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Co-occurrence of Alzheimer's disease ß-amyloid and ? pathologies at synapses.


ABSTRACT: Although beta-amyloid (Abeta) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Abeta and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop in triple transgenic mice harboring mutations in APP, tau and presenilin 1, we utilized these well-characterized mouse models to explore the relation between Abeta and tau pathologies. We now report that pathological accumulation of Abeta and hyperphosphorylation of tau develop concomitantly within synaptic terminals.

SUBMITTER: Takahashi RH 

PROVIDER: S-EPMC2909664 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature

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Co-occurrence of Alzheimer's disease ß-amyloid and τ pathologies at synapses.

Takahashi Reisuke H RH   Capetillo-Zarate Estibaliz E   Lin Michael T MT   Milner Teresa A TA   Gouras Gunnar K GK  

Neurobiology of aging 20080903 7


Although beta-amyloid (Abeta) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Abeta and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precursor protein (APP) Swedish mutant transgenic mice, and since neurofibrillary tangles develop  ...[more]

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