anti-aging tagged posts

Hidden Secret of Immortality Enzyme Telomerase

This figure depicts the enzyme telomerase as well as telomeres relative to a chromosome.

This figure depicts the enzyme telomerase as well as telomeres relative to a chromosome.

Can we stay young forever, or even recapture lost youth? Can we stay young forever, or even recapture lost youth? Research from the laboratory of Professor Julian Chen in the School of Molecular Sciences at Arizona State University recently uncovered a crucial step in the telomerase enzyme catalytic cycle. This catalytic cycle determines the ability of the human telomerase enzyme to synthesize DNA “repeats” (specific DNA segments of six nucleotides) onto chromosome ends, and so afford immortality in cells. Understanding the underlying mechanism of telomerase action offers new avenues toward effective anti-aging therapeutics.

Typical human cells are mortal and cannot forever renew themselves...

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Combating Iron in the Brain: Researchers find anti-aging micromolecule

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members 2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri. Three different clusters were isolated (pri-mir-29 1, 2, 3) encoding four different mature members miR-29a, b, d, e. In red, seed sequence is reported, single nucleotide differences in blue. b Age-dependent expression of miR-29 primary transcripts (Pri-miR-29-1, 2, 3) in the brain of N. furzeri. The relative expression was evaluated by RT-qPCR, data were normalized on TATA binding protein (TBP), pri-miR-29-2 results much more expressed than the other clusters and shows a clear age-dependent up-regulation (1 way ANOVA with post-test for trend: R = 0.5285 P < 0.0001, n = 4 animals for age group). c Correlation of miR-29 with its predicted targets. Blue bars show the distribution of Pearson’s correlation coefficients between miR-29a and its predicted target. Light-blue bars show the distribution of correlation values extracted from a bootstrap (P = 10–14, Kolmogorov–Smirnoff). d, e Pri-miR-29-2 expression pattern in N. furzeri brain. d Pri-miR-29-2 signal (red) and HuC/D expression (green) in the optic tectum (TeO). Pri-miR-29-2 shows a nuclear staining and a co-localization with neuronal marker HuC/D along the periventricular gray zone (PGZ), white arrows show neurons in the optic tectum (TeO) negative for pri-miR-29-2. Scale bar = 50 μm. Cerebellum overview picture (e) shows a clear and strong expression of pri-miR-29-2 just in the granular cell layer (GCL), it is instead absent in the Purkinje cell (white arrow) and molecular layer (ML). Scale bar 100 μm

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members
2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri.

The older we get, our brain ages. Cognitive abilities decline and the risk of developing neurodegenerative diseases like dementia, Alzheimer’s and Parkinson’s disease or having a stroke steadily increases...

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Certain Plant Extracts may keep you young – and alive

An extract of willow bark has shown to be one of the most potent longevity-extending pharmacological interventions yet described in scientific literature.

An extract of willow bark has shown to be one of the most potent longevity-extending pharmacological interventions yet described in scientific literature.

A new Concordia-Idunn Technologies research collaboration provides insights into how 6 groups of molecules can slow biological aging. For the study, the research team combed through Idunn Technologies’ extensive biological library, conducting more than 10,000 trials to screen for plant extracts that would increase the chronological lifespan of yeast.

Why yeast? Cellularly speaking, aging progresses similarly in both yeast and humans. It’s the best cellular model to understand how the anti-aging process takes place...

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Anti-Aging Tricks from Dietary Supplement seen in Mice: Alpha-lipoic acid

 

Alpha-lipoic acid stimulates telomerase in vascular smooth muscle. Telomerase is the enzyme that lengthens chromosomes’ protective caps, with positive effects in a mouse model of atherosclerosis. The discovery highlights a potential avenue for the treatment for chronic diseases.

“Alpha-lipoic acid has an essential role in mitochondria, the energy-generating elements of the cell,” says Wayne Alexander, MD, PhD, professor of medicine at Emory University School of Medicine. “It is widely available and has been called a ‘natural antioxidant’. Yet ALA’s effects in human clinical studies have been a mixed bag.”

ALA appears to exert its effects against atherosclerosis by spurring the smooth muscle cells that surround blood vessels to make PGC1 (peroxisome proliferator-activated receptor gam...

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