Lifeboat Foundation

Short-lived proteins control gene expression in cells and execute critical roles ranging from assisting brain connectivity to fortifying the body’s immune response. Originating in the nucleus, these proteins are swiftly degraded after fulfilling their purpose.

For decades, the mechanism behind the degradation and removal of these essential proteins from cells remained a mystery to researchers — until now.

In a cross-departmental collaboration, researchers from Harvard Medical School identified a protein called midnolin that plays a key role in degrading many short-lived nuclear proteins. The study shows that midnolin does so by directly grabbing the proteins and pulling them into the cellular waste-disposal system, called the proteasome, where they are destroyed.

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In this episode, filmed during Abundance360, Peter and David discuss David’s groundbreaking research on reversing aging through epigenetic changes, emphasizing that aging is not just damage to the body but a loss of information. They talk about age reversal as a possibility, rejuvenating brains, and regaining lost memories.

Continue reading “Aging is Now Optional w/ David Sinclair | EP #60” »

The Human Brain Project wraps up in September after a decade. It had notable achievements and a troubled past.

Vaccinations against tetanus and diphtheria, pneumococcus, and herpes zoster (HZ)- better known as shingles, are linked to a reduced risk of Alzheimer’s disease (AD). The corresponding study was published in the Journal of Alzheimer’s Disease.

Viral, bacterial, and fungal infections increase the risk of neuroinflammation, which may cause or exacerbate neurodegeneration and dementia. Vaccines may thus reduce neurodegeneration and dementia risk by reducing the risk of infection. Previous research, for example, shows that people who receive at least one influenza vaccine are 40% less likely than unvaccinated peers to develop AD.

Currently, the Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) recommends older adults receive vaccines against tetanus, diphtheria and herpes zoster, and pneumococcus. The researchers behind the current study thus sought to see how these common vaccines may affect AD risk.

Most of us who’ve reached middle age have noticed a slowing in memory and cognition, but scientists don’t have a clear picture of the molecular changes that take place in the brain to cause it.

Now, a study in mice has determined that the most pronounced changes occur in the white matter, a type of nervous system tissue that’s integral to transmitting signals across the brain. The study also examined two treatments — caloric restriction and infusions of plasma from young mice — that affect certain regions of the brain, with the plasma appearing to slow the age-related decline.

Continue reading “Stanford Medicine-led research identifies gene ‘fingerprint’ for brain aging” »

How looks life with na implant in brain.

Brain-computer interface technology is a fast-growing field but how does it feel to live with an implant inside of you?

In 2014, Ian Burkhart looked down at his hand and imagined closing it. To his astonishment, his hand did just that.

Continue reading “How does it feel to live with a cerebral implant?” »

The viral ALS Ice Bucket Challenge a few years ago raised major funding that resulted in the discovery of new genes connected to the disease. One of those genes is NEK1, in which mutations have been linked to as much as 2% of all ALS cases, making it one of the top-known causes of the disease.

But it wasn’t known how the mutated gene disrupts the function of the motor neuron and causes it to degenerate and die.

Northwestern Medicine scientists have discovered for the first time how this mutated gene leads to ALS (amyotrophic lateral sclerosis).

We know that humans are an intelligent species. But this biologist breaks down the intelligence of each of our cells — and it will blow your mind.

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Continue reading “Can cells think? | Michael Levin” »

A research team headed by investigators at Brigham and Women’s Hospital reported on the results of a study in which they used stem cells from Alzheimer’s disease (AD) patients to identify a potential mechanism by which a gene known as SORL1 may impact the risk for the neurodegenerative disorder. Their work found that loss of normal SORL1 function leads to a reduction in two key proteins, APOE and CLU, which are known to be involved in AD, and which play an essential role in the neurons of healthy individuals. The study findings suggest a potential new strategy for AD treatment, especially for patients not responsive to existing therapies.

“Understanding the subtypes of AD is relatively new in the field of neurology research,” said Tracy Young-Pearse, PhD, of the Ann Romney Center for Neurological Diseases. “This is getting at a precision neurology approach, with which we can better predict which patients may be responsive to Alzheimer’s treatment strategies that attack specific genes or target the problems they cause.” Young-Pearse is corresponding author of the team’s published paper in Cell Reports, which is titled, “ Cell-type-specific regulation of APOE and CLU levels in human neurons by the Alzheimer’s disease risk gene SORL1,” in which they concluded, “Taken together, we demonstrate that AD-relevant SORL1 loss of function results in neuron-specific reduction in APOE and CLU and dysregulated lipid homeostasis.”

AD varies widely in its age of onset, presentation, and severity. Key neurological features of AD, including the accumulation of amyloid-beta (Aβ) plaques in the brain, also vary across individuals. The anti-amyloid therapies, aducanumab and lecanemab, have received FDA accelerated and traditional approval, respectively, but not all patients respond to these drugs, warranting other treatment options.