A Mitochondrial Peptide, “Humanin,” Can Protect Against Dementia’s Disease

A Mitochondrial Peptide, “Humanin,” Can Protect Against Dementia’s Disease

A new study conducted by the Universtiy of Southern California found a new, never-before-seen genetic risk factor for Alzheimer’s disease and related dementias. According to the new research, a mitochondrial peptide known as “humanin” is causing dementia and other aging-related disorders as its levels are reducing as we age.

“Because of the beneficial effects of “humanin,” a decrease in circulating levels could lead to an increase in several different diseases of aging, particularly in dementia,” said study’s senior author Pinchas Cohen.

The recent research, headed by Kelvin Yen of the USC Leonard Davis School, and published today in the Nature-published journal Scientific Reports, also revealed a considerable difference between the mitochondrial peptide “humanin” in African-Americans, the group most affected by Alzheimer’s disease and other aging-related conditions, in comparison with Caucasians.

“We have now discovered a novel underlying biological factor that may be contributing to this health disparity,” stated Kelvin Yen.

“Humanin,” a mitochondrial peptide, involved in Alzheimer’s disease

“Humanin,” which is encoded in the mitochondrial genome, is affected by a genetic variation. That causes the levels of the before-mentioned mitochondrial peptide to drop by 14 percent with aging.

This new study is the first of its kind to find scientific evidence that a variation in the sequence of a mitochondrial peptide associated with alterations in the levels of peptides such as “humanin.”

Then, after analyzing the data of about 20,000 US-based individuals over the age of 50, the researchers also found that low levels of the “humanin” peptide are also linked to accelerated cognitive aging which causes Alzheimer’s disease and other cognitive-related conditions.

Also, injections with the “humanin” mitochondria peptide delayed the cognitive decline linked to aging in mice subjects, which could also be available in humans. However, even though that might pave the way to new treatments or prevention drugs for Alzheimer’s disease, the research must continue with humans subjects.


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