Genetic Variations that Boost PKC Enzyme Contribute to Alzheimer’s Disease
PKC alpha is required towards pathological consequences of amyloid beta plaques; mutations that heighten its activity found in patients with the disease
In Alzheimer’s infirmity, plaques of amyloid beta protein accumulate in the brain, damaging connections between neurons. Now, researchers at University of California San Diego School of Medicine and Harvard Medical School be seized of found that the enzyme Protein Kinase C (PKC) alpha is needful for amyloid beta to damage neuronal connections. They also identified genetic variations that enhance PKC alpha activity in patients with Alzheimer’s ailment.
The study, published May 10 in Science Signaling, may largess a new therapeutic target for the disease.
“Until recently, it was thinking that PKC helped cells survive, and that in addition much PKC activity led to cancer. Based in c~tinuance that assumption, many companies tested PKC inhibitors at the same time that drugs to treat cancer, but they didn’t operate,” said co-senior author Alexandra Newton, PhD, professor of pharmacology at UC San Diego School of Medicine.
“Instead, we not long ago found that the opposite is granted. PKC serves as the brakes to organic unit growth and survival, so cancer cells service when PKC is inactivated. Now, our latest study reveals that also much PKC activity is also depressing, driving neurodegeneration. This means that drugs that failed in clinical trials against cancer may provide a new therapeutic opportunity for Alzheimer’s disease.”
The study was a three-highroad collaboration between experts in PKC (Newton), neuroscience (Roberto Malinow, MD, PhD, Distinguished Professor of Neurosciences and Neurobiology and possessor of the Shiley-Marcos Endowed Chair in Alzheimer’s Disease in Honor of Dr. Leon Thal at UC San Diego School of Medicine) and genomics (Rudolph Tanzi, PhD, professor of neurology at Harvard Medical School).
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