Cited by 151Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses

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Takahashi, Reisuke H., Capetillo-Zarate, Estibaliz, Lin, Michael T., Milner, Teresa A., Gouras, Gunnar K.·2010·Neurobiology of Aging

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.

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Crossref · 10.1016/j.neurobiolaging.2008.07.021

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  1. Mori C Spooner ET Wisniewsk KE Wisniewski TM Yamaguch H Saido TC Tolan DR Selkoe DJ Lemere CA Intraneuronal Abeta42 accumulation in Down syndrome brain Amyloid 2002 9 88 102 12440481

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Authors
Takahashi, R. H., Capetillo-Zarate, E., Lin, M. T., Milner, T. A., & Gouras, G. K.
Affiliations
Weill Cornell Medicine (US)
Venue
Neurobiology of Aging
Publisher
Elsevier BV
Published
2010-07
Volume
31
Issue
7
Pages
1145-1152
ISSN
0197-4580 (ISSN-L)
OpenAlex
W2000668585
Cited by
150
References
47
Citations by year
2026: 4 · 2025: 9 · 2024: 1 · 2023: 1 · 2022: 6 · 2021: 18 · 2020: 15 · 2019: 3 · 2018: 9 · 2017: 12 · 2016: 6 · 2015: 9 · 2014: 13 · 2013: 10 · 2012: 3
FWCI
7.02
Type
journal article
Language
en
Open access
Locations
  • Neurobiology of Aging (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
Funders
  • University of Minnesota
  • National Institutes of Health
  • National Institute on Aging (R01AG027140, K02AG028174, AG028174, AG027140)
  • National Heart, Lung, and Blood Institute (HL-18974, P01HL018974)
  • National Institute of Neurological Disorders and Stroke (R01NS045677, NS 045677)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, amyloid-beta, tau hyperphosphorylation, synapses, synaptic loss, amyloid plaques, neurofibrillary tangles, triple transgenic mice, presenilin 1
MeSH terms
Adult, Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Middle Aged, Peptide Fragments, Phosphorylation, Amyloid beta-Peptides, tau Proteins, Presynaptic Terminals, Mice

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