The DOI matches its Crossref record; 151 of the 153 references it cites were found in a registry or an index.
Intracellular amyloid-β in Alzheimer's disease
Abstract
The primal role that the amyloid-beta (Abeta) peptide has in the development of Alzheimer's disease is now almost universally accepted. It is also well recognized that Abeta exists in multiple assembly states, which have different physiological or pathophysiological effects. Although the classical view is that Abeta is deposited extracellularly, emerging evidence from transgenic mice and human patients indicates that this peptide can also accumulate intraneuronally, which may contribute to disease progression.
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In the citing paper
“verified that plaque deposition requires BACE1 activity, as previously shown [17-20].”
From Neuron loss in the 5XFAD mouse model of Alzheimer’s disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation (2013) · cites this paper as [17]
In the citing paper
“In PD, intracellular inclusions of alpha-synuclein (αSYN) are found in neurons and glia, while both extracellular and intracellular deposits of amyloid-beta (Aβ) are present in the AD brain [2, 3].”
From Crosstalk between astrocytes and microglia results in increased degradation of α-synuclein and amyloid-β aggregates (2021) · cites this paper as [3]
In the citing paper
“A accumulation occurs prior to extracellular amyloid formation, has been implicated in the onset of early cognitive alterations, and may contribute to the pathological cascade of events that leads to neuronal dysfunction and, eventually, to AD (12,13).”
From Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4 (2014) · cites this paper as [12]
In the citing paper
“Furthermore, the 42-amino acid A (A42) constitutes the majority of intraneuronal A (12).”
From Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4 (2014) · cites this paper as [12]
In the citing paper
“Accumulation of A, the majority of which is A42, occurs prior to extracellular amyloid formation, has been implicated in the onset of early cognitive alterations, and may contribute to the pathological cascade of events that lead to neuronal dysfunction and, eventually, to AD (12,13).”
From Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4 (2014) · cites this paper as [12]
In the citing paper
“Since accumulation of Aβ42 within AD vulnerable neurons has been associated with physiological, pathological and behavioral abnormalities even prior to plaques [12, 140, 187, 188], the evidence is mounting that intraneuronal Aβ42 is the driving force in Aβ-related AD pathogenesis [9, 58, 92].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [92]
Citations
Cites
1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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Amyloid plaque core protein in Alzheimer disease and Down syndrome.
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Triple-Transgenic Model of Alzheimer’s Disease with Plaques and Tangles
Oddo, S., Caccamo, A., Shepherd, J. D., Murphy, M. P., Golde, T. E., Kayed, R., Metherate, R., Mattson, M. P., Akbari, Y., & LaFerla, F. M. (2003) · Neuron · doi:10.1016/s0896-6273(03)00434-3 · Cited by 4,126
Self-citationVassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., et al. (1999) · Science · doi:10.1126/science.286.5440.735 · Cited by 3,876
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Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Schenk, D., Barbour, R., Dunn, W., Gordon, G., Grajeda, H., Guido, T., Hu, K., Huang, J., Johnson-Wood, K., Khan, K., et al. (1999) · Nature · doi:10.1038/22124 · Cited by 3,160
Cited by
Sorted by citations
Pathological roles of MAPK signaling pathways in human diseases
Kim, E. K., & Choi, E.-J. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.12.009 · Cited by 2,472
Amyloid Precursor Protein Processing and Alzheimer's Disease
O'Brien, R. J., & Wong, P. C. (2011) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113613 · Cited by 2,061
The Amyloid-β Pathway in Alzheimer’s Disease
Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01249-0 · Cited by 1,952
Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Tönnies, E., & Trushina, E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161088 · Cited by 1,750
Amyloid-β and tau--a toxic pas de deux in Alzheimer’s disease
Ittner, L. M., & Götz, J. (2011) · Nature Reviews Neuroscience · doi:10.1038/nrn2967 · Cited by 1,269
Metadata
- Authors
- LaFerla, F. M., Green, K. N., & Oddo, S.
- Affiliations
- University of California, Irvine (US)
- Corresponding author
- LaFerla, Frank M.
- Venue
- Nature Reviews Neuroscience
- Published
- 2007-07
- Volume
- 8
- Issue
- 7
- Pages
- 499-509
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W1602771322
- Cited by
- 1,942
- References
- 153
- Citations by year
- 2026: 69 · 2025: 74 · 2024: 106 · 2023: 73 · 2022: 87 · 2021: 110 · 2020: 137 · 2019: 122 · 2018: 129 · 2017: 117 · 2016: 119 · 2015: 111 · 2014: 107 · 2013: 96 · 2012: 118
- FWCI
- 9.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- 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
- amyloid-beta, intraneuronal amyloid-beta, Alzheimer's disease, amyloid plaques, amyloid-beta production, neuronal pathology, transgenic mouse model
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Intracellular Fluid, Synaptic Transmission, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Extracellular Fluid, Proteasome Endopeptidase Complex, Plaque, Amyloid
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