Amyloid β-Peptide: The Inside Story
Abstract
The amyloid beta-peptide (Abeta) plays an early and critical role in the pathogenic cascade leading to Alzheimer's disease (AD). Abeta is typically found in extracellular amyloid plaques that occur in specific brain regions in the AD and Down syndrome brain. Mounting evidence, however, indicates that intraneuronal accumulation of this peptide may also contribute to the cascade of neurodegenerative events that occur in AD and Down syndrome. A pathogenic role for intracellular Abeta is not without precedent, as it is known to be an early and integral component of the human muscle disorder inclusion body myositis (IBM). Therefore, it is plausible that intracellular Abeta may likewise induce cytopathic effects in the CNS, causing neuronal and synaptic dysfunction and perhaps even neuronal loss. Here we review recent evidence supporting a pathogenic role for intracellular Abeta in AD, Down syndrome, and IBM.
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Recent studies have described intraneuronal Aβ accumulation in AD and DS brain and have reported that amyloid plaques appear to originate from neuron cell bodies or processes.
“Recent studies have described intraneuronal A 𝛃 accumulation in AD and DS brain and have reported that amyloid plaques appear to originate from neuron cell bodies or processes (for review, see Echeverria and Cuello, 2002; Tseng et al., 2004; Gouras et al., 2005).”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Tseng et al., 2004
Recent studies have reported intraneuronal Aβ in AD, Down's syndrome, and APP transgenic brains, suggesting that intraneuronal Aβ may play a role in AD pathology.
“Recent studies have reported intraneuronal A 𝛃 in AD, Down's syndrome, and APP transgenic brains (for review, see Echeverria and Cuello, 2002; Tseng et al., 2004; Gouras et al., 2005), suggesting that intraneuronal A 𝛃 may play a role in AD pathology.”
From Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006) · cites this paper as Tseng et al., 2004
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“5XFAD mice have robust intraneuronal A labeling Recent studies have reported intraneuronal A in AD, Down’s syndrome, and APP transgenic brains (for review, see Echeverria and Cuello, 2002; Tseng et al., 2004; Gouras et al., 2005), suggesting that intraneuronal A may play a role in AD pathology.”
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TSPO contributes to neuropathology and cognitive deficits in Alzheimer’s diseasePreprint
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- Authors
- Tseng, B., Kitazawa, M., & LaFerla, F.
- Affiliations
- University of California, Irvine (US)
- Venue
- Current Alzheimer Research
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2004-11-01
- Volume
- 1
- Issue
- 4
- Pages
- 231-239
- ISSN
- 1567-2050 (ISSN-L)
- OpenAlex
- W2004646459
- Cited by
- 72
- References
- 0
- Citations by year
- 2025: 3 · 2020: 1 · 2017: 2 · 2015: 1 · 2014: 3 · 2013: 5 · 2012: 3
- FWCI
- 5.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Alzheimer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG212982, AG 26175)
- 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
- amyloid-beta, Alzheimer's disease, Down syndrome, inclusion body myositis, amyloid plaques, neurodegeneration, neuronal dysfunction, synaptic dysfunction, neuronal loss
- MeSH terms
- Alzheimer Disease, Animals, Down Syndrome, Humans, Amyloid beta-Peptides, Myositis, Inclusion Body
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