Taking Back the Brain

A promising novel target for potentially treating Alzheimer's disease has been identified in mice by a team at the University of California, Davis. The researchers will present their findings at the Biophysical Society's 56th Annual Meeting in San Diego, Calif., held Feb. 25-29.
The team’s focus is on controlling cells in the brain known to be major inflammatory agents. These cells, called microglia, are activated by toxic beta amyloid proteins that accumulate as plaques in the brain and disrupt neuronal function, and they are major players in the initiation and progression of Alzheimer's disease. To turn off the microglia, and therefore stop their neurotoxic effects, the UC Davis team blocked the flow of potassium ions through a voltage-gated potassium channel on the microglial membrane.
"Our observations raise the exciting possibility that potassium channel blockers might preferentially inhibit the action of microglia related to killing neurons without affecting the beneficial functions associated with them, as such as scavenging of debris,” says UC Davis’ David P. Jenkins, first author of the study.
In their investigation, the researchers examined microglia from mice specially bred to develop a mouse-mimic of Alzheimer's disease. They found that the adult mouse brains with high levels of beta amyloid also expressed higher levels of potassium channels on their microglia compared to microglia isolated from normal mouse brains. The researchers tested the functional importance of microglial potassium channels by administering a potassium channel blocker to brain tissue specimens. Results showed that the blocker inhibited plaque-induced microglia activation and the toxicity associated with it, but that it did not interfere with the useful "housecleaning" tasks that microglia perform.
"With the rise of Alzheimer's disease,” says Jenkins, “finding a novel pharmacological target for curbing the harmful effects of beta amyloid-induced microglia activation is highly desirable in developing new therapies."
The presentation, “Microglial KV1.3 channels as a potential target for Alzheimer’s disease,” is at 10:30 a.m. on Wednesday, Feb. 29, 2012, in the San Diego Convention Center, Hall FGH. ABSTRACT: http://tinyurl.com/7t2u4f5
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This news release was prepared for the Biophysical Society (BPS) by the American Institute of Physics (AIP).