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Worldwide, 50 million people are living with Alzheimer’s disease and other dementias. According to the Alzheimer’s Association, every 65 seconds someone in the United States develops this disease, which causes problems with memory, thinking and behavior.

It has been more than 100 years since Alois Alzheimer, M.D., a German psychiatrist and neuropathologist, first reported the presence of senile plaques in an Alzheimer’s patient brain. It led to the discovery of that produces deposits or plaques of fragments in the brain, the suspected culprit of Alzheimer’s disease. Since then, amyloid has been extensively studied because of its association with Alzheimer’s disease. However, amyloid precursor protein distribution within and on neurons and its function in these cells remain unclear.

A team of neuroscientists led by Florida Atlantic University’s Brain Institute sought to answer a fundamental question in their quest to combat Alzheimer’s disease—” Is amyloid precursor protein the mastermind behind Alzheimer’s disease or is it just an accomplice?”

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Sirtuins have long been implicated in playing a role in the longevity of various species, including our own, and researchers at the University of Rochester have now discovered more supporting evidence that they do.

What are sirtuins?

Sirtuins are a family of proteins that facilitate cellular function and have long been known to play a role in aging. In particular, they are responsible for functions such as gene expression and are involved in DNA repair. It has long been understood that sirtuins played a role in aging, but the key factor in how well they function is the presence of nicotinamide adenine dinucleotide (NAD+), a coenzyme found in all living cells. NAD+ biology is central to deregulated nutrient sensing and a reason why we age, and sirtuins play a key role in this biology.

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