When scientists blocked AMP-activated protein kinase (AMPK) in mice, neurons were protected from the loss of synapses — neuron-to-neuron connection points — that are typical of the early phase of Alzheimer’s disease, according to Scripps researchers.
“These findings open up many new avenues of investigation, including the possibility of developing therapies that target the upstream mechanisms leading to AMPK over-activation in the brain,” said TSRI professor Franck Polleux, who led the study.
His team’s report appears in this week’s edition of the journal Neuron.
Alzheimer’s disease, a fatal neurodegenerative disorder that afflicts more than 25 million people worldwide, has no cure or disease-delaying therapy.
TSRI said its been known for years that patients in the early stages of Alzheimer’s diseases lose synapses in areas of the brain that involve memory, but scientists didn’t know how. Recent studies have shown that AMPK might lead to tangles of the protein tau that are seen in the brains of patients.
The enzyme is also tied to regulation of insulin synthesis and secretion in pancreatic cells, and modulation of hypothalamic functions, according to themedicalbiochemistrypage.org.
Polleux said the discovery not only could impact potential Alzheimer’s treatments, but also suggests a need for further safety studies on an existing drug, metformin, a popular treatment for Type 2 Diabetes. He said metformin causes AMPK over-activation.
TSRI said the scientists are now studying what else the over-activation of the AMPK enzyme causes, and how it might contribute to the progression of Alzheimer’s disease over the long term.