Fight Aging! Newsletter, November 30th 2020
We examined specific aspects of metabolism in male PolG+/mut mice at 6 and 12 months of age under three dietary conditions: normal chow (NC) feeding, high-fat feeding (HFD), and 24-hr starvation. We performed mitochondrial proteomics and assessed dynamics and quality control signaling in muscle and liver to determine whether mitochondria respond to mtDNA point mutations by altering morphology and turnover. In the current study, we observed that the accumulation of mtDNA point mutations failed to disrupt metabolic homeostasis and insulin action in male mice, but with aging, metabolic health was likely preserved by countermeasures against oxidative stress and compensation by the mitochondrial proteome.
An Overview of the Mechanisms of Transthyretin Amyloidosis
https://www.fightaging.org/archives/2020/11/an-overview-of-the-mechanisms-of-transthyretin-amyloidosis/
A score or so different types of amyloid can form in the human body, each a protein that can become altered or misfolded in a way that encourages other molecules of the same protein to also alter or misfold. These broken proteins aggregate together into sheets and fibrils, forming solid deposits in and around cells that interfere with the normal function of tissues, or are actively toxic. Transthyretin is one such protein, and transthyretin amyloidosis is present to some degree in all older people. Evidence of recent years suggests that it is a factor in 10% of heart failure cases in old people in ge...
Source: Fight Aging! - Category: Research Authors: Reason Tags: Newsletters Source Type: blogs
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