Chapter category: Neurodegenerative Disease

Cell Cycle and Chromosome Segregation Defects in Alzheimer’s Disease

This chapter appears in the following book:

Cell-Cycle Mechanisms and Neuronal Cell Death

Edited by: Agata Copani and Ferdinando Nicoletti
ISBN: 0-306-47850-1
» Get more information about this book at landesbioscience.com «

Chapter authors:
Huntington Potter

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Despite a common set of hallmark neuropathological lesions and clinical symptoms, Alzheimer’s disease has an apparently complex etiology. The disease can be caused by autosomal dominant mutations in at least three genes (encoding the amyloid precursor protein (APP) and the two presenilins). In addition, it can be influenced by certain allelic variants of at least three “risk factor“ genes (apolipoprotein E, antichymotrypsin, and interleukin-1), or may arise “sporadically” with no evident genetic component. In the end, as many as 30-40% of individuals over the age of 85 may have some symptoms of Alzheimer’s— underscoring the fact that age itself is the strongest risk factor for the disease. It has been known for almost twenty years that individuals with trisomy 21 (Down syndrome) exhibit Alzheimer neuropathology by the time they are 30-40 years old. Somewhat later, they also develop dementia, and eventually die of Alzheimer’s disease. Because the gene for amyloid precursor protein (APP) resides on chromosome 21, its consequent overexpression in trisomy 21 cells presumably contributes to the development of Alzheimer’s disease in Down syndrome individuals.

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Chapter category: Neurodegenerative Disease

Cell Cycle and Chromosome Segregation Defects in Alzheimer’s Disease

Additional chapters from this book:

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