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Mina Yaar, MD; Barbara A. Gilchrest, MD

Arch Dermatol. 1997;133(10):1287-1291.

Abstract
The aging process leads to increased vulnerability to injury and disease, resulting in a decline in 1 or more organ systems that is incompatible with life. One of the most devastating age-associated neurodegenerative disorders, Alzheimer disease, is characterized by neuronal loss and the extracellular deposition in the brain of β-amyloid peptide, which is presumed to be causally related. Using cultured neural crest-derived cutaneous melanocytes, we find that in the presence of β-amyloid, melanocytes, like neurons, undergo programmed cell death (apoptosis). Nerve growth factor, which has been reported to attenuate the loss of cholinergic neurons in Alzheimer disease, protects melanocytes from apoptosis induced by β-amyloid. Moreover, β-amyloid is a ligand for the 75-kD transmembrane neurotrophin receptor that belongs to the family of apoptotic receptors that generates a cell-death signal on activation. Our data suggest that neuronal death in Alzheimer disease is mediated by the interaction of β-amyloid with the 75-kD neurotrophin receptor. Human melanocytes provide a valuable in vitro model for studies of Alzheimer disease and for development of potential therapies. Arch Dermatol. 1997;133:1287-1291

Author Affiliations
From the Department of Dermatology, Boston University School of Medicine, Boston, Mass.

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