Aluminium is an element suspected to contribute to the pathogenesis of Alzh
eimer's disease, but its mechanism of action is not clear. Neuropeptide Y (
NPY) plays a significant role in feeding behaviour. Our spectroscopic, ELIS
A, and western blot studies indicate that aluminium interacts with neuropep
tide Y and alters significantly the a-helical content. We found that alumin
ium reduced levels of NPY in the hypothalamus of aged rabbits. NPY polyclon
al antibody interaction was found to depend upon the alpha-helical content
of NPY. These results clearly show that aluminium alters NPY structure and
this could explain the abnormality in feeding behaviour seen in patients wi
th Alzheimer's disease.