The basic hypothesis we are testing is that, in Alzheimer’s disease (AD), the delicate balance of brain Zn is disrupted and may play a role in the pathogenesis of neuron degeneration. Previous neutron activation analysis (NAA) studies showed an increase in total Zn in multiple AD brain regions at the bulk level. Recent micro-particle-induced X-ray emission (PIXE) measurements from our lab revealed a significant elevation of Zn in senile plaques (SP) in AD brain compared with adjacent neuropil and a significant increase in AD neuropil compared to control neuropil. The observation of elevated Zn in SP is of interest because the amyloid precursor protein contains a Zn binding site that prevents normal cleavage leading to the generation of a toxic fragment of beta amyloid, the constituent of SP. We are investigating cellular levels of Zn in AD using micro-PIXE analysis and are comparing levels of Zn in post-mortem serum and hippocampus in AD and control subjects using NAA.
This work is performed in collaboration with Dr. Mark Lovell at the University of Kentucky Sanders Brown Center on Aging.
Senile plaques (20 to 40 µm in diameter) in the brain tissue from an AD patient
