The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Amyloid β protein (Aβ) deposition in chromosome 14–linked Alzheimer's disease: Predominance of Aβ42(43)
Abstract
Amyloid beta protein (Abeta) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of Abeta40 and Abeta42(43), respectively. In all patients, Abeta42(43) was the predominant peptide species present. The total amount of Abeta40 and Abeta42(43) deposited was more than twice the amount deposited in cases of sporadic AD of similar disease duration, although the ratio between the extent of Abeta40 and Abeta42(43) deposition was unaltered, compared with sporadic AD. Therefore, (one of) the effects of the mutations in the presenilin 1:PS-1 (S182) gene may be to cause or at least promote an early and excessive deposition of Abeta42(43) within the brain, a property shared with other inherited forms of AD, such as those due to amyloid precursor protein mutations, and Down's syndrome (trisomy 21).
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In the citing paper
“Human PSEN1 mutation carriers have notable BBB breakdown and cerebrovascular dysfunction including cerebellar amyloid angiopathy and CAA (143, 183, 274, 280, 354, 389, 440, 500, 544, 573, 639, 668); disrupted meningeal, subpial, and cortical arterioles (274, 389, 440); degeneration of pericytes and SMCs (573); cerebral perivascular amyloid deposits (25, 274, 289, 354, 573, 668); and diminished FDG”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [389]
In the citing paper
“Particularly, cerebrovascular pathology with BBB breakdown was shown by neuropathological studies in patients with PSEN1 T113-114 insertion (544), P117L (573, 639), M139V (183, 389), M146V (389), L153V (289), H163R (280), E184D (668), G209V (389), A260V (389), C260T (274), E280A (354), L282V (143), C285T (274), and L420R (440) missense mutations, and 𝚫 e9 deletion (280).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [389]
Citations
Cites
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
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Candidate gene for the chromosome 1 familial Alzheimer’s disease locus
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Mutation of the Alzheimer's Disease Amyloid Gene in Hereditary Cerebral Hemorrhage, Dutch Type
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Genetic Linkage Evidence for a Familial Alzheimer's Disease Locus on Chromosome 14
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Self-citationA Familial Alzheimer's Disease Locus on Chromosome 1
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Research works printed but not linked: 1
- Mann DMA, 1996, Predominant deposition of Aβ42(43) in plaques in cases of Alzheimer's disease and hereditary cerebral haemorrhage associated with mutations in the APP gene, Am J Pathol, 148, 1257
Cited by
Sorted by citations
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Blood-Brain Barrier: From Physiology to Disease and Back
Sweeney, M. D., Zhao, Z., Montagne, A., Nelson, A. R., & Zlokovic, B. V. (2019) · Physiological Reviews · doi:10.1152/physrev.00050.2017 · Cited by 2,312
Translating cell biology into therapeutic advances in Alzheimer's disease
Selkoe, D. J. (1999) · Nature · doi:10.1038/399a023 · Cited by 1,166
Amyloid, the presenilins and Alzheimer’s disease
Hardy, J. (1997) · Trends in Neurosciences · doi:10.1016/s0166-2236(96)01030-2 · Cited by 1,370
Self-citationThe Amyloid Beta Peptide: A Chemist’s Perspective. Role in Alzheimer’s and Fibrillization
Hamley, I. W. (2012) · Chemical Reviews · doi:10.1021/cr3000994 · Cited by 892
Metadata
- Authors
- Mann, D. M. A., Iwatsubo, T., Cairns, N. J., Lantos, P. L., Nochlin, D., Sumi, S. M., Bird, T. D., Poorkaj, P., Hardy, J., Hutton, M., Prihar, G., Crook, R., Rossor, M. N., & Haltia, M.
- Affiliations
- University of Manchester (GB)
- The University of Tokyo (JP)
- University of Washington (US)
- University of South Florida (US)
- National Hospital for Neurology and Neurosurgery (GB)
- University of Helsinki (FI)
- Corresponding author
- Mann, D. M. A.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1996-08
- Volume
- 40
- Issue
- 2
- Pages
- 149-156
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2076606883
- Cited by
- 184
- References
- 36
- Citations by year
- 2026: 1 · 2024: 1 · 2022: 1 · 2021: 3 · 2020: 5 · 2019: 2 · 2018: 5 · 2017: 1 · 2016: 3 · 2015: 2 · 2014: 5 · 2013: 3 · 2012: 3
- FWCI
- 15.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG 05136, U01AG006781, AG06781-06, P50AG005136)
- 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, Aβ40, presenilin 1 mutations, frontal cortex, amyloid deposition, sporadic Alzheimer's disease, familial Alzheimer's disease, Down syndrome, amyloid precursor protein mutations
- MeSH terms
- Adult, Alzheimer Disease, Antibodies, Monoclonal, Apolipoproteins E, Chromosomes, Human, Pair 14, Female, Frontal Lobe, Humans, Male, Membrane Proteins, Middle Aged, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, Point Mutation, Presenilin-1
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