In Alzheimer’s disease, glutamate excitotoxicity which can damage neurons through chronic activation is exacerbated by deficiency of ABCA7, the second strongest genetic risk factor for the disease. The findings highlight ABCA7 and glutamate–GABA signaling as potential therapeutic targets.

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In Alzheimer’s disease, glutamate excitotoxicity which can damage neurons through chronic activation is exacerbated by deficiency of ABCA7, the second strongest genetic risk factor for the disease. The findings highlight ABCA7 and glutamate–GABA signaling as potential therapeutic targets.

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