The scientists observed that species which are already predisposed to long life, including the naked mole rat had high levels of humanin, while mice, in contrast, experience a 40% decrease in humanin over the first 18 months of their life and primates experienced a similar notable decrease between the ages of 19 and 25.
Interestingly, the research showed higher, more sustained, humanin levels in children of centenarians compared to a control group. In some species, including worms and mice, the team went on to discover that modifying their genes to increase humanin levels increased lifespan. However, this was at the expense of the number of offspring the animals produced.
Scientists also looked at cerebral spinal fluid from Alzheimer’s patients and a control group, finding that humanin levels were significantly lower in the group with Alzheimer’s.
This new study is part of a growing body of research into the importance of humanin in delaying the aging process, and it is now hoped that it could pave the way for the development of mitochondrial protein-based treatments for age-related disease and conditions.
Results look good in mice and worms. There is less fat and more lean body mass and longer lives.
Humanin is a member of a new family of peptides that are encoded by short open reading frames within the mitochondrial genome. It is conserved in animals and is both neuroprotective and cytoprotective. Here we report that in C. elegans the overexpression of humanin is sufficient to increase lifespan, dependent on daf-16/Foxo. Humanin transgenic mice have many phenotypes that overlap with the worm phenotypes and, similar to exogenous humanin treatment, have increased protection against toxic insults. Treating middle-aged mice twice weekly with the potent humanin analogue HNG, humanin improves metabolic healthspan parameters and reduces inflammatory markers. In multiple species, humanin levels generally decline with age, but here we show that levels are surprisingly stable in the naked mole-rat, a model of negligible senescence. Furthermore, in children of centenarians, who are more likely to become centenarians themselves, circulating humanin levels are much greater than age-matched control subjects. Further linking humanin to healthspan, we observe that humanin levels are decreased in human diseases such as Alzheimer’s disease and MELAS (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes). Together, these studies are the first to demonstrate that humanin is linked to improved healthspan and increased lifespan.
SOURCES – Aging Journal, USC
Written By Brian Wang, Nextbigfuture.com