Abstract
During recent years, many reports have indicated that in addition to the progressive neuropathology observed in Alzheimer's disease (AD), there are also plasticity-related changes in the AD brain. It is thought that these plastic events are an attempt by the brain either to try to restore structure and function or to compensate for the damage caused by the disease. Alternatively, it is possible that these changes are a part of the disease's pathologic cascade. Here we discuss our recent findings on highly polysialylated neural cell adhesion molecule (PSA-NCAM) and neuronal-expressed calcium-binding proteins in the hippocampus and entorhinal cortex of controls and patients with AD in relation to the other findings which suggest that structural plasticity is an integral part of the disease process of AD.
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