Abstract
One of the pathological characteristics of Alzheimer's disease (AD) is the formation of dystrophic neurites accompanied by aberrant neuronal sprouting. Although a number of studies have focussed on the formation of amyloid plaques and neurofibrillary tangles, the mechanism of neuronal sprouting in AD is not fully understood. The protein levels of neural Wiskott–Aldrich syndrome protein (N-WASP), WASP interacting SH3 protein (WISH) and WASP family verprolin-homologous protein (WAVE) were significantly increased in AD brains. In addition, N-WASP, WISH and WAVE were co-localized with filamentous actin in abnormal dendrite-like processes sprouting from staurosporine-treated human SH-SY5Y cells. These results suggest that N-WASP, WISH and WAVE may participate in the neurodegenerative aberrant sprouting in AD neurons.
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