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Gladstone scientists uncover mechanism for the major genetic risk factor of Alzheimer's disease
Date:10/13/2010

obarbital, a compound that enhances GABA action. They found that the injections rescued the learning and memory deficits in the mice. They also examined the effects of apoE4 on tau, another protein implicated in Alzheimer's disease. When they genetically eliminated the mouse's own tau, the loss of the GABAergic interneuron was halted and the learning and memory deficits were prevented.

"We previously showed that suppressing the protein tau can prevent Aβ from causing memory deficits and other abnormalities in mouse models of Alzheimer's disease," said Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease. "This new study demonstrates that tau also acts downstream of apoE4. Thus, tau might be a general causative factor in Alzheimer's disease pathogenesis."

ApoE4 seems to increase the concentration of a particular species of tauphosphorylated tau known to be toxic in some kinds of neurodegeneration. Increases in the levels of phosphorylated tau eventually kill the GABAergic interneurons, and this loss leads to learning and memory deficits. The Gladstone team showed that giving the mice pentobarbital to boost the GABA function could stop this chain of events. In effect, they were providing a product of a reaction downstream from where apoE4 disrupts the pathway.

"Clinical studies have shown that apoE4 is associated with increased activity in the hippocampus at rest and in response to memory tasks in humans. Our study suggests that this may reflect the impaired GABAergic inhibitory neuronal functions in the presence of apoE4," said Dr. Huang. "Our study also demonstrates that increasing GABA signaling and reducing tau are potential strategies to treat or prevent apoE4-related Alzheimer's disease."


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Contact: Valerie Tucker
vtucker@gladstone.ucsf.edu
415-734-2019
Gladstone Institutes
Source:Eurekalert

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