Researchers in Nature reveal what could be one of the earliest molecular seeds of Alzheimer's disease - an assembly of amyloid-b peptides that accumulates outside cells and affects memory. This finding could potentially be used to detect, and perhaps prevent, the disease long before more serious signs of memory loss arise.
People at high risk of Alzheimer's disease show subtle memory problems and brain abnormalities several years before the onset of more serious clinical symptoms. Karen Ashe and her colleagues examined mice that have been genetically engineered to make a form of human amyloid-b precursor protein (APP) that is linked to Alzheimer's disease. Like humans, these mice show memory problems in middle age, before formation of the insoluble amyloid-b plaques classically associated with the disease.
The researchers found that early memory deficits in these mice are caused by the accumulation of complexes of 12 amyloid-b peptides outside cells. When they injected these complexes into the brains of healthy rats, their memory was temporarily disrupted. The authors propose that these amyloid-b assemblies impair memory independently of plaques or neuronal death and that, under certain circumstances, they can trigger a series of events leading to Alzheimer's disease.
Karen Ashe (University of Minnesota, Minneapolis, MN, USA)
Richard Morris (University of Edinburgh, Edinburgh, UK)
(C) Nature press release.
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