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Alzheimer's disease: synaptic dysfunction and Aβ
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In Alzheimer's disease, accumulation, aggregation, and deposition of Aβ peptides in the brain are critical steps in pathogenesis.
“Increasing evidence supports the hypothesis that accumulation, aggregation, and deposition of amyloid-β (Aβ) peptides in the brain are critical steps in its pathogenesis (Selkoe, 2001; Shankar and Walsh, 2009).”
From Heparan Sulphate Proteoglycan and the Low-Density Lipoprotein Receptor-Related Protein 1 Constitute Major Pathways for Neuronal Amyloid-β Uptake (2011) · cites this paper as Shankar and Walsh, 2009
In the Introduction section “Aβ exists in many different assembly forms” (page unavailable), the paper describes a proposed pathogenic cascade beginning with Aβ accumulation and discusses its aggregation into multiple forms. It does not establish deposition in plaques as a critical step; instead, it notes that plaque quantity and progression correlate poorly with clinical progression. (LLM, conf=0.85)
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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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Metadata
- Authors
- Shankar, G. M., & Walsh, D. M.
- Venue
- Molecular Neurodegeneration
- Published
- 2009
- Volume
- 4
- Issue
- 1
- Pages
- 48
- ISSN
- 1750-1326
- PMC
- PMC2788538
- Cited by
- 486
- References
- 40
- Language
- en
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