Jan 8, 2011

Pathological changes induced by amyloid-β in Alzheimer's disease

Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
Kazuyuki TakataTakashi Taniguchi

Abstract

The pathologic hallmarks of Alzheimer's disease (AD) include senile plaque, neurofibrillary tangles (NFTs), synaptic loss, and neurodegeneration. Senile plaque and NFTs are formed by accumulation of amyloid-β (Aβ) and hyperphosphorylated tau, respectively. Progressive synaptic dysfunction and loss closely correlate with cognitive deficits in AD. Based on studies of the genes responsible for familial AD and temporal patterns of pathologic changes in AD brains, the Aβ accumulation is thought to be a primary event that influences other AD pathologies in the developmental cascade of AD. However, the details of Aβ effects on the other AD pathologies remain poorly understood. In this review, we provide an overview of the effects of Aβ in AD brains, especially focusing on synaptic dysfunction and microglia. We have recently found abnormal accumulation of a key molecule for actin assembly in NFTs of AD brains, and it was revealed that the accumulation requires not only tau pathology but also an Aβ burden in a study using transgenic mouse models of AD. Synaptic integrity is morphologically maintained by the precise regulation of actin assembly. Therefore, the results suggest the possibility that Aβ may promote NFT maturation and induce ...Continue Reading

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Mentioned in this Paper

Familial Alzheimer Disease (FAD)
APP protein, human
Neurofibrillary Degeneration (Morphologic Abnormality)
Isoactin
Actins
N-Actin
Brain
Nerve Degeneration
Retrograde Degeneration
Plaque, Amyloid

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