Alzheimer’s disease (AD) is insidious, occurring gradually and resulting in memory loss, behavior and personality changes, and a decline in thinking or cognitive abilities. These losses are related to a breakdown in the connections between nerve cells in the brain (neurons), and the eventual demise of many of these cells. Two abnormal lesions in the brain are the hallmarks of AD: Neurofibrillary tangles and amyloid plaques.

Tau and Amyloid Precursor Protein (APP) are normal proteins that change in type and concentration in the brains of those with Alzheimer’s disease, forming these lesions, which are believed to damage and shrink neurons. Memory function is impaired when tangles and plaques form in the memory centers of the brain. In these studies, we will examine the cerebrospinal fluid (CSF) level of abnormal by-products of these proteins in people with and without memory changes. CSF is the fluid that surrounds and cushions the brain and the spinal chord. Our body is constantly making it and it is constantly circulating in our central nervous system. Because of close association, this fluid may act as a window to brain levels of tau proteins and amyloid beta proteins, which are abnormal breakdown products of APP.

Studies at the Center for Brain Health have demonstrated alterations in CSF levels of certain tau and amyloid proteins in people with or at risk for developing AD. We have also found, using MRI, that there is a decrease in volume in the entorhinal cortex of the hippocampus, a memory center in the brain in many of these individuals. This finding has since been corroborated around the world. Currently, the only way to definitively diagnose AD is post-mortem. By correlating CSF tau and amyloid protein levels with results from brain MRI scans and cognitive tests, we believe the ability to accurately diagnosis early Alzheimer’s disease is at hand.

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