Alzheimer's disease (AD) is the major cause of serious dementia and memory loss in several million elderly Americans. The most prominent lesions in the brains of these patients are the depositions of two types of abnormal filaments: the predominantly intraneuronal neurofibrillary tangles (NFT), which consist of paired helical filaments (PHF), and the extracellular amyloid fibers. These changes are characteristic of AD, and a final diagnosis of this disease is based on the presence of large numbers of these abnormal filamentous structures in the patient's brain. The amyloid fibers consist of a peptide subunit termed β-protein or A4 peptide, which derives from a larger precursor protein. In this study we review the structural characteristics, regulation of expression, and metabolism of the Alzheimer amyloid precursor in brain tissue and cell cultures.
- Neuritic plaques