FOXO3 tagged posts

How a Longevity Gene protects Brain Stem Cells from Stress

cells under a microscope
Antioxidant treatment boosts the birth of new neurons from stem cells by suppressing stress signaling. Image courtesy of the Paik lab.

A gene linked to unusually long lifespans in humans protects brain stem cells from the harmful effects of stress, according to a new study by Weill Cornell Medicine investigators.

Studies of humans who live longer than 100 years have shown that many share an unusual version of a gene called Forkhead box protein O3 (FOXO3). That discovery led Dr. Jihye Paik, associate professor of pathology and laboratory medicine at Weill Cornell Medicine, and her colleagues to investigate how this gene contributes to brain health during aging.

In 2018, Dr...

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Genetic influence on Aging into the 90s but not beyond

The role of FoxO3 in longevity may involve upregulation of target genes involved in stress resistance, metabolism, cell cycle arrest, and apoptosis. Effective control of FoxO3 in response to environmental stimuli is likely critical to prevent ageing and age-related diseases including cardiovascular disease, type 2 diabetes, cancer and neurodegenerative diseases. The diagram shows how the well-known longevity-associated intervention of caloric restriction helps to maintain the redox state of the cell by cycling calories through the mitochondria so as to restore NAD+. Caloric restriction results in activation of sirtuins, leading to activation of FoxOs, improved autophagy, amino acid recycling via inhibition of mTOR activity, and other mechanisms leading to a healthy ageing phenotype. On the other hand, excess calories, particularly from carbohydrates, increase the NADH/NAD+ ratio and leads to lipogenesis, overproduction of ROS by mitochondria, poor autophagy and activation of mTOR as a result of an excess of protein intake. AKT1 is a term derived from the ‘Ak' mouse strain that develops spontaneous thymic lymphomas (AKT1 is also known as protein kinase B). CAD = Coronary artery disease; HNF4a = hepatocyte nuclear factor 4α; GCN1l1 = general control of amino acid synthesis 1-like 1; O-GlcNAc = O-linked N-acetylglucosamine; OXPHOS = oxidative phosphorylation; PPARγC1α = peroxisome proliferator-activated receptor-γ coactivator 1α; TCA = tricarboxylic acid.

The role of FoxO3 in longevity may involve upregulation of target genes involved in stress resistance, metabolism, cell cycle arrest, and apoptosis. Effective control of FoxO3 in response to environmental stimuli is likely critical to prevent ageing and age-related diseases including cardiovascular disease, type 2 diabetes, cancer and neurodegenerative diseases. The diagram shows how the well-known longevity-associated intervention of caloric restriction helps to maintain the redox state of the cell by cycling calories through the mitochondria so as to restore NAD+. Caloric restriction results in activation of sirtuins, leading to activation of FoxOs, improved autophagy, amino acid recycling via inhibition of mTOR activity, and other mechanisms leading to a healthy ageing phenotype...

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1st-of-its-kind exploratory study ID’s potential Gene a/w Most Common Cause of Liver Damage

NASHprogression

NAS/ Nonalcoholic‬ ‪‎fatty‬ liver disease progression

Nonalcoholic fatty liver disease is the most common cause of liver damage. In this study, TGen scientists sequenced microRNAs from liver biopsies, spelling out their biochemical molecules to identify several potential gene targets associated with NAFLD-related liver damage.

The miRNAs – RNA molecules that regulate gene expression – were obtained from liver biopsies of 30 female candidates for gastric bypass surgery: 15 with, and 15 without, NAFLD liver damage. Using the most advanced technology to refine the data, researchers identified several potential gene targets associated with NAFLD-related liver damage...

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