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Implications of Amyloid Precursor Protein and Subsequent β‐Amyloid Production to the Pharmacotherapy of Alzheimer's Disease
Author(s) -
RojasFernandez Carlos H.,
Chen Ming,
Fernandez Hugo L.
Publication year - 2002
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1592/phco.22.17.1547.34116
Subject(s) - neurodegeneration , dementia , disease , amyloid precursor protein , amyloid (mycology) , alzheimer's disease , amyloid precursor protein secretase , biochemistry of alzheimer's disease , medicine , neuroscience , psychology , pathology
Alzheimer's disease is the most common type of dementia in older people. It is highly prevalent, affecting 35–45% of those aged 85 years or older. This disease has devastating consequences to patients, their families, caregivers, and the health care system. Much has been learned about its pathobiology, which has led to the β‐amyloid (Aβ) hypothesis. This hypothesis continues to be the predominant postulate of the pathobiology of Alzheimer's disease. Under this hypothesis, abnormal accumulation of Aβ is followed by a cascade of neurotoxic effects, which eventually result in neurodegeneration and development of Alzheimer's disease. This is thought to be the result of altered processing of the amyloid precursor protein (APP), preferentially by β‐ and γ‐secretase enzymes rather than nonamyloidogenic processing by α‐secretase. The growing body of knowledge regarding the processing of APP to various forms of Aβ has resulted in new approaches to the investigation of putative anti‐Alzheimer's disease compounds, including immune‐based therapies and various agents that can positively affect APP processing.