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The post Could a Popular Joint Supplement Increase Alzheimer’s Risk? appeared first on Knowridge Science Report.

Alzheimer’s disease is the most common cause of dementia, affecting millions of people worldwide. It gradually damages brain cells, leading to memory loss, confusion, difficulty with daily activities, and changes in thinking and behavior. As populations continue to age, the number of people living with Alzheimer’s is expected to rise sharply in the coming decades, […]

The post Simple Blood Test Could Help Doctors Detect and Track Alzheimer’s Disease appeared first on Knowridge Science Report.

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For five years, an elderly woman with advanced Alzheimer’s disease had spoken mostly in single words, needed help walking, and showed little spontaneous interaction with the people around her. Then, roughly 19 hours after receiving a high dose of psilocybin-containing mushrooms, she emerged from a prolonged, deep sleep-like state and began talking about her life.

The striking episode, described in a new case report published in Frontiers in Neuroscience, does not show that psilocybin reverses Alzheimer’s disease. The researchers are careful to stress that this was a single patient, observed in a real-world private clinical setting without brain imaging, formal sleep monitoring, or standardized cognitive testing.

Still, the study’s authors say the case raises the interesting possibility that in late-stage dementia, some functional abilities may indeed remain dormant rather than be completely lost.

“Advanced Alzheimer’s disease is generally regarded as a stage of irreversible functional decline,” researchers write. “This case documents transient multidomain functional improvement in advanced Alzheimer’s disease following psilocybin administration.”

The case involved a Japanese-American woman in her 80s with a 10-year history of Alzheimer’s disease. The patient was described as being in an advanced stage of dementia, with the previous five years being noted for severe decline.

Her speech had become mostly monosyllabic, and she had chronic urinary incontinence, executive dysfunction, dysphagia, dependent mobility, flat affect, prolonged somnolence, and a severe reduction in spontaneous communication.

Her diagnosis had been made clinically about a decade earlier, based on a steadily progressive neurodegenerative course, memory impairment, language reduction, executive dysfunction, and functional decline.

The intervention was a single oral dose of 5 grams of psilocybin-containing mushrooms from the “Enigma” strain. Researchers note that no established psilocybin dosing framework exists for advanced dementia, and the dose was high by almost any comparison.

Recreational users commonly describe 1 to 3 grams of dried Psilocybe cubensis mushrooms as a typical range, while doses around 3.5 grams or more are generally considered strong. A 5-gram dose is often treated as an especially intense experience. However, direct comparisons are imprecise because psilocybin content can vary widely between mushroom species, strains, batches, and even different parts of the same mushroom.

The study also notes that the dose was “relatively high compared with dosing approaches commonly used in modern clinical trials,” which typically use carefully measured amounts of purified psilocybin rather than whole mushrooms.

One month later, after some improvements persisted, the patient underwent a second supervised session using 3 grams.

The first session produced a dramatic acute response. The patient experienced autonomic activation, profuse sweating, suspected hyperthermia, and what the researchers describe as a prolonged deep sleep-like state. Exact temperature measurements were not available.

The study’s timeline shows that the first 12 hours were dominated by autonomic and sleep-like effects. At about 19 hours, the patient spontaneously awakened and produced roughly four hours of autobiographical speech.

By the first day, she showed increased alertness and recognition of family. By the second day, she was independently walking. By days two and three, she was dressing herself and showing spontaneous initiative. Around the same time, her diapers remained dry, including at night.

The improvement in continence was particularly notable to researchers because urinary control depends on more than a single simple reflex. It requires awareness of bodily signals, executive inhibition, and coordination among brain networks affected by dementia. The report states that the patient remained continent one month after the initial session, which was one reason a second session was performed.

During that second session, the patient reportedly remained more verbally expressive and described positive imagery involving surfing with her son on a peaceful island.

Researchers also observed improved facial expressivity, emotional reciprocity, spontaneous humor, and greater agility while walking. At one point during follow-up, the patient spontaneously said, “It is pleasant to come here.”

The study’s broader importance is in what it may suggest about the brain in advanced neurodegenerative disease. Alzheimer’s is usually understood as a progressive condition in which neurons and networks progressively deteriorate, stripping away memory, communication, mobility, and autonomy. By the advanced stage, treatment is largely supportive, and meaningful functional recovery is generally considered unlikely.

Psilocybin, however, is known to transiently alter large-scale brain dynamics via activation of the serotonin 5-HT2A receptor. Researchers point to prior human neuroimaging studies showing changes in default mode network integrity, network segregation, and functional connectivity after psilocybin administration. They also cited preclinical research suggesting psychedelics may promote structural and functional plasticity, including dendritic growth and synaptic remodeling.

That does not mean psilocybin repaired the patient’s Alzheimer’s disease. Instead, researchers suggest a more measured interpretation. The drug may have temporarily altered brain network activity, allowing remaining functional systems to reintegrate or become accessible again, at least for a limited period.

The report does not claim that plaques, tangles, or neurodegeneration were reversed. It also does not show that other patients would experience similar results. Because this was a single case, there was no control group, no placebo comparison, no formal biomarker confirmation, and no standardized cognitive testing to measure the degree of change.

Researchers acknowledge that mixed or alternative neurodegenerative contributions, including vascular components, cannot be fully excluded. Although they found no evidence of acute delirium, intoxication, or another acute neurological diagnosis during the observation period, the case remains observational. Causality cannot be established, and fluctuations in neurodegenerative disease cannot be completely ruled out.

The safety picture is also incomplete. While no severe persistent adverse effects, prolonged agitation, clinically significant cardiovascular instability, persistent psychotic symptoms, delayed neurological deterioration, or delayed medical complications were observed during follow-up, the acute phase included suspected hyperthermia and profuse sweating. In frail elderly patients, especially those with advanced dementia, such responses could carry serious risks.

For that reason, the findings should not be read as a green light for unsupervised psychedelic use in dementia patients. Psilocybin is still a powerful psychoactive compound, and older adults with complex neurological disease may be especially vulnerable to complications.

Ultimately, the value of the report doesn’t lie in providing a treatment recommendation but in documenting an unusual clinical observation that researchers say warrants controlled investigation.

The case also lands amid a flood of scientific interest in psychedelics as tools for studying brain plasticity, perception, memory, and large-scale network dysfunction.

As The Debrief has previously reported, recent brain-imaging work has found that psilocybin can temporarily dissolve familiar brain-network patterns tied to the sense of self, while other studies suggest psychedelics may redirect visual processing toward memory-related regions. Additional research has analyzed how a single dose of psilocybin may produce lasting brain changes, how the compound can reshape neural pathways associated with depression, and how psychedelic effects may be influenced by factors such as exercise, food restriction, and immune signaling.

However, most clinical work with psilocybin has centered on psychiatric conditions such as depression, anxiety, PTSD, and substance use disorders.

More recently, researchers have begun asking whether similar neuromodulatory effects might have relevance for people with mild cognitive impairment or early Alzheimer’s disease.

Published clinical data involving advanced dementia remain extremely limited, which is why the new report is best understood not as evidence of a treatment, but as a provocative case study that may help guide future controlled research.

This recent case does not prove efficacy, but it questions assumptions about what may remain possible in a brain already deeply affected by Alzheimer’s disease.

If future studies find similar effects under supervised conditions, the implications could be significant, not only for dementia care but also regarding understanding how much latent function can persist beneath the outward appearance of severe decline.

“Residual functional capacity may persist in advanced Alzheimer’s disease and may become transiently accessible following psilocybin induced modulation of large-scale brain networks,” researchers conclude. “Systematic investigation is warranted.”

Tim McMillan is a retired law enforcement executive, investigative reporter and co-founder of The Debrief. His writing typically focuses on defense, national security, the Intelligence Community and topics related to psychology. You can follow Tim on Twitter: @LtTimMcMillan.  Tim can be reached by email: tim@thedebrief.org or through encrypted email: LtTimMcMillan@protonmail.com 

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Brown rot is a common fungal disease in the Southeastern United States that affects stone fruits like peaches, cherries, and plums. Monilinia fructicola is a tan, fuzzy fungus that grows on tree flowers, twigs, and fruit, and is the most common cause of brown rot. Once brown rot infects a tree, the damage is irreversible, causing significant crop losses in commercial orchards. Farmers try to control the spread of M. fructicola by applying chemical sprays, called fungicides, to fruit trees in the spring.

In M. fructicola, a biosynthesis gene named MfCYP51 encodes a major protein critical to the fungi’s survival. Certain fungicides, called demethylation inhibitor (DMI) fungicides, stop M. fructicola from growing by targeting this protein. Over the last 20 years, DMI fungicides have become less effective against brown rot as M. fructicola becomes more resistant. 

Living microorganisms and their metabolites can control fungal diseases as an alternative to chemical fungicides, known as biofungicides. Many bacteria produce compounds like hydrogen cyanide and pyrrolnitrin that damage fungal cells. However, scientists have not found a biofungicide suitable for commercial production.​ A group of researchers at Clemson University in the USA and Huazhong Agricultural University in China set out to test whether the soil bacteria Pseudomonas chlororaphis and Bacillus subtilis could be effective biofungicides against brown rot. 

The researchers performed an incubation experiment to analyze how the fungal cells make their critical protein from the MfCYP51 gene, a process called gene expression, under different fungicide treatments. They used 3 M. fructicola strains sensitive to traditional DMI fungicides and 3 resistant strains. They tested these with 5 different fungicide treatments: a DMI fungicide, a mixture of P. chlororaphis metabolites, a mixture of living B. subtilis cells, a DMI fungicide + P. chlororaphis metabolites, and a DMI fungicide +  B. subtilis cells. They also set up a control treatment with sterile water instead of fungicide.  

After 6 hours, the researchers extracted the molecule that measures gene expression, called RNA, from the fungi. They found that both the P. chlororaphis treatment and the DMI fungicide + P. chlororaphis treatment substantially reduced MfCYP51 expression in both the sensitive and resistant isolates compared to the controls. In contrast, the DMI fungicide, B. subtilis, and DMI fungicide + B. subtilis treatments increased MfCYP51 expression in the resistant isolates. The researchers concluded that P. chlororaphis has a unique ability to reduce gene expression, unlike other biofungicides.

​To further investigate how the biofungicide treatments work, the team tested whether P. chlororaphis and B. subtilis produced the anti-fungal metabolite pyrrolnitrin. They added 1 milliliter of each treatment to a machine that separates and identifies liquid compounds using high pressure, called a high-performance liquid chromatograph. They found that the P. chlororaphis treatment contained pyrrolnitrin, so they hypothesized that it was responsible for reducing gene expression.

Additionally, the researchers tested their 5 treatments on brown rot in fruit. For each treatment, they took 10 Gala apples, washed and sterilized their surfaces, and sprayed them with the fungicides. After 24 hours, they poked holes in the apples with toothpicks and added 20 microliters of liquid containing M. fructicola cells to the poked holes. They placed the apples in a humid chamber for 5 days and measured the number and size of brown rot spots that developed on their surfaces. 

Despite decreasing MfCYP51 expression, ​the researchers found that P. chlororaphis treatment alone didn’t reduce brown rot disease compared to the control, but the DMI fungicide and B. subtilis treatments did. The mixed treatments of DMI fungicide + P. chlororaphis and DMI fungicide + B. subtilis both reduced brown rot disease compared to the control, but only the DMI fungicide + P. chlororaphis treatment prevented it. 

​The researchers concluded that although biofungicides may not be fully effective on their own, commercializing them could allow farmers to use less DMI fungicide. They explained that scaling back the use of DMI fungicides would slow M. fructicola resistance. Finally, they proposed that future researchers test biofungicide mixtures containing pyrrolnitrin in the field to observe real-world effects on stone fruit trees.

The post Using bacteria to fight fungal brown rot appeared first on Sciworthy.

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