The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Cerebral Amyloid Angiopathies: A Pathologic, Biochemical, and Genetic View
Abstract
Amyloid deposition can take place in the walls of arteries, arterioles, and, less often, capillaries and veins of the central nervous system, a phenomenon known as cerebral amyloid angiopathy (CAA). The major clinicopathological manifestations of CAA include cerebral hemorrhage, ischemic lesions, and dementia. CAA may be classified according to the amyloid protein deposited. In the most common form, sporadic CAA, and in CAA related to sporadic Alzheimer disease (AD). A beta deposition is characteristic. CAA can also be severe in variants of familial AD caused by mutations of the amyloid-beta precursor protein or presenilin-1 genes in which deposition of A beta variants and/or wild-type A beta occurs. Other amyloid proteins involved in familial CAAs include 1) the mutant cystatin C (ACys) in hereditary cerebral hemorrhage with amyloidosis of Icelandic type, 2) variant transthyretins (ATTR) in meningo-vascular amyloidoses, 3) mutated gelsolin (AGel) in familial amyloidosis of Finnish type, 4) disease-associated prion protein (PrP(Sc)) in a variant of the Gerstmann-Sträussler-Scheinker syndrome, and 5) ABri and ADan in CAAs observed in the recently described BRI2 gene-related dementias, familial British dementia and familial Danish dementia, respectively. This review addresses issues related to the correlation between morphology, biochemistry, and genetics, and briefly discusses both the pathogenesis and animal models of CAAs.
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Cites
Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study
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Cerebral amyloid angiopathy and cognitive function: The HAAS autopsy study
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Self-citationMann, D. M. A., Pickering-Brown, S. M., Takeuchi, A., & Iwatsubo, T. (2001) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)64688-3 · Cited by 182
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Furin mediates enhanced production of fibrillogenic ABri peptides in familial British dementia
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Dense-Core Senile Plaques in the Flemish Variant of Alzheimer's Disease Are Vasocentric
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Cited by
Amyloid ion channels: A common structural link for protein-misfolding disease
Quist, A., Doudevski, I., Lin, H., Azimova, R., Ng, D., Frangione, B., Kagan, B., Ghiso, J., & Lal, R. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0502066102 · Cited by 982
Self-citationCerebral amyloid angiopathy and Alzheimer disease — one peptide, two pathways
Greenberg, S. M., Bacskai, B. J., Hernandez-Guillamon, M., Pruzin, J., Sperling, R., & van Veluw, S. J. (2020) · Nature Reviews Neurology · doi:10.1038/s41582-019-0281-2 · Cited by 947
Charidimou, A., Gang, Q., & Werring, D. J. (2012) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp-2011-301308 · Cited by 611
ApoE and Aβ in Alzheimer’s Disease: Accidental Encounters or Partners?
Kanekiyo, T., Xu, H., & Bu, G. (2014) · Neuron · doi:10.1016/j.neuron.2014.01.045 · Cited by 608
Cognitive status correlates with neuropathologic stage in Parkinson disease
Braak, H., Rüb, U., Jansen Steur, E. N. H., Del Tredici, K., & de Vos, R. A. I. (2005) · Neurology · doi:10.1212/01.wnl.0000158422.41380.82 · Cited by 560
Metadata
- Authors
- Revesz, T., Ghiso, J., Lashley, T., Plant, G., Rostagno, A., Frangione, B., & Holton, J. L.
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-09
- Volume
- 62
- Issue
- 9
- Pages
- 885-898
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W148771838
- Cited by
- 288
- References
- 10
- FWCI
- 11.60
- Type
- journal article
- Language
- en
- Open access
- closed
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- Revesz, T., Ghiso, J., Lashley, T., Plant, G., Rostagno, A., Frangione, B., & Holton, J. L. (2003). Cerebral Amyloid Angiopathies: A Pathologic, Biochemical, and Genetic View. Journal of Neuropathology & Experimental Neurology. https://doi.org/10.1093/jnen/62.9.885
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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