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Managing microglia in Alzheimer's

Microglia are often found near damaged tissue in Alzheimer's disease patients, but whether the brain's innate immune cells are helpful or harmful in the disease has been an open question. Now, German researchers have evidence that both camps got it right. A pair of studies reveals that microglia play opposing roles in AD pathogenesis: they not only eliminate b-amyloid aggregates via phagocytosis but also kill nearby neurons by causing inflammation and the release of neurotoxic proteases.

Importantly, the reports suggest that the two functions of microglia are controlled by different cell-surface receptors, thus providing a road map for how to clear b-amyloid (Ab) plaques without destroying healthy neurons that are in close proximity.

One report makes a case for antagonizing chemokine CX3C motif receptor 1 (CX3CR1), which promotes inflammation and neuron killing by microglia.1The other shows that an adrenergic receptor agonist from Chelsea Therapeutics International Ltd.and Dainippon Sumitomo Pharma Co. Ltd. stimulates a microglial mechanism for clearing Ab deposits while suppressing inflammation.2

Together, the studies are "a good demonstration and proof of principle that targeting microglia can be beneficial" if it can be done selectively, said Douglas Feinstein, research professor of anesthesiology at the University of Illinois at Chicago and a research career scientist at the Department of Veterans Affairs.

Chilling, not killing

The chemokine receptor study, from a team led by Jochen Herms, professor of neurology at Ludwig Maximilian University of Munich, connects the dots and orders the events in AD pathology.

The group created an AD mouse model with microglia that lacked Cx3cr1, which is known to help microglia

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