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

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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

DOI 10.1016/j.neurobiolaging.2008.07.021PMC PMC2909664

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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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Authors: Takahashi, R. H., Capetillo-Zarate, E., Lin, M. T., Milner, T. A., & Gouras, G. K.
Affiliations: Weill Cornell Medicine (US)
ORCID: Takahashi, Reisuke H.
Milner, Teresa A.
Gouras, Gunnar K.
Venue: Neurobiology of Aging
Publisher: Elsevier BV
Published: 2010-07
Volume: 31
Issue: 7
Pages: 1145-1152
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2008.07.021
PMC: PMC2909664
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: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses

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