AANS Neurosurgeon | Volume 26, Number 1, 2017

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Genetic Variations that Boost PKC Enzyme Contribute to Alzheimer's Disease

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PKC alpha is required for pathological consequence of amyloid beta plaques; mutations that enhance its activity found in patients with the disease

Researchers have recently discovered that the enzyme Protein Kinase C (PKC) alpha must be present for amayloid beta to begin accumulating in the brain. Amayloid beta accumulations, or plaques, are what damage the brain and neuronal connections in patient’s who have been diagnosed with Alzheimer’s disease. “Until recently, it was thought that PKC helped cells survive, and that too much PKC activity led to cancer. Based on that assumption, many companies tested PKC inhibitors as drugs to treat cancer, but they didn’t work,” said co-senior author Alexandra Newton, PhD, professor of pharmacology at UC San Deigo School of Medicine. “Instead, we recently found that the opposite is true. PKC serves as the brakes to cell growth and survival, so cancer cells benefit when PKC is inactivated. Now, our latest study reveals that too much PKC activity is also bad, driving neurodegeneration. This means that drugs that failed in clinical trials for cancer may provide a new therapeutic opportunity for Alzheimer’s disease.” To read more, click here.

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