Diabetes gene linked to degeneration of enzyme involved in Alzheimer's disease onset and progression

October 12, 2010

Mount Sinai School of Medicine researchers have found that a gene associated with the onset of Type 2 diabetes also is found at lower-than-normal levels in people with Alzheimer's disease. The research, led by Giulio Maria Pasinetti, MD, PhD, The Saunder Family Professor in Neurology, and Professor of Psychiatry and Geriatrics and Adult Development at Mount Sinai School of Medicine, was published this month in Aging Cell.

The new study provides insight into a potential mechanism that might explain the relationship between Type 2 diabetes and the onset and progression of Alzheimer's disease. Recent evidence indicates that healthy elderly subjects affected by Type 2 diabetes are twice as likely to develop Alzheimer's disease, but researchers have been unable to explain how.

"The relationship between Type 2 diabetes and Alzheimer's disease has been elusive," said Dr. Pasinetti. "This new evidence is of extreme interest, especially since approximately 60 percent of Alzheimer's disease cases have at least one serious medical condition primarily associated with Type 2 diabetes."

Using mice that were genetically engineered to have Alzheimer's disease comparable to that seen in humans, Dr. Pasinetti and colleagues found that a gene known as proliferator-activated receptor coactivator 1 (PGC-1), a key regulator of currently investigated as a potential for Type 2 , is decreased in Alzheimer's disease. The team reports that this decrease might be causally linked to promotion of Alzheimer's disease. They found that PGC-1 promotes degradation of a specific enzyme known as beta-secretase (BACE). ACE is directly involved in the processing and eventually generation of β-amyloid, an abnormal protein highly linked to Alzheimer's disease and brain degeneration.

"Our research is the first to find that PGC-1 is a common denominator between and Alzheimer's disease," said Dr. Pasinetti. "This discovery will have significant implications for the more than five million Americans affected by Alzheimer's disease, a number that is expected to skyrocket in the next three decades as the population ages. We look forward to continuing to research this discovery and translate it into the development of novel approaches for disease prevention and treatment."

Dr. Pasinetti and his colleagues are optimistic that if they find that PGC-1 can be manipulated pharmacologically to prevent BACE accumulation in the brain, these studies will provide important insights for the formulation of novel treatments and possible preventative strategies in Alzheimer's disease.

Related Stories

Recommended for you

Artificial beta cells

December 8, 2016

Researchers led by ETH Professor Martin Fussenegger at the Department of Biosystems Science and Engineering (D-BSSE) in Basel have produced artificial beta cells using a straightforward engineering approach.

Key regulator of bone development identified

December 8, 2016

Loss of a key protein leads to defects in skeletal development including reduced bone density and a shortening of the fingers and toes—a condition known as brachydactyly. The discovery was made by researchers at Penn State ...

Researchers question lifelong immunity to toxoplasmosis

December 8, 2016

Medical students are taught that once infected with Toxoplasma gondii—the "cat parasite"—then you're protected from reinfection for the rest of your life. This dogma should be questioned, argue researchers in an Opinion ...

0 comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.