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Molecular basis of Alzheimer's disease: From amyloid hypothesis to treatment in the foreseeable future
Author(s) -
Tabira Takeshi
Publication year - 2004
Publication title -
geriatrics and gerontology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 57
eISSN - 1447-0594
pISSN - 1444-1586
DOI - 10.1111/j.1447-0594.2004.00141.x
Subject(s) - tangle , senile plaques , pathological , medicine , neuroscience , dementia , neurofibrillary tangle , alzheimer's disease , mechanism (biology) , disease , atrophy , amyloid (mycology) , pathology , autopsy , senile dementia , psychology , philosophy , mathematics , epistemology , pure mathematics
Alzheimer's disease (AD) is the most common dementing disorder in the elderly. It is clinically characterized by insidious onset of memory disturbance followed by slowly progressive global dementia. The patient's brain at autopsy shows diffuse cerebral atrophy, and microscopic findings are characterized by the presence of intraneuronal neurofibrillary tangle (NFT), senile plaques with extraneuronal β amyloid deposits, and dystrophic changes of neuronal processes with synaptic and neuronal loss. The pathological mechanism of these hallmarks are now well understood on the molecular basis, and new strategies to prevent and reverse these pathological changes are now being developed. Here I review some personal interest of the mechanism, and describe future strategies for prevention and treatment of AD.

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