He found that once TGF-beta activated a cell, it triggered the CTGF gene to make its protein (see chart).

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The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein.

ECONOMIST: Alzheimer's disease

The idea that more brain cell activity could lead to more amyloid-beta build up is an exciting, if sobering, finding.

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By 1992 Grotendorst, who had done work at the University of South Florida and is now at the University of Miami, concluded that it was CTGF, not TGF-beta, that triggers collagen production by binding to specific cell receptors.

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An experimental new class of drugs is aimed at rendering TGF-beta and CTGF ineffective by blocking their ability to bind with cell receptors.

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The dominant explanation of Alzheimer's disease contends that the massive brain cell death is due to the buildup of plaques containing a protein called beta amyloid built up in the brain.

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