The blood–brain barrier (BBB) is a dynamic interface that tightly regulates the transport of substances from the blood into the brain. BBB dysfunction can occur with ageing and is a hallmark of many major diseases but is underappreciated as a therapeutic target. Here, Searson and Banks review studies on BBB repair and rejuvenation, highlighting common mechanisms across disorders and potential strategies for pharmacological intervention.
First dogs, then …
Biotechnology group says treated animals showed improved survival and functional measures in early-stage study
Genflow Biosciences Ltd (LSE: GENF, OTCQB: GENFF, FRA: WQ5) said positive preliminary interim results from its SLAB clinical trial showed improved survival and functional outcomes in aged dogs treated with its proprietary SIRT6 centenarian gene therapy.
The biotechnology company, which focuses on developing gene therapies for age-related diseases, said the randomised, blinded study enrolled 24 beagle dogs aged over 10 years and was conducted by an independent contract research organisation.
National Institutes of Health (NIH) researchers have developed a digital replica of crucial eye cells, providing a new tool for studying how the cells organize themselves when they are healthy and affected by diseases. The platform opens a new door for therapeutic discovery for blinding diseases such as age-related macular degeneration (AMD), a leading cause of vision loss in people over 50. The study is published in the journal npj Artificial Intelligence.
“This work represents the first-ever subcellular resolution digital twin of a differentiated human primary cell, demonstrating how the eye is an ideal proving ground for developing methods that could be used more generally in biomedical research,” Kapil Bharti, Ph.D., scientific director at the NIH’s National Eye Institute (NEI).
The researchers created a highly detailed, 3D data-driven digital twin of retinal pigment epithelial (RPE) cells, which perform vital recycling and supportive roles to light-sensing photoreceptors in the retina. In diseases such as AMD, RPE cells die, which eventually leads to the death of photoreceptor cells, causing loss of vision.
Recent advancements in immunotherapy have led to the first successful application of chimeric antigen receptor (CAR) T-cell therapy in treating neurodegenerative diseases, specifically Alzheimer’s disease. In a study conducted by researchers at Washington University in St. Louis and the Weizmann Institute of Science, T-cells were genetically engineered to recognize and target toxic beta-amyloid plaques. When tested on mouse models, three injections of these modified cells resulted in a significant reduction of protein aggregates within just ten days of the final administration. Beyond plaque clearance, the treatment successfully mitigated neuroinflammation, as evidenced by decreased microglial and astrocytic activity. These findings demonstrate the potential of CAR-T technology to rapidly clear pathological protein deposits and restore nervous tissue function, offering a promising new frontier for the treatment of Alzheimer’s and other proteinopathies.
Alzheimer’s disease (AD) is the prevailing cause of age-associated dementia worldwide. Current standard of care relies on antibody-based immunotherapy. However, antibody-based approaches carry risks for patients, and their effects on cognition are marginal. Increasing evidence suggests that T cells contribute to AD onset and progression. Unlike the cytotoxic effects of CD8+ cells, CD4+ T cells capable of regulating inflammation show promise in reducing pathology and improving cognitive outcomes in mouse models of AD and in aging. Here, we sought to exploit the beneficial properties of CD4+ T cells while circumventing the need for TCR and peptide-MHC antigen discovery, thereby providing a potential universal therapeutic approach. To achieve this, we engineered CD4+ T cells with chimeric antigen receptors (CARs) targeting fibrillar forms of aggregated amyloid-β. Our findings demonstrate that optimized CAR-T cells can alter amyloid deposition in the dura and reduce parenchymal pathology in the brain. Furthermore, we observed that CAR-T treatment promotes the expansion and recruitment of endogenous CD4+ T cells into the brain parenchyma and leptomeninges. In summary, we established the feasibility of amyloid plaque-specific CAR-T cells as a potential therapeutic avenue for AD. These findings highlight the potential of CD4+ CAR-T therapy not only to modify amyloid pathology but also to reshape the immune landscape of the CNS, paving the way for future development of cellular immunotherapies for neurodegenerative disease.
Keywords: Alzheimer’s disease; CAR T cells; T cell; chimeric antigen receptors; neurodegeneration.
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What I like is the idea of metabolic momentum — seeing whether your daily habits are accelerating or slowing your pace of aging, based on sleep, stress, and activity over time.
It’s very “longevity-optimized” thinking: push when it’s smart, recover when it’s not, and let the data guide sustainable decisions without blood tests or guesswork.
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Our brains age along with the rest of our bodies, and as they do, they produce fewer new brain cells. Now, researchers have found a key mechanism through which the typical age-related decline in neuron production might be slowed.
In later life, the neural stem cells (NSCs) that turn into fully fledged neurons become more dormant – almost as if they’re going into retirement after a long lifetime of service. As that happens, cognitive decline creeps in.
A major reason why NSC activity fades with age is the wear and tear on telomeres, the protective caps on the ends of DNA. Telomeres fray a little more each time a cell divides, and over time, this impairs cells’ ability to grow and divide, leading to increasing cell death.
NewLimit just announced something that could be a major step toward real anti-aging medicine:
their first therapy is designed to regenerate the liver potentially making it 10–20 years younger.
Human trials are still ahead, but they’re already working on similar approaches for the immune system and vascular system.
Cartilage. Teeth. Liver.
Regeneration is moving from science fiction to clinical reality.
And it raises a bigger question:
medicine today often requires lifelong dosing like GLP-1 weight loss drugs (Ozempic, Wegovy).
What if the future is different?
What if one shot could actually repair the system instead of managing it forever?
Aging doesn’t rewrite your DNA, it scrambles how your cells read it.
This clip explains epigenetic drift and how Life Biosciences’ therapy, ER100, uses Yamanaka factors to restore youthful epigenetic patterns in aged cells. By resetting the chemical marks that control gene expression, cells can behave as if they’re young again without changing the underlying DNA.
It’s the same biological process that happens early in embryonic development, applied in a controlled way to adult cells.