Alzheimer's Disease and Brain Minerai Metabolism

Dementia constitutes one of the greatest médical and social problems facing the aging populations of developed countries. Alzheimer's disease is the main cause of dementia in the eiderly, and the cognitive décline that characterizes this disorder clinically is accompanied by the development of hallmark neuropathological changes, including loss of neurons and synapses and the development of senile plaques and neurofibrillary tangles. Plaques consist of extracellular deposits of an abnormal protein fragment, the β-amyloid peptide, which aggregates in fibrils in a "star-burst" array to form the core of mature plaques. This plaque core is surrounded by neuritic processes and glial cells and there is loss of synapses in the adjacent neuropil (1). Neurofibrillary tangles are lésions in which paired helical filaments (PHFs) are deposited intracellularly. A major component of PHFs is an abnormally phosphorylated form ofthe microtubule-associated protein, tau, indicating a dérangement of cytoskeletal function in affected neurons (2).