be properly directed to the next steps of diagnosis and treatment.

How are Alzheimer's disease blood tests used?

Currently in the U.S., Alzheimer's blood tests are approved for use only for adults ages 55 and older who have signs of cognitive impairment, like memory problems. Palmqvist said these tests are best used by specialists with knowledge of dementia, such as doctors in memory clinics. They aren't approved for use by primary care doctors in the U.S.

"The clinicians working there [at memory clinics] have many, many years of experience of interpreting these types of biomarkers," he explained.

Before the advent of these blood tests, memory clinics had to rely solely on expensive brain scanning technology or invasive lumbar punctures to identify physical signs of Alzheimer's disease. The new tests greatly simplify diagnosis, Palmqvist said, but they still need to be used in combination with other tests.

So currently, if a patient receives a positive blood test, they must undergo further cognitive testing, brain scans or invasive biomarker analyses to confirm the diagnosis.

While for now the blood tests are best used by specialists, data that Palmqvist presented at the conference suggested that access to a blood test result may improve a primary care physician’s diagnostic accuracy to levels closer to a memory clinic specialist's. That hints that the test may eventually be usable in primary care, without more invasive diagnostics.

How well do the approved Alzheimer's tests work?

In clinical trials, the approved Lumipulse test had a sensitivity of 97.6% and a specificity of 90.8%. Sensitivity refers to the percentage of people who do have amyloid in their brains that test positive — so it's the rate of true positives. Specificity refers to the percentage of healthy people who test negative, meaning true negatives.

However, the test was recalled in February because it returned an unusually high percentage of false-positive results when it was used in the real world, compared to clinical trials. Palmqvist said there's now a newer version of the same test that avoids this problem.

Analyses comparing pTau217 and pTau181, the two tau biomarkers that Roche uses in its tests, have concluded that pTau217 is a more accurate indicator of Alzheimer's disease. That means it more closely matches results from gold-standard amyloid brain scans.

Dr. Ashton Harper, global medical affairs lead for neurosciences at Roche Diagnostics, said the Roche pTau217 test correctly spotted Alzheimer's-linked proteins 96.1% of the time and accurately ruled out that pathology 94.7% of the time in trials. By comparison, pTau181 — the Roche test approved in the U.S. — correctly identified Alzheimer's pathology 83.6% of the time and ruled out pathology in healthy brains 72.2% of the time.

Patients who take this more-accurate test are given one of three possible results based on two cutoff points, Harper said. If their tau level comes back above the upper cutoff — giving a positive result — clinicians can be "highly certain" that the patient has disease-linked amyloid in their brain, he said.

Below the lower of the two cutoffs, clinicians can be confident that their patient doesn't have any disease-linked amyloid in their brain. If the reading comes back in between the two cutoffs, though, the result is uncertain.

Current guidelines set by the Alzheimer’s Association require that patients end up in that gray area no more than 20% of the time, and the pTau217 test meets that requirement, Harper said. As with patients who get a positive test result, patients who receive these uncertain results are also advised to undergo further testing, such as scans or cognitive tests.

There are other reasons a person without Alzheimer's disease might get a positive test result; rare cases of severe kidney disease, for example, can artificially inflate the test's readings.

Harper said early data suggests that Roche's pTau217 test is roughly as accurate at detecting Alzheimer's disease proteins in cognitively unimpaired people as it is in those with symptoms. This may someday open the door to prevent Alzheimer's in patients who have not yet developed symptoms, he suggested, clarifying that Roche's test is not intended for that use yet.

How do Alzheimer's tests actually affect patients' care?

In the U.S., these tests can help patients get a diagnosis more quickly, but treatment options for the condition remain limited.

The approved antibody drugs are available through both private and government insurers, but they still cost the patient thousands of dollars each month. And again, these drugs only slow, rather than stop, the progression of the disease.

Researchers hope that early treatment with the drugs will enhance their effectiveness, but as of yet, there's no published data to back this idea up.

In the U.K., disease-modifying drugs like the antibodies have not been approved by the U.K.'s National Health Service (NHS) yet. Because the drugs only modestly slow Alzheimer's progression, ultimately, the NHS determined that they were too costly to cover without clearer signs of efficacy. That means British patients cannot access the drug for free.

Still, Hazan said a positive test could be beneficial for patients.

"Diagnostic accuracy is important in its own right so that people feel more certain about the diagnosis and also there are management implications," Hazan said. While they can't access antibody drugs, patients do have access to drugs that help ease the condition's cognitive and behavioral symptoms, as well as non-pharmacological treatments like behavior management.

Diagnosed patients can also access one of the many clinical trials for the condition. It's estimated that 50,000 patients are needed to populate these ongoing trials worldwide.

Hazan and Palmqvist agreed that, despite the blood tests' accuracy, they should not be used to preventively screen for Alzheimer's in people with no symptoms. That's because testing in a wider population, where fewer people will have Alzheimer's disease, naturally increases the number of false-positive results, even while the assay itself retains the same level of accuracy. This could lead many healthy people to be incorrectly diagnosed with Alzheimer's disease, which would cause stress for patients and have significant financial implications for healthcare systems.

Newer tests that are still in development may help reduce the likelihood of false positives by measuring only a subset of tau protein that comes directly from the brain rather than from the rest of the body, Palmqvist said. But for now, mass screening remains a goal, rather than a reality, for these blood-based Alzheimer's diagnostics.

"I think that's the next frontier," Palmqvist said.

This article is for informational purposes only and is not meant to offer medical advice.

See how much you know about the most complex organ in the human body with our brain quiz!

Bats have long posed an immunological mystery: They can harbor viruses that cause severe diseases in other animals, including humans, yet they rarely show signs of illness. Now, scientists have discovered a big clue as to why that is.

Researchers uncovered an unusual feature of bat immunity that could help to explain how these mammals evade infections. Vesper bats, the world's largest family of bats, may possess two separate genetic systems for producing the building blocks of antibodies, the immune proteins that latch onto germs. This configuration has never been found before in mammals.

"It was really surprising," study co-author Hannah Frank, an associate professor of ecology and evolutionary biology at Tulane University, told Live Science. "The only other vertebrates we see something similar in are fish."

The findings, published Wednesday (July 29) in the journal Science Advances, could open new avenues for studying viral infections and the evolution of immunity.

"The study provides a novel view into the evolution and diversity of adaptive immunity in bats," said Daniel Becker, an associate professor of biology at the University of Oklahoma who was not involved in the study. "The duplication seen in vesper bats is really intriguing and suggests that we need more immunological study of this globally distributed family of bats," Becker told Live Science in an email.

'More diversity in their antibodies'

Antibodies are Y-shaped proteins that help the immune system recognize and neutralize foreign invaders, including viruses, as well as other threats, like toxins. Each antibody contains two "heavy chains" and two "light chains," structures that work together to recognize and bind to specific features of viruses, bacteria or other targets.

The tips of the Y shape are responsible for recognizing the targets, while other parts of the antibody help determine how the immune system responds — by blocking pathogens from infecting cells or flagging them for destruction by other immune cells, for instance.

In humans and most other mammals, the genes that build antibody heavy chains are organized into a single region of the genome, called a locus. Cells create a wide range of antibodies by mixing and matching the proteins encoded in different segments of that locus.

But when Frank and her team examined 26 bat species, they found two complete heavy-chain loci located on different chromosomes. The team then showed that both sets of genes were functional and actively used by immune cells to build antibodies. The finding was initially surprising enough that the researchers considered whether it could be an error in how they'd assembled the bats' genomes after sequencing them.

However, Frank's collaborator and former graduate student Dr. Taylor Pursell thought the finding might be genuine, rather than an experimental fluke.

"She said, 'No, Hannah; this is really weird ‪—‬ like, this doesn't happen,'" Frank recalled. "And I said, 'Oh my God; you're right. This is not just an experimental annoyance. This is actually super cool.'"

Using genetic analysis, the team found that one of the two loci contained a larger and more varied collection of gene segments that could be used to create a broad, ready-made repertoire of antibodies. The other had fewer of these building blocks but appeared to rely more heavily on a process called somatic hypermutation, in which antibody-producing cells make small genetic changes after encountering a pathogen.

Those changes can help antibodies become more "customizable" to whatever threatens the immune system, Frank said.

She compared this system to the different layers of defense seen in the 1998 Disney movie "Mulan." Upon seeing invaders at the Great Wall of China, guards raised an alarm to alert others without yet knowing the specific threat; this is like the innate immune system, the body's first, broad line of defense. The adaptive immune system is more like the heroine Mulan: highly targeted and capable of responding to a specific enemy, but slower to develop.

These two layers of immune defense are not unique to bats, but bats' two antibody systems may provide an additional layer of protection.

From each loci, bats can create a "cache of trainable, customizable cells," Frank said. This degree of customization could help the bats immune system ward off a wider range of threats than other mammals can.

"This extra set of genes gives the animals more diversity in their antibodies," said Michael Letko, a molecular virologist at Washington State University who was not involved in the study. "This study suggests bats have more diversity to start with, which may allow for faster and more effective responses from the start of an infection," Letko told Live Science in an email.

Letko added that the genetic analysis in the study was impressive and lends credibility to the results. "It is hard to dispute the validity of information solidly founded on the genetic organization of these bats," he said.

That interpretation remains a hypothesis, though; Frank and her team will need to study how these two systems behave when bats are exposed to viruses before they can determine exactly what advantages they provide.

"We think this discovery is an important piece of the puzzle," Frank said in a statement. "It doesn't fully explain why bats are such effective viral reservoirs, but it reveals a level of immune variety we didn't know existed and gives us an entirely new direction to explore."

Past studies of bat immunity have found that hotter body temperatures and a larger number of virus-filled packages in stem cells could also help bats' tolerate viruses better.

Understanding how bats tolerate viruses could help scientists predict which kinds of bats are most likely to affect human health and how we can mitigate those risks, Becker noted. Separately, bats have a notably low incidence of tumors and cancer, Letko said, and he wonders if their unique immune systems might hold clues as to why.

While bats are often viewed through the lens of the infectious diseases they carry, their story is far more complex, Frank said.

"Let's learn from the guys who've been evolving with them [viruses] for millions and millions of years," Frank said. "But let's try not to villainize them for surviving for millions and millions of years."

An outbreak of parasitic illness linked to iceberg lettuce is affecting nine U.S. states, federal health officials have announced. That's up from the five affected states that were identified in earlier stages of the officials' investigation.

This lettuce-related outbreak is one of several in the U.S. that are being caused by the parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the organism. The federal government has not officially identified a source of contamination in the other Cyclospora outbreaks yet, although some state officials have mentioned potential culprits. (North Carolina officials have pointed to cilantro and parsley, for example.)

The nine-state outbreak linked to iceberg lettuce includes cases in Illinois, Indiana, Kansas, Kentucky, Michigan, Ohio, Oklahoma, Pennsylvania and West Virginia, according to the Food and Drug Administration (FDA). To date, 1,947 people have been infected across these states and reported eating Taco Bell before they got sick. There have been 98 hospitalizations and no deaths.

Data collected by federal officials had previously pointed to shredded lettuce served at Taco Bell as a common source of exposure, and from there, they identified the supplier as Taylor Farms de Mexico. "Taco Bell has indicated they are no longer using lettuce from Taylor Farms de Mexico as of July 17, 2026," the FDA noted.

Specifically, the infections have been linked to lettuce sourced from central Mexico, prompting Taylor Farms to remove all of its iceberg lettuce from that region from the U.S. market. The company has also issued a recall. A complete list of recalled products can be found on the FDA's website.

The recall affects products that were distributed in the nine states listed above, as well as additional states, all of which are listed on the FDA's website. Consumers, restaurants and retailers that purchased or received recalled lettuce are advised to discard it immediately and not consume it.

"We also expect to continue to see the number of confirmed cases rise, despite the recall, due to the fact that it can take as long as six weeks for CDC [Centers for Disease Control and Prevention] and state officials to determine if a sick person is part of this outbreak," the FDA's latest update notes. "FDA will continue to work with federal and state partners to investigate this multistate outbreak and ensure products implicated in this outbreak have been removed from the market."

This article is for informational purposes only and is not meant to offer medical advice.

U.S. health officials have identified shredded iceberg lettuce served at Taco Bell as one source of contamination behind an outbreak of parasitic infections affecting over 1,000 people.

The outbreak has been caused by the protozoan parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the parasite. Since May 1, there have been 1,644 confirmed cases across Indiana, Kentucky, Ohio, West Virginia and Michigan, which is currently the hardest-hit state.

(Health officials are also investigating additional cases of Cyclospora infection in the U.S. that have yet to be linked to this specific lettuce-related outbreak. Those other potential cases remain under investigation and total over 5,100, per the Centers of Disease Control and Prevention (CDC).)

In the five-state outbreak, there have been 94 hospitalizations and no deaths to date.

Through an investigation, health officials found that all 1,644 of the sickened people with confirmed cases of Cyclospora reported eating Taco Bell in Indiana, Kentucky, Michigan, Ohio or West Virginia before becoming ill. Interviews with the affected individuals suggested that shredded lettuce might be a common source of exposure.

The Food and Drug Administration (FDA) then investigated the source of the lettuce, identifying a single supplier of iceberg lettuce from Mexico that was used by Taco Bell locations where the people ate before becoming ill. News reports have named California-based Taylor Farms as the supplier.

"FDA is working directly with the identified supplier to determine if potentially contaminated shredded iceberg lettuce remains on the market," an FDA notice states. "As part of this investigation, FDA and state partners have initiated collection of product samples for testing and analysis."

The investigation is ongoing, and additional sources of contamination or affected restaurants could possibly be identified later, the FDA noted. In the meantime, Taco Bell has said it will stop using lettuce from the implicated supplier.

"Taco Bell is working to stop use of all lettuce implicated by this investigation. Not all Taco Bell locations in these states received implicated product," the FDA statement says.

Currently, the CDC is warning consumers not to eat shredded iceberg lettuce served at Taco Bell locations in Indiana, Kentucky, Michigan, Ohio or West Virginia.

Case counts reported by individual states may differ from the FDA's and CDC's counts, because states may include both probable and confirmed cases. The FDA and CDC will update their totals once they can confirm additional cases reported to them.

Symptoms of Cyclospora infection typically emerge two to 14 days after a person consumes the parasite. These symptoms include watery diarrhea, fatigue, cramping, bloating, gas and loss of appetite, and without treatment, they can last between a few days to a month or more. The infection is treated with an antibiotic, which blocks the parasite's ability to multiply.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: An 83-year-old man in Belgium

The symptoms: The man sought medical attention at a hospital because the muscles on one side of his face had weakened suddenly, causing it to droop — a condition called unilateral peripheral facial-nerve palsy. He had also recently had a fever, which had since resolved.

Tests run by the neurology department found the man had anemia, fatty liver disease and an enlarged spleen. Combined with his recent fever, these findings led the team to assume he had a viral infection. However, he tested negative for a variety of germs, including Epstein-Barr virus, which causes mono; cytomegalovirus; human immunodeficiency virus (HIV); and hepatitis A, B, C, and E.

The man's liver abnormalities hadn't resolved by one week later, but his facial-nerve palsy cleared following a 10-day course of a strong corticosteroid. But then, over the next month, the man's knees and ankles became stiff and painful, and his legs and feet — and occasionally his face, arms and hands — began to swell. He reported feeling generally unwell, he had gained 11 pounds (5 kilograms), and his urine had darkened even though he had been drinking more water than usual. All of these signs pointed to problems with his kidney function.

Besides the conditions uncovered on his recent medical examinations, the patient had long-standing high blood pressure, high cholesterol, an enlarged prostate and chronic obstructive pulmonary disease (COPD), for which he was taking medications. He had also been diagnosed with rectal cancer 20 years beforehand and received various treatments over the years. He and his wife of 50 years had been sexually inactive since that cancer treatment, he told his doctors.

What happened next: After weeks spent in and out of the hospital, the man went to an emergency room after his skin suddenly became intensely itchy. He had a red, scaly rash on his calves. A neurological exam revealed "normal motor strength, sensation, reflexes, coordination, and gait," the doctors wrote in a report of the case.

At the ER, the patient was questioned further about his medical history, at which point he told doctors that, during his military service as a young man, he'd had unprotected sex with multiple casual partners. He reported being treated for various sexually transmitted infections (STIs) during that time but had forgotten the specific diagnoses.

Tests revealed that the patient was anemic and that his urine contained blood and an abnormal amount of protein. Additionally, a test for autoimmune diseases found abnormally high levels of antinuclear antibodies, which target the control centers of cells that house DNA. Because the patient had recently had facial-nerve palsy, the doctors analyzed his cerebral spinal fluid — the clear fluid that surrounds the brain and spinal cord. This revealed elevated levels of white blood cells, which hinted at an active infection.

The diagnosis: While tests for HIV and tuberculosis came back negative, an assay for Treponema pallidum, the bacterium that causes syphilis, was positive, confirming that the patient had an active syphilis infection.

Syphilis infections can progress through four stages, each with different symptoms. If an infected person doesn't get effective treatment during the primary and secondary stages, the bacteria can go latent, sometimes for decades. And in a minority of cases, latent syphilis can awaken and cause a late, or tertiary, infection.

Based on his positive T. pallidum test, rash, general unwell feeling, abnormal liver results, high urinary protein count, leg swelling, facial drooping and swollen lymph nodes, the man's doctors diagnosed him with secondary syphilis with early neurosyphilis, in which the bacteria attack the nervous system.

The treatment: The patient had been given a single injection of penicillin before the test results confirmed that his infection had neurological involvement. He was subsequently given a 14-day course of intravenous penicillin, which is the recommended treatment for neurosyphilis, according to the case report.

The severe itching was treated with antihistamines, and he was prescribed diuretics to reduce the swelling in his legs. The rash, itching and swelling had improved by his one-month follow-up appointment, and his liver tests and urinary output had normalized.

Public health authorities were informed of the patient's diagnosis, and his wife was referred for testing. The case report does not note whether his wife tested positive for syphilis.

What makes the case unique: Secondary syphilis normally occurs within the first year of an untreated infection and only rarely develops after four years have passed. Normally, smooth, hard sores appear on the mouth or genitals during primary syphilis, and once those sores disappear, secondary syphilis sets in within months, if left untreated.

"Although the patient's history of multiple sexually transmitted infections as a young man prompted testing for syphilis, an exposure from that period would not be expected to explain his current presentation," his doctors wrote.

There's a possibility that the man had a latent infection that recently reactivated, perhaps due to the immune-suppressing effect of his recent steroid treatment. But you'd expect the reactivation to cause only symptoms of tertiary syphilis — like nervous system problems — not symptoms associated with secondary syphilis, like fever, rash and weight loss.

Therefore, exactly when the man contracted the infection is uncertain. "A more recent, unreported exposure must be considered," the doctors wrote.

It is also rare for syphilis to affect the liver and kidneys, occurring in less than 10% of cases, according to the case report.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

This article was first published Feb. 18, 2026.

A years-long malaria control campaign in the Brazilian Amazon nearly eliminated the disease from a city — but then cases rebounded. Now, scientists think they've uncovered why.

The campaign took place in northern Brazil during the construction of the Belo Monte Dam in the Xingu River, one of the largest hydroelectric dams in the world. From 2013 to 2017, the initiative slashed annual malaria rates from more than 1,200 cases to fewer than 60. But the program ended, and within a few years, infections had rebounded to more than 700 cases a year. This time, they were concentrated in the rural communities surrounding the river in the city of Altamira.

In a study published Thursday (July 9) in the journal GeoHealth, scientists analyzed 15 years of malaria surveillance records alongside satellite images of forests around Altamira. Earlier studies have pointed to deforestation and dam construction as a driver of malaria because they can provide habitats for mosquito larvae, which inhabit the forest edge. In Altamira, large stretches of rainforest have been cleared for cattle ranching, logging and settlement along the Xingu River in the decades since the region was first opened up by road-building, leaving a patchwork of cleared land pressed up against the remaining forest.

However, the study found that the malaria resurgence wasn't simply a result of how much forest had been cut down. Instead, cases tracked most closely with the forest edge, the boundary where intact forest meets cleared or open land. There, mosquitoes get everything they need to thrive: shade from the tree line, sunlit pools of standing water for their larvae, and people living or working close by.

The findings highlight how the environment contributes to malaria risk, suggesting that maintaining surveillance in these high-risk landscapes could be just as important as driving cases down in the first place.

"What made Altamira compelling was that the timing gave us something rare, close to a natural experiment," study co-author Eloise Skinner, an epidemiologist and postdoctoral research fellow at the University of Queensland in Australia, told Live Science in an email. The results of that natural experiment could help Brazil in its efforts to eliminate malaria from the country in the next decade, she said.

A program tied to temporary funding

The researchers tracked malaria trends before, during and after the construction of the Belo Monte Dam. Before construction began, malaria was already a persistent problem in the region; Altamira city alone reported more than 1,200 cases a year.

As thousands of workers moved in, local health authorities and the dam's developers rolled out an intensive control program that involved spraying insecticides indoors, using mosquito nets, and deploying rapid diagnosis and treatment when cases did emerge. The goal was to head off outbreaks spread by Nyssorhynchus darlingi, the mosquito that carries the malaria-causing parasite in the Brazilian Amazon.

Mosquitoes pick up the parasite that causes malaria by feeding on the blood of infected people, and they can then spread that parasite to others they bite. Treating infected people quickly can help break that chain of transmission.

Cases plummeted despite the influx of workers, but once construction wrapped up and the program lost its funding, malaria came back.

To understand what drove the resurgence, the researchers combined three streams of data. Case records came from Brazil's national malaria surveillance system and covered 150 health centers in Altamira over 15 years. The team layered on temperature, forest cover and rainfall data, since both shape how favorable an area is for mosquito breeding and how efficiently the malaria parasite develops inside mosquitos. Plus, they added an estimate of travel time between each cluster of cases and the nearest town, as a proxy for how easily people and the diseases they carry might move around.

From the observations, the forest edge consistently emerged as the strongest predictor of increased malaria cases. For every 1% increase in the perimeter of the forest edge, malaria cases rose by roughly 0.7%; for every 1% increase in Altamira's population, who are located at the forest edge, cases rose by about 1.4%.

The rebound wasn't evenly distributed. Before the dam was built, most of Altamira's malaria cases came from clusters inside the city itself. Afterward, that pattern flipped: by 2020, the roughly 700 annual cases were concentrated almost entirely in remote, rural clusters near forest edges. Meanwhile, Altamira's urban center stayed comparatively protected, much as it had during construction.

"When the funded program wound down, malaria came back to the communities that are hardest for the health system to reach," Skinner said. "The city stayed protected, most likely because fast diagnosis and treatment are easier to deliver and keep going in a town."

That leaves the same communities exposed twice over, Skinner said. The places that are already the hardest to reach with health services also sit where the ecological risk is the highest.

But this pattern could point to solutions. The resurgence didn't scatter unpredictably. It came back to the same kind of place — rural communities at the forest edge — each time. That's the kind of risk that can be anticipated in the future.

Brazil aims to eliminate locally acquired malaria by 2035. Skinner said Altamira's near elimination of the disease, and its rebound within a few years of the control program ending, is a warning for that effort. When a community contains a strong environmental driver for malaria, like forest-edge ecosystems, stopping a control program short is sure to let the disease climb back.

"Because the resurgence wasn't diffuse, we can predict where malaria is likely to return first," Skinner said. "The message for a 2035 goal isn't only that elimination needs sustained investment. It is that where the environment drives risk, that risk is predictable, and planning for it from the start is what lets the money go where it matters most."

At least 20 people across 17 states have been hospitalized due to severe gastrointestinal illness as more than 1,000 cases of the parasitic infection cyclosporiasis have been reported across the country, the U.S. Centers for Disease Control and Prevention (CDC) reports.

The CDC and the Food and Drug Administration (FDA) are investigating several clusters of the illness in Illinois, New York, Pennsylvania and Texas, according to CNN. However, the worst-hit state so far is Michigan, with 1,251 cases reported as of July 9, the Michigan Department of Health and Human Services (MDHHS) reported. According to the Associated Press (AP), this marks the biggest cyclosporiasis outbreak in the state's history.

Cyclosporiasis is a gastrointestinal illness caused by the protozoan parasite Cyclospora cayetanensis, which can enter the body when someone consumes food or water contaminated with the parasite. It then infects the small intestines, invading epithelial cells that line the gut, causing inflammation and leading to watery and often "explosive" diarrhea, according to the CDC. Symptoms usually kick in around a week after infection and can last over a month without antibiotic treatment. While the illness can go away on its own, it is also common for symptoms to disappear for a bit and then return.

Cyclosporiasis is not usually life-threatening, but it can cause severe illness and dehydration, particularly in young children, older adults and people with compromised immune systems. In rare cases, the condition may lead to complications like biliary disease, in which the flow of bile gets blocked and impacts the liver and digestive health, according to the MDHHS.

As of July 1, there was no evidence of a single, multistate outbreak of cyclosporiasis, but the CDC is investigating several clusters. According to an email from the health agency, many of the clusters appear to be linked to Mexican-style restaurants, a chain of grocery stores and a catered event, CNN reported. The FDA is conducting trace-back investigations on white and green onions, cucumbers and cilantro, according to CNN.

Meanwhile, the MDHHS warned that, while the source of the current outbreak is still uncertain, previous Cyclospora outbreaks have been linked to contaminated fresh produce, including raspberries, basil and bagged salad.

Cyclosporiasis cases tend to rise during the spring and summer, with May 1 to Aug. 31 considered "cyclosporiasis season," according to the CDC. However, there have been more cases than usual this year: Whereas Michigan typically reports 50 cases over a whole year, the state has seen over 1,000 cases in just a few weeks, the AP reported.

Compared with outbreaks of E. coli and Salmonella, clusters of Cyclospora are much harder to trace back to their source. This is because the parasite can reproduce sexually, meaning its genetic material is mixed up with each generation, according to Charles River Laboratories. However, Dr. Natasha Bagdasarian, Michigan's chief medical executive, told the AP that "there is clearly a linked outbreak happening right now."

To minimize your risk of becoming infected with Cyclospora, wash all fruits and vegetables thoroughly before eating them; cut away any bruised or damaged areas; and refrigerate cut, peeled or cooked produce as soon as possible, the Michigan Department of Agriculture and Rural Development recommends. If you are experiencing sudden gastrointestinal issues, health officials suggest you visit your local health care provider.

This article is for informational purposes only and is not meant to offer medical advice.

The hantavirus outbreak that struck a cruise ship in April, killing three people and sparking fears of further spread, is over, the World Health Organization (WHO) has announced.

"Today, the final contact of a person exposed to hantavirus on the cruise ship MV Hondius completed their quarantine period, tested negative and returned home. No further cases have been reported since the 25th of May," Tedros Adhanom Ghebreyesus, the WHO's director-general, said in his opening remarks at a news conference Thursday (July 2). "We are therefore very pleased to say that WHO considers the outbreak of hantavirus over."

The total number of cases linked to the outbreak was 13. All those affected were either passengers or crew on the ship.

The outbreak began aboard the Dutch-flagged cruise ship MV Hondius after it departed southern Argentina on April 1. It involved the Andes virus, the only known hantavirus that can spread between people.

Hantaviruses are rodent-borne viruses that are found in the Americas, Europe and Asia and spread to humans relatively rarely, usually via contact with the urine, droppings or saliva of infected rodents. The Andes virus, however, has sparked short chains of human-to-human transmission in the past.

Before public health authorities were informed of the cases on MV Hondius, several dozen people disembarked the vessel on the island of St. Helena. To find them, authorities launched an international contact-tracing operation, tracking down more than 650 contacts in total who were then followed by health authorities in 33 countries and territories, according to the WHO.

Additionally, health authorities coordinated the monitoring, care and transport of the remaining passengers and crew aboard MV Hondius.

Of these contacts, those considered at the highest risk of infection were then quarantined and monitored for up to 42 days, because sometimes, hantavirus symptoms don't show up until weeks after exposure to the virus. Depending on their jurisdiction and degree of exposure, some contacts quarantined at home while others stayed in specialized facilities.

The initial unchecked travel of some contacts, alongside the virus's long incubation period, prompted concern from the public that the cluster of cases could explode into an enormous outbreak, or even a global pandemic. Many infectious-disease experts emphasized that the Andes virus does not spread easily between people and that the containment effort was going well, so the risk of a large outbreak was low. Still, some experts raised concerns that the international travel of contacts could trigger pockets of the deadly disease, and some argued that the Andes virus does have "pandemic potential."

Now, with the final contact having completed their quarantine period and no further cases reported, the WHO has declared the outbreak over. All of the contacts who were repatriated to the U.S. completed their quarantine period by June 21.

"WHO will continue working with governments and partners to advance our understanding of this outbreak and of hantavirus more generally," Tedros said. "We are also coordinating a study involving 21 countries to understand how the disease develops, which will support the development of diagnostics, therapeutics and vaccines for future outbreaks."

Besides rigorous contact tracing, the WHO credited the coordinated actions of national public health bodies as being vital to preventing the further spread of the disease. These measures included the response of the Spanish government, which created a safe zone on the island of Tenerife for the ship's remaining passengers to disembark before they were repatriated under quarantine.

As the hantavirus outbreak concludes, there's an ongoing Ebola outbreak in the Democratic Republic of the Congo and an outbreak of the Marburg virus in Uganda. These and future outbreaks will require similarly robust international cooperation, the WHO emphasized.

"The outbreaks of hantavirus, Ebola and Marburg all show why there is no alternative to international cooperation in the face of international threats," Tedros said. "No country alone can fight."

This article is for informational purposes only and is not meant to offer medical advice.

An 11-year-old boy in Ontario, Canada, has died after being bitten by a rabid bat that was resting on his face as he slept. The boy had no obvious bite or scratch marks and didn't show symptoms for the first 19 days after the incident, his doctors report.

While on vacation with his parents at a cottage in northern Ontario in 2024, the boy was woken up in the night by a bat on his nose and mouth, according to a report published in the Canadian Medical Association Journal on June 29. His father caught the bat in a cooking pot and released it outside, and because the child had no visible injuries and the bat did not seem to be particularly aggressive, his parents decided not to seek a medical assessment, the report noted.

A few weeks later, the child began to experience tingling, numbness and swelling on the right side of his face. When he was examined at his local hospital his vital signs appeared to be normal, aside from an elevated heart rate and white blood cell count.

The next day, the boy's symptoms worsened: he lost feeling in the right side of his face and his speech was beginning to slur. While waiting in hospital, he developed a fever, confusion, hallucinations and difficulty swallowing, followed by excessive production of saliva.

After four days in intensive care at McMaster Children's Hospital in Hamilton, Ontario, the child tested positive for rabies, and after five days his brain stem reflexes were absent, indicating a total loss of brain stem function. Seventeen days after admission, following a consultation between his family and medical experts, he was taken off life support and died.

Rabies is a viral disease that primarily affects the central nervous system, according to the CDC. It is mainly spread through bites and scratches from infected animals, with bats accounting for the majority of cases in North America, according to the boy's doctors.

"Bats pose a particular risk because bites or scratches may be small and are easily overlooked, and patients may not recollect or recognize a bat exposure," the medical team wrote in their report.

According to a report in the Journal of Virology in 2013, silver-haired bats (Lasionycteris noctivagans), are responsible for the majority of rabies cases in Canada. Skunks, foxes and raccoons also often carry the disease.

The rabies virus must travel to the brain before symptoms can occur, but once a patient develops symptoms the infection is almost 100% fatal, with most deaths occurring within one to two weeks of symptom development. However, prompt treatment after exposure — including wound cleaning, antibody administration and a series of vaccines — is nearly always effective at preventing the disease, according to the CDC.

Rabies in humans is very rare in North America, with fewer than 10 deaths reported in the U.S. every year, according to the CDC. In Canada, only 28 human fatalities have been reported since 1924, according to the Canadian Veterinary Medical Association. Even so, the boy's doctors have emphasized the importance of prompt medical attention following exposure to bats and other animals that could carry the disease.

"Early recognition of exposure and timely PEP [postexposure prophylaxis] remain the only effective means of rabies prevention," they wrote. "Any direct human contact with a bat, even in the absence of a visible bite or scratch, is an indication for PEP."

They added that rabid bats do not always display the classic symptoms commonly associated with rabies, such as aggressive behavior and frothing at the mouth. "Any direct human contact with [a] bat is considered high risk," they added.

This article is for informational purposes only and is not meant to offer medical advice.