In a large-scale proteomic study of biological aging of 11 organs from 44,498 individuals in the UK Biobank, the biological ages of the brain and immune system emerged as strong predictors of healthspan and longevity.
Category: life extension – Page 4
17y Younger Biological Age (Test #4 in 2025): Supplements, Diet
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Role of plasmin in metastatic tumors
FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient’s immune system, use apoptosis to kill cancer cells.
The team discovered that in human genes, a single evolutionary amino acid change — serine instead of proline at position 153 — makes FasL more susceptible to being cut and inactivated by plasmin.
Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.
This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons — FasL — can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.
The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.
Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.
DunedinPACNI estimates the longitudinal Pace of Aging from a single brain image to track health and disease
Differences in the Pace of Aging are important for many health outcomes but difficult to measure. Here the authors describe the Dunedin Pace of Aging Calculated from NeuroImaging measure, an approach that uses a single brain image to measure how fast a person is aging and can help predict mortality or the risk of developing chronic disease.
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 college football players, 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.