DYSTROPHIC NEURITES OF SENILE PLAQUES ARE DEFECTIVE IN PROTEINS INVOLVED IN EXOCYTOSIS AND NEUROTRANSMISSION

Dystrophic neurites are major components of neuritic (both immature an d mature) senile plaques in Alzheimer disease. Previous studies have s hown strong immunoreactivity for different neuropeptides, and chromogr anin A, a protein associated with dense-core vesicles, in dystrophic n eurites. In the present study, antibodies to synaptophysin, synapsin, Rab3a and synaptotagmin (synaptic vesicle proteins), and SNAP-25 (syna ptosomal-associated protein of 25 kD) and syntaxin (presynaptic plasma membrane proteins) have been used to learn about the dystrophic neuri te equipment of proteins that are necessary for the docking and fusion of synaptic vesicles, and then for exocytosis and neurotransmission. The present results have shown that, although most neuritic senile pla ques have chromogranin A-and SNAP-25-immunoreactive dystrophic neurite s, only a percentage of them contain synaptophysin, and a minority con tain synaptotagmin and Rab3a. Dystrophic neurites do not contain synap sin and syntaxin. These results show that dystrophic neurites of senil e plaques are defective in proteins that control exocytosis and neurot ransmission.