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Study suggests a second dimension to Alzheimer's disease

and genetic inheritance.

The two forms of the disease otherwise share many common characteristics, Bezprozvanny said, and it is generally assumed that study of familial Alzheimer's can lead to new insights into general mechanisms underlying the disease.

Earlier studies had linked mutations in the presenilin gene to abnormal calcium signaling and suggested that calcium might have some relevance to Alzhiemer's disease. However, the mechanistic basis for presenilin's apparent effects on calcium remained unclear, leaving a question as to whether the proteins played a direct role.

The researchers now report from studies in mice that presenilins can form ion channels. The effects of presenilin could account for about 80% of the calcium leaked from a membrane bound cellular compartment called the endoplasmic reticulum, they found.

Cells with the mutant presenilin become "overloaded" with calcium, Bezprozvanny explained, which heightens the strength of the calcium signal. Moreover, the heightened calcium signal was reversed in mutant cells in which the scientists restored normal presenilin. They further showed presenilin's role in calcium signaling to be independent of its role in the production of amyloid .

The findings suggest that drugs that restore normal calcium levels might be useful for treating Alzheimer's disease, Bezprozvanny said. Indeed, he added, a drug called memantine, which is already in use against Alzheimer's, acts on receptors that are a component of the calcium pathway.

The development of Alzheimer's drugs has almost exclusively focused on amyloid plaques, he said. The current findings begin to suggest the possibility that a combination therapy targeting both amyloid and calcium signaling might be a "best case scenario," Bezprozvanny speculated.

Aberrant calcium signaling might also be a common link among multiple neurodegenerative diseases, he added. For example, he noted that his group ea
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
7-Sep-2006


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