Disturbances in this critical sense are often linked to problems with brain health, researchers are learning

Most people know the ketogenic diet as a popular way to lose weight. Celebrities, athletes, and people trying to improve their health have embraced the low-carbohydrate eating plan over the past decade. But scientists are increasingly discovering that the keto diet may have effects far beyond the bathroom scale. According to a new review published […]

The post This Weight-Loss Diet May Also Fight Alzheimer’s and Parkinson’s Diseases appeared first on Knowridge Science Report.

Alzheimer’s disease gradually steals memories, independence, and quality of life from millions of people worldwide. Despite decades of research, scientists still struggle to find treatments that can stop the disease from progressing. Most available medications provide only modest benefits and cannot fully prevent the loss of brain cells that characterizes the condition. A new study […]

The post Scientists Find a New Way to Fight Alzheimer’s After 20 Years of Research appeared first on Knowridge Science Report.

Compound 10 slowed dementia-like decline in mice.

The saying that the eyes are the window to the soul may contain more truth than people realize. Scientists now believe that our eyes may also provide valuable information about the health of our brains. A new study suggests that simple photographs of the retina, the light-sensitive tissue at the back of the eye, may […]

The post Your Eyes May Reveal Your Future Risk of Alzheimer’s Disease appeared first on Knowridge Science Report.

In a groundbreaking advance poised to transform the landscape of age-related immune decline, University College London (UCL) researchers are spearheading a pioneering clinical trial aimed at rejuvenating worn-out T cells through an innovative immune restoration therapy. This Phase 1 first-in-human study will explore the therapeutic potential of metabolically resetting exhausted or senescent T cells, a subset of immune cells that accumulate with age and chronic disease and lose their robustness in coordinating immune responses. The initiative promises to reopen avenues for combating a spectrum of diseases, including cancer, HIV, and neurodegenerative disorders like dementia, by profoundly modifying the immune system’s intrinsic capacity to defend and repair.

Central to the research is the recognition that immune ageing, characterized by the progressive dysfunction and decline in immune cell performance, is a key factor leading to increased vulnerability in the elderly and those with chronic infections. T cells, particularly the CD4+ subtype—often regarded as the conductors of the immune orchestra—become less effective with time, diminishing the immune system’s ability to coordinate defenses accurately. These cells, rendered senescent or exhausted, exhibit impaired proliferation, cytokine production, and cytotoxic activity, undermining responses to pathogens, malignancies, and cellular damage.

The novel therapy, developed by SenTcell, a biotech startup founded by Dr. Alessio Lanna from UCL Medicine, employs a liquid formulation administered intramuscularly akin to conventional vaccines. This delivery method facilitates patient-friendly administration while targeting key metabolic pathways within dysfunctional T cells. By reprogramming the intracellular environment of these immune cells, the treatment aims to restore youthful functional properties, including enhanced proliferative capacity and efficient pathogen recognition, thereby revitalizing the immune system’s broad protective functions.

Dr. Lanna explains that although antiretroviral advancements have significantly improved lifespans for individuals living with HIV, many still experience premature immune ageing. Similar patterns of immune exhaustion are also detected in cancer patients and other chronic disease cohorts. The imminent clinical trial represents a critical stepping stone towards verifying whether exhausted immune cells can be safely and effectively rejuvenated in human subjects, with the potential to redefine therapeutic paradigms for diseases rooted in immune dysregulation.

At the molecular level, one of the intriguing aspects under investigation involves the role of telomeres—protective caps on chromosome ends whose shortening serves as a hallmark of biological ageing. Laboratory studies have suggested that rejuvenated CD4+ T cells may release telomere-containing extracellular structures, whimsically termed “telomere Rivers,” into the bloodstream. The presence and behavior of these structures might offer novel insights into how restored immune cells influence systemic health, extending their benefits beyond immediate immune niches to broader tissue health. Although this phenomenon has yet to be validated in human clinical contexts, it highlights the sophisticated interplay between immune rejuvenation and organismal aging.

The clinical trial enjoys regulatory support from the UK’s Medicines and Healthcare products Regulatory Agency (MHRA) through its Innovative Licensing and Access Pathway (ILAP), underscoring the therapy’s potential to meet the pressing unmet medical needs associated with immune senescence. This endorsement accelerates development timelines and affirms the significance of targeting immune metabolic dysfunction as a viable therapeutic strategy.

Participants in the upcoming Phase 1 trial will be meticulously selected adults exhibiting characteristics of immune dysfunction, including evidence of premature immune ageing or persistent viral infections. Comprehensive immune profiling will be conducted before and after therapeutic administration to discern immunological changes and safety outcomes. Although the initial focus is on evaluating biological activity and tolerability, successful results could pave the way for advanced trials assessing clinical efficacy.

Unlike conventional treatments that combat diseases by targeting individual pathogens or tumor cells directly, this therapy seeks to recalibrate the immune system itself—restoring its intrinsic resilience and regenerative functionality. Such a paradigm shift holds profound implications; by enhancing the immune system’s natural defensive repertoire, it may afford broad-spectrum protection and facilitate healthier ageing trajectories.

Beyond chronic infections like HIV and cancer, this approach could ultimately apply to autoimmune disorders characterized by immune exhaustion, wherein overly active yet dysfunctional immune cells drive pathology. Immune rejuvenation strategies offer a novel means of restoring balance without broadly suppressing immune activity, potentially mitigating disease progression while improving quality of life.

This research aligns with a growing global focus on understanding the cellular and molecular underpinnings of ageing and immune decline. By intervening at the level of T cell metabolism and function, scientists hope to extend not only lifespan but healthspan—preserving cognitive and physical function while reducing susceptibility to infections, cancer, and degenerative diseases.

As UCL celebrates two centuries of academic excellence and innovation, this project embodies the institution’s commitment to translating bold scientific ideas into therapies capable of reshaping medicine. If validated through clinical trials, this immune rejuvenation therapy could herald a transformative era in treating age-associated diseases, offering hope for millions affected by immune dysfunction worldwide.

Subject of Research: People
Article Title: Immune Rejuvenation: UCL’s Pioneering Trial Targets T Cell Exhaustion to Combat Age-Related Immune Decline
News Publication Date: Not provided
Web References: www.ucl.ac.uk
References: Not provided
Image Credits: Not provided
Keywords: Immune ageing, T cell exhaustion, CD4+ T cells, immune rejuvenation, senescent immune cells, telomeres, immune dysfunction, chronic disease, HIV, cancer, metabolic resetting, Phase 1 clinical trial

In an unprecedented advancement for neurodegenerative disease research, a team led by Busquets, Li, Syed, and colleagues has unveiled iSCORE-PD, an innovative isogenic stem cell repository designed explicitly to accelerate Parkinson’s disease studies. Published in Nature Communications in 2026, this comprehensive collection represents a pivotal leap toward resolving the complex pathophysiology of Parkinson’s, a condition affecting millions worldwide yet still eluding curative therapies. The iSCORE-PD platform promises to redefine experimental paradigms by providing scientists with genetically matched cellular models that mirror the intricate genetic underpinnings of Parkinson’s disease.

Parkinson’s disease is characterized primarily by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to debilitating motor symptoms such as tremors, rigidity, and bradykinesia, alongside a spectrum of non-motor complications. Despite extensive research, there remains a conspicuous gap between clinical observations and mechanistic understanding at the cellular and molecular levels. Existing animal models and conventional stem cell lines often fall short in recapitulating the exact human pathology. The iSCORE-PD initiative addresses this deficiency head-on by harnessing isogenic stem cell lines, which are genetically identical except for defined Parkinson’s-relevant mutations, thus enabling unprecedented control over genetic variables.

The technical foundation of iSCORE-PD relies on advanced genome editing methodologies, most notably CRISPR/Cas9 technology. By precisely introducing or correcting mutations in key genes implicated in Parkinson’s pathogenesis such as SNCA, LRRK2, PINK1, and PARKIN, researchers have generated isogenic pairs of induced pluripotent stem cells (iPSCs). These iPSC lines can subsequently be differentiated into dopaminergic neurons or other relevant cell types, facilitating side-by-side comparisons that isolate the effects of specific genetic alterations without the confounding noise of inter-individual genetic variability.

One of the remarkable features of the iSCORE-PD collection is its extensive genomic validation pipeline. Whole genome sequencing and transcriptomic analyses are systematically employed to ensure the integrity and authenticity of the edited lines, confirming that off-target effects are minimized and that the genetic landscape conforms precisely to intended edits. This meticulous validation is crucial for downstream experiments intending to dissect subtle cellular phenotypes attributable to Parkinson’s mutations with a high degree of confidence.

The availability of these isogenic cell lines dramatically enhances the fidelity of disease modeling. Scientists can now observe, in real time and within a human cellular context, the cascade of pathological events triggered by individual mutations. For instance, iSCORE-PD lines harboring the G2019S mutation in LRRK2 have already demonstrated distinct lysosomal dysfunction and mitochondrial impairment, hallmarks of Parkinson’s-related neurodegeneration. These insights provide vital clues about the molecular mechanisms that underpin neuronal vulnerability and death.

Beyond mechanistic studies, iSCORE-PD serves as an invaluable platform for drug discovery and therapeutic screening. High-throughput assays conducted on these standardized cellular models allow for robust evaluation of candidate compounds’ efficacy and toxicity. The isogenic background ensures that drug responses can be directly attributed to genetic contributors and not extraneous genomic differences, thereby accelerating the identification of promising therapeutic leads with increased translational potential.

Moreover, the iSCORE-PD repository supports integrative omics approaches. By coupling proteomics, metabolomics, and epigenomic profiling with the genetically defined cell lines, researchers can generate comprehensive molecular atlases elucidating the multifaceted alterations engendered by Parkinson’s-associated mutations. Such data-rich resources augment our understanding of disease heterogeneity and may reveal novel biomarkers for early diagnosis and progression monitoring.

The initiative also pioneers robust methodologies for modeling non-cell autonomous effects in Parkinson’s pathology. By co-culturing isogenic dopaminergic neurons with glial cells or other brain cell types derived from similarly engineered iPSC lines, investigators can explore the cell–cell interactions and inflammatory pathways that contribute to disease propagation. These complex in vitro systems increasingly resemble the in vivo brain microenvironment, bridging translational gaps.

In addition to its scientific hinge, iSCORE-PD represents a significant step forward in reproducibility and collaborative science. By providing open-access to a rigorously characterized and genetically standardized stem cell collection, the project promotes harmonization of experimental models across laboratories worldwide. This standardization mitigates discrepancies often observed in Parkinson’s research due to genetic heterogeneity of patient-derived cells and disparate culture conditions.

Ethical considerations have been front and center in the development and dissemination of the iSCORE-PD lines. The team has implemented stringent protocols to ensure donor anonymity, informed consent, and compliance with international guidelines for stem cell research. This ethical diligence is fundamental to fostering public trust and enabling broad scientific utilization with responsibility.

The iSCORE-PD research consortium envisions future expansion of the collection to encompass additional mutations, gene variants, and epigenetic modifications implicated in Parkinson’s disease, thereby creating an ever-more comprehensive toolkit for the field. This evolving repository will facilitate the study of gene–environment interactions and provide models for the sporadic forms of Parkinson’s that constitute the majority of cases.

Importantly, the development of iSCORE-PD aligns synergistically with advances in single-cell sequencing and live-cell imaging technologies. These combined approaches empower real-time monitoring of neuronal dynamics, synaptic connectivity, and intracellular trafficking in disease-relevant contexts. Such capabilities promise to unravel the temporal progression of neuronal dysfunction in unprecedented detail.

The translational impact of iSCORE-PD extends beyond fundamental research, holding profound implications for personalized medicine. Patient-specific isogenic lines can be derived, enabling evaluation of individualized drug responses and prediction of disease progression trajectories. This precision medicine paradigm could revolutionize clinical management and therapeutic development for Parkinson’s patients.

Finally, iSCORE-PD serves as a testament to the power of interdisciplinary collaboration, integrating expertise in stem cell biology, genome editing, neuroscience, bioinformatics, and clinical neurology. This concerted effort exemplifies how cutting-edge technologies, when harnessed collectively, can illuminate complex diseases and hasten the arrival of effective treatments.

In sum, the iSCORE-PD isogenic stem cell collection stands as a groundbreaking resource that transforms the landscape of Parkinson’s disease research. By providing genetically precise, highly validated cellular models, it enables unparalleled mechanistic insights, drug discovery opportunities, and personalized medicine applications. As the Parkinson’s field grapples with its most urgent challenges, iSCORE-PD promises to be a beacon guiding innovative interventions and ultimately improving patient outcomes worldwide.

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Subject of Research: Parkinson’s disease; isogenic stem cell models; neurodegeneration; genome editing; induced pluripotent stem cells.

Article Title: iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.

Article References:

Busquets, O., Li, H., Syed, K.M. et al. iSCORE-PD: an isogenic stem cell collection to research Parkinson’s disease.
Nat Commun (2026). https://doi.org/10.1038/s41467-026-74355-8

Image Credits: AI Generated

Microplastics: Unseen Threats to Liver Health Revealed Through Cutting-Edge Spatial Transcriptomics

In recent years, microplastics have emerged as pervasive environmental contaminants, infiltrating virtually every corner of the globe. These minuscule plastic particles, derived from the breakdown of larger plastic debris, have invaded air, water, and soil, exposing humans to continuous contact via inhalation, ingestion, and dermal absorption. Despite the ubiquity of microplastics, understanding their direct impact on biological systems has remained a formidable challenge within the scientific community. A groundbreaking study by researchers at the University of Oklahoma, recently published in the journal Science Advances, delves into this critical area by examining how microplastics particularly affect liver health under dietary stress conditions.

Tae Gyu Oh, Ph.D., an assistant professor of oncology science at the University of Oklahoma College of Medicine and lead author of the study, highlights the pressing concern: “Exposure to microplastics is inevitable. Their presence in human tissues has been confirmed across multiple studies. However, we wanted to investigate how microplastic exposure interacts with a high-fat, high-cholesterol diet, known to independently induce liver damage.” The study offers compelling evidence that the combination of a typical Western diet and microplastic exposure exacerbates liver injury, potentially accelerating the progression of metabolic liver diseases.

Central to the study is the focus on polyethylene, the most prevalent plastic polymer globally, commonly found in everyday items such as plastic bags and milk containers. The research team administered polyethylene microplastics to mice over eight weeks, with one cohort receiving a standard diet and another subjected to a diet mimicking metabolic dysfunction-associated steatohepatitis (MASH). This severe form of fatty liver disease is characterized by inflammation and liver cell damage, often culminating in cirrhosis and liver failure if untreated.

The findings were striking: mice consuming the high-fat diet alongside microplastic exposure exhibited blood markers indicating liver injury more than twice as elevated as those on a standard diet experiencing similar exposure. This synergistic effect underscores the intricate interplay between environmental pollutants and diet-induced metabolic stressors, intensifying hepatic damage beyond what each factor causes independently.

To unravel the molecular and cellular underpinnings of this phenomenon, the research employed an array of sophisticated analytical techniques, culminating in the use of spatial transcriptomics. Unlike conventional bulk transcriptomic approaches, which average gene expression across millions of cells and can obscure localized responses, spatial transcriptomics enables researchers to map transcriptional activity within intact tissue sections at near single-cell resolution. This technique revealed precise “hot spots” of inflammation and tissue injury within the liver, a breakthrough insight unattainable by earlier methodologies.

Analysis of gene regulatory networks through spatial transcriptomics indicated a pivotal role for PPAR-alpha (peroxisome proliferator-activated receptor-alpha), a nuclear receptor that orchestrates fat metabolism and energy homeostasis in liver cells. PPAR-alpha appears to engage in cross-talk with Anxa2, a gene implicated in tissue repair and membrane dynamics. The altered activity of this axis in microplastic-exposed livers suggests that microplastics may disrupt the liver’s natural defense and regenerative processes, impairing its capacity to recover from metabolic insults.

This discovery has profound implications for understanding the mechanistic pathways by which environmental contaminants like microplastics contribute to liver pathology. The perturbation of PPAR-alpha and Anxa2 signaling potentially links microplastic exposure with the dysregulation of lipid metabolism and compromised repair, exacerbating the severity of conditions such as nonalcoholic fatty liver disease (NAFLD) and MASH.

While these findings were generated in a murine model, they establish an essential framework that informs potential human health risks. Given the parallels between murine and human liver physiology, it is plausible that microplastic exposure combined with high-fat diets could similarly predispose humans to aggravated liver damage. However, the researchers caution that further studies are necessary to confirm this translation and to elucidate the long-term implications for populations worldwide.

Dr. Oh emphasizes the broader relevance of this research: “Microplastics are now inextricably linked to daily life, yet their biological impact is only beginning to be understood. Through advanced spatial transcriptomic mapping, we have visualized the precise loci of hepatic damage induced by microplastics, revealing a novel environmental dimension to liver disease pathogenesis.” This nuanced comprehension paves the way for future investigations targeting environmental and dietary risk factors in liver health.

Moreover, these insights open avenues for therapeutic targeting. Modulating the PPAR-alpha-Anxa2 pathway could become a strategy to mitigate microplastic-induced liver injury or fortify the liver’s resilience against environmental toxins. Understanding such molecular crosstalk also facilitates improved diagnostic markers sensitive to environmental damage, allowing for earlier intervention in vulnerable populations.

This pioneering study exemplifies the intersection of environmental health, genomics, and hepatology, demonstrating how innovative technologies can elucidate complex biological interactions. It underscores the urgent need to address microplastic pollution not only as an ecological crisis but as a public health priority, particularly in societies where high-fat diets are prevalent.

As humanity grapples with escalating plastic waste and its fragmentary descent into invisible pollutants, research such as this serves as a clarion call for comprehensive strategies. Reducing plastic production, enhancing waste management, and fostering healthier dietary practices collectively form the cornerstone of mitigating hidden dangers to liver health and overall well-being.

The University of Oklahoma study, titled “Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity,” stands as a seminal contribution offering unprecedented mechanistic clarity. Through employing spatial transcriptomics, the researchers have achieved a level of resolution that redefines how environmental toxicology and metabolic disease research can coalesce to confront emergent health threats posed by our plastic-saturated environment.

Subject of Research: Animals
Article Title: Spatial transcriptome mapping identifies Ppara-Anxa2 cross-talk in microplastic-induced hepatotoxicity
News Publication Date: 17-Jun-2026
Web References: https://doi.org/10.1126/sciadv.aec8681
References: Oh, T.G., Jung, W., Joshi, A.D., et al. Spatial Transcriptome Mapping Identifies Ppara-Anxa2 Crosstalk in Microplastic-Induced Hepatotoxicity. Science Advances, 2026.
Image Credits: University of Oklahoma
Keywords: Microplastics, Liver Disease, Fatty Liver Disease, Polyethylene, High-Fat Diets, Spatial Transcriptomics, PPAR-alpha, Anxa2, Hepatotoxicity, Environmental Health, Metabolic Dysfunction, Inflammation

Ebola Virus Finds Sanctuary in the Brain: Breaking Ground with Human Cerebral Organoids

In a landmark study published in Nature Microbiology, researchers from the Icahn School of Medicine at Mount Sinai and the Bernhard Nocht Institute for Tropical Medicine (BNITM) have uncovered how the deadly Ebola virus can persist and replicate stealthily within the human central nervous system. By leveraging cutting-edge cerebral organoid models—three-dimensional brain-like structures derived from human pluripotent stem cells—the team has shed light on the viral mechanisms that allow long-term survival, raising critical implications for treatment and prevention strategies of Ebola virus disease (EVD).

It has long been a harrowing clinical observation that survivors of acute Ebola infections sometimes suffer relapses or develop inflammatory syndromes months or even years after recovery. This enduring threat is attributed to the virus’s ability to hide out in “immune-privileged” regions of the body—such as the central nervous system (CNS)—where the immune surveillance is deliberately restrained to protect vulnerable tissue from damaging inflammation. This latest research elucidates the ways Ebola virus exploits this sanctuary and endures prison-like conditions inside cerebral tissue without fully succumbing to immune clearance.

The team engineered cerebral organoids by coaxing human induced pluripotent stem cells (iPSCs) into forming spherical, differentiated structures composed of multiple neural cell types: neurons, astrocytes, and microglia alike. These organoids mimic the cellular environment of the human brain closely enough to serve as a viable model to explore viral persistence with unprecedented resolution and relevance. Unlike traditional animal models, these human-derived organoids enable direct examination of host-virus interactions in a context that recapitulates human neuroanatomy and immunology.

Longitudinal infection experiments revealed that Ebola virus and related filoviruses—including Sudan, Reston, and Marburg viruses—could sustain active replication within these cerebral organoids for up to 120 days. More intriguingly, Ebola virus infected not just neurons but also astrocytes and microglia, the brain’s resident immune cells. The virus exhibited two spreading modalities: direct cell-to-cell contact transmission as well as classical budding from host cells. This productive persistence clearly places the virus in an infectious, replicative state rather than a latent or inactive one.

Despite the robust production of pro-inflammatory cytokines by infected organoids, the innate immune responses orchestrated within this model failed to clear the infection entirely. The study observed an upregulation of immune and inflammatory markers at later stages, mirroring clinical presentations seen in Ebola virus disease survivors who develop delayed meningoencephalitis and other inflammatory sequelae. The data affirm that persistent filovirus infection in immune-privileged tissues contributes to localized inflammation, fostering neurological disease conditions even after primary viremia subsides.

At the molecular level, whole-genome sequencing of viral populations recovered from persistently infected organoids uncovered the presence of defective viral genomes (DVGs) and a spectrum of mutations emerging during chronic replication. DVGs are truncated or mutated forms of viral genomes known to modulate replication dynamics and immune evasion in other viral families. These defective genomes may allow the Ebola virus to dampen replication while maintaining a foothold inside host tissue, facilitating long-term survival without triggering overwhelming immune destruction.

Several mutations identified in the viral sequences corresponded to variants previously reported to attenuate replication in natural infections, while others were novel and uncharacterized. This emerging mutational landscape hints at an ongoing evolutionary arms race as the virus adapts to the CNS environment and immune pressures. Such adaptations could be critical determinants in the capacity of Ebola virus to establish persistent reservoirs and cause relapses.

This cerebral organoid model’s faithful recapitulation of human Ebola virus infection patterns underscores its utility as a powerful platform for mechanistic studies of viral persistence. Unlike animal models, which often fail to mimic intricate human neural immunology adequately, organoids offer a nearer-to-human experimental system. This breakthrough has potential ramifications for testing and optimizing targeted antiviral therapies aimed specifically at reservoirs residing in immune-privileged compartments.

Moreover, cerebral organoids provide an ethically favorable and scalable alternative to animal experiments, fostering more humane and potentially faster progress in infectious disease research. This innovation aligns with global efforts to reduce animal use in biomedical studies and to increase translational fidelity to human conditions.

Looking ahead, the research team emphasizes expanding their investigations to include other lesser-studied filoviruses such as Taï Forest, Bombali, and Bundibugyo viruses. Comprehensive deciphering of host–virus dynamics in such a model may unravel universal persistence mechanisms across filovirus species, informing cross-cutting therapeutic strategies. Crucially, this work also lays groundwork for exploring how viral persistence in the CNS intersects with immune modulation, neuroinflammation, and long-term neurological sequelae in EVD survivors.

Persistent Ebola infection in the brain highlights a formidable challenge for public health, given the potential for virus reactivation or even transmission from immune-privileged sanctuaries. This study delivers a compelling window into that hidden battleground, leveraging state-of-the-art human cellular models to confront a deadly pathogen’s stealth strategies. Unlocking the biology of Ebola’s cerebral persistence may ultimately pave the way for interventions that not only save lives during acute infection but also circumvent post-recovery complications and community outbreaks.

As our understanding deepens, harnessing cerebral organoids as investigative tools promises to revolutionize the study of neurotropic viral infections. The Mount Sinai and BNITM collaboration exemplifies how multidisciplinary, translational research can illuminate the dark corners of viral pathogenesis and guide clinical innovation for diseases once deemed intractable.

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Subject of Research: Animals (via human-derived cerebral organoids)

Article Title: Host–virus determinants of Ebola virus persistence in a human cerebral organoid model

News Publication Date: 12-Jun-2026

Web References:
https://www.nature.com/articles/s41564-026-02388-2
http://dx.doi.org/10.1038/s41564-026-02388-2

Keywords: Ebola virus, cerebral organoids, central nervous system, viral persistence, filoviruses, neuroinflammation, antiviral therapy, immune evasion, defective viral genomes, virus-host interaction