Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses Academic Article uri icon

Overview

MeSH Major

  • Alzheimer Disease
  • Amyloid beta-Peptides
  • Peptide Fragments
  • Presynaptic Terminals
  • tau Proteins

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.

publication date

  • July 2010

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2909664

Digital Object Identifier (DOI)

  • 10.1016/j.neurobiolaging.2008.07.021

PubMed ID

  • 18771816

Additional Document Info

start page

  • 1145

end page

  • 52

volume

  • 31

number

  • 7