Scientists discover new risk factor for Alzheimer’s

In a recent study, researchers from USC discovered a new genetic risk factor for Alzheimer’s disease and related dementias.

The research sheds new light on the protective role of a naturally occurring mitochondrial peptide, known as humanin.

Amounts of the peptide decrease with age, leading researchers to believe that humanin levels play an important function in the aging process and the onset of diseases linked to older age.

The researchers discovered a significant difference between the circulating levels of humanin in African-Americans.

This population is more impacted by Alzheimer’s disease and other diseases of aging, as compared to Caucasians.

Because humanin is encoded within the mitochondrial genome, the research team examined the mitochondrial DNA for common genetic variations known as SNPs (pronounced snips) that could explain the differences between humanin levels.

After sequencing the entire mitochondrial genome of all samples to determine if any SNPs correlated with humanin levels, they identified a genetic variation that was associated with a 14% decrease in circulating humanin levels.

This finding provides the first evidence that a variation in the sequence of a mitochondrial peptide is associated with a change in the level of peptides.

It is the first conclusive demonstration that mitochondrial peptides are encoded in and regulated through mitochondrial DNA.

The team subsequently examined the effect of this SNP in a separate large cohort of participants from the Health and Retirement Study.

It is a longitudinal study of approximately 20,000 individuals over the age of 50 in the United States, of which more than 12,500 individuals consented to DNA analysis.

Using this data set, the researchers report finding that the unfavorable version of this SNP, associated with low levels of the humanin peptide, is also associated with accelerated cognitive aging.

This provides the first demonstration linking a humanin SNP in the mitochondria to cognitive decline in people.

The study also shows that in mice, injections of humanin delay cognitive decline associated with aging, proposing a possible therapeutic role for humanin-related drugs.

The mechanism through which humanin acts to mediate these effects involves the suppression of inflammation systemically, as well as specifically in the brain.

The researchers suggest that their study provides insights on how these conditions, and other diseases of aging, might one day be treated and prevented.

The study is led by Kelvin Yen of the USC Leonard Davis School and published in the Nature-published journal Scientific Reports.

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Source: Scientific Reports.