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Category: life extension – Page 29

AI-assisted technique can measure and track aging cells

A combination of high-resolution imaging and machine learning, also known as artificial intelligence (AI), can track cells damaged from injury, aging, or disease, and that no longer grow and reproduce normally, a new study shows.

These senescent cells are known to play a key role in wound repair and aging-related diseases, such as cancer and heart disease, so tracking their progress, researchers say, could lead to a better understanding of how tissues gradually lose their ability to regenerate over time or how they fuel disease. The tool could also provide insight into therapies for reversing the damage.

The study included training a computer system to help analyze animal cells damaged by increasing concentrations of chemicals over time to replicate human aging. Cells continuously confronted with environmental or biological stress are known to senesce, meaning they stop reproducing and start to release telltale molecules indicating that they have suffered injury.

Cross-omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging

We developed single-and multi-omics risk scores to assess blood inflammation markers and validated them across three cohorts. Our multi-omics models outperformed blood markers in predicting all-cause mortality, offering a more comprehensive approach to capturing inflammation burden. This may help identify at-risk populations for targeted interventions to reduce inflammation-related mortality.

Abstract: Synaptic plasticity is obstructed by pathogenic tau in the brain

Representing a key mechanism that underlies memory loss in Alzheimer’s disease (AD) and related tauopathies. Here, we found that reduced levels of the memory-associated protein KIdney/BRAin (KIBRA) in the brain and increased KIBRA protein levels in cerebrospinal fluid are associated with cognitive impairment and pathological tau levels in disease. We next defined a mechanism for plasticity repair in vulnerable neurons using the C-terminus of the KIBRA protein (CT-KIBRA). We showed that CT-KIBRA restored plasticity and memory in transgenic mice expressing pathogenic human tau; however, CT-KIBRA did not alter tau levels or prevent tau-induced synapse loss. Instead, we found that CT-KIBRA stabilized the protein kinase Mζ (PKMζ) to maintain synaptic plasticity and memory despite tau-mediated pathogenesis. Thus, our results distinguished KIBRA both as a biomarker of synapse dysfunction and as the foundation for a synapse repair mechanism to reverse cognitive impairment in tauopathy.

1Buck Institute for Research on Aging, Novato, California, USA.

2Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, California, USA.

3Gladstone Institutes, San Francisco, Califoria, USA.

4Weill Institute for Neurosciences, Department of Pathology, University of California San Francisco, San Francisco, California, USA.

CTE and normal aging are difficult to distinguish, new study finds

In recent years, some scientists and advocates have warned that playing contact sports like football and hockey may increase the risk of brain diseases like Alzheimer’s disease or chronic traumatic encephalopathy (CTE) due to a buildup of a specific protein in the brain.

But a new Northwestern Medicine study of 174 donated brains, including some from former high school and , pumps the brakes on that theory.

“The long and short of it is no, this protein in this specific brain region is not increased in people who played football at the amateur level. It throws a little bit of cold water on the current CTE narrative,” said corresponding author Dr. Rudolph Castellani, professor of pathology at Northwestern University Feinberg School of Medicine and a Northwestern Medicine neuropathologist.

More misfolded proteins than previously known may contribute to Alzheimer’s and dementia

For decades, the story of Alzheimer’s research has been dominated by a battle between A-beta and tau amyloids, both of which can kill neurons and impact the brain’s ability to function. A new study suggests, however, that these sticky brain plaques may not be operating alone.

Johns Hopkins University researchers have identified more than 200 types of in rats that could be associated with age-related cognitive decline.

The findings could lead the way to finding new therapeutic targets and treatments in humans that could provide relief for the millions of people over 65 who suffer from Alzheimer’s, dementia, or other diseases that rob them of their memories and independence as they age.

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