Cited by 206Alzheimer's disease research and treatmentsNeuroscience and Neuropharmacology ResearchNeuroinflammation and Neurodegeneration Mechanisms

The synaptic Aβ hypothesis of Alzheimer disease

Tanzi, Rudolph E·2005·Nature Neuroscience

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Crossref · 10.1038/nn0805-977

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  • Soluble Ab oligomers cause early memory problems by disrupting LTP and LTD mechanisms.

    “The cognitive decline, however, starts well before this stage, and there is growing evidence that one of the toxic protein species believed to be etiologically related to AD, soluble Ab oligomers, causes early memory problems by disrupting LTP and LTD mechanisms (Walsh et al. 2002;Tanzi 2005;Shankar et al. 2008;Cisse et al. 2011).”

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References 14 · Cited by 206

Authors
Tanzi, R. E.
Affiliations
Harvard University (US)
Corresponding author
Tanzi, Rudolph E
Venue
Nature Neuroscience
Published
2005-08
Volume
8
Issue
8
Pages
977-979
ISSN
  • 1097-6256 (ISSN-L)
  • 1546-1726
OpenAlex
W2030320815
Cited by
206
References
14
Citations by year
2025: 3 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 13 · 2020: 4 · 2019: 9 · 2018: 8 · 2017: 14 · 2016: 14 · 2015: 10 · 2014: 12 · 2013: 7 · 2012: 11
FWCI
8.93
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid-beta, Alzheimer's disease, NMDA receptor, synaptic dysfunction, receptor internalization, endocytosis, synaptic toxicity
MeSH terms
Alzheimer Disease, Brain, Endocytosis, Humans, Models, Neurological, Synapses, Receptors, N-Methyl-D-Aspartate, Amyloid beta-Peptides

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