Researchers Prevent Memory Loss in Alzheimer's Model

Their findings were reported in the January 2004 issue of Neuron.

The researchers used behavioral, biochemical, and electrophysiologic methods to analyze beta-secretase (BACE1), which is required for the production of beta-amyloid, in mice bred to lack the enzyme but to also overproduce amyloid precursor protein, which BACE "clips” into fragments of beta-amyloid that eventually form the plaques associated with Alzheimer's disease. The mice were healthy and had no serious neurologic abnormalities. The beneficial effects were seen well before beta-amyloid plaques formed, indicating that the soluble forms of the protein can disrupt learning and memory in early stages of the disease.

"Potential compounds that block BACE1 should be useful in counteracting Alzheimer's. We clearly show for the first time that genetic reduction of brain beta-amyloid levels prevents memory deficits and brain cell functional abnormalities in a laboratory model of Alxheimer's disease,” said Masuo Ohno, research assistant professor of physiology at the Feinberg School of Medicine at Northwestern University (IL, USA).




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