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Category: life extension

So gene therapy administered during the operation can extend bypass life

Extending the life of the bypass, the operation that saves the heart when the coronary arteries close, by intervening in the biological behaviour of the implanted vessels. This is the idea behind the first gene therapy administered during a heart bypass. The first patient in the world to receive it was a 73-year-old man in Scotland’s Golden Jubilee University National Hospital.

Bypass allows blood flow to the heart to be restored by bypassing blocked arteries, using vessels taken from other parts of the body to act as a graft, i.e. a ‘bridge’ to the blocked arteries. In most cases, veins taken from the leg (usually the great saphenous vein) are used because they are readily available and simple to implant. In the case of the 73-year-old British man, gene therapy was added to the bypass, which consists of carrying the TIMP-3 gene into the vein before implanting it as a graft. The new gene therapy aims to make the vessel more stable and resistant right from the start by affecting its biological behaviour before it is implanted in the heart. The researchers are thus attempting to overcome one of the main limitations of the bypass procedure: once connected to the heart, the veins have to withstand much higher pressure than they are designed for, which in time leads them to shrink and reduce blood flow, until they lose their function.

Aging brains pile up damaged synaptic proteins in microglia

It is increasingly clear, though, that the loss of synapses—the flexible and adaptive relay stations central to our brains’ ability to think, learn, and remember—is central to the rise of cognitive decline and dementia in old age.

Now, researchers have discovered clues that may tie synapse loss to another hallmark of brain aging: the declining ability of brain cells to break down and recycle damaged proteins.

Published in Nature, the study shows that synaptic proteins are particularly susceptible to this age-related garbage-disposal problem: In old age, synaptic proteins break down much more slowly, they become more likely to pile up into the tangled clumps of protein characteristic of neurodegenerative disease, and they are more likely to make their way into microglia, immune cells that prune away damaged synapses.

Those findings are the latest in a series of discoveries that suggest new links between the brain’s waste management systems, microglia, and neurodegeneration—and they could yield new insights into human brain aging and neurodegeneration, said the study’s lead author. ScienceMission sciencenewshighlights.

Strategies for blood–brain barrier rejuvenation and repair

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.

Genflow reports positive interim data from SIRT6 gene therapy trial in aged dogs

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.

Digital twin reveals how eye cells lose their organization in leading cause of vision loss

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.

Engineering chimeric antigen receptor CD4 T cells for Alzheimer’s disease

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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A group of researchers compared the DNA of Italian centenarians with prehistoric genomes… and what they discovered left them stunned: the secret to living to 100 could lie in genes from 14,000 years ago

Italian centenarians share DNA links to Ice Age hunter gatherers, hinting that ancient genes may support extreme longevity.

Scientists Have Discovered a Protein That Reverses Brain Aging in The Lab

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.

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