The DOI matches its Crossref record, with a small difference in title or year; 46 of the 47 references it cites were found in a registry or an index.
Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses
Open accessAbstract
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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“A number of studies have associated intraneuronal Ab buildup with hyperphosphorylation of tau protein, 8 disturbed protein trafficking and sorting, 9 reduced expression of synaptic proteins, 10 and mitochondrial dysfunction.11,12”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [8]
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Cites
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BackgroundIntracellular amyloid-β in Alzheimer's disease
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Basic mechanisms of neurodegeneration: a critical update
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Synaptic degeneration in Alzheimer's disease
Arendt, T. (2009) · Acta Neuropathologica · doi:10.1007/s00401-009-0536-x · Cited by 517
Reduced IGF-1 signaling delays age-associated proteotoxicity in mice
Cohen, E., Paulsson, J. F., Blinder, P., Burstyn-Cohen, T., Du, D., Estepa, G., Adame, A., Pham, H. M., Holzenberger, M., Kelly, J. W., et al. (2009) · Cell · doi:10.1016/j.cell.2009.11.014 · Cited by 488
Metadata
- 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)
- 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
- 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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