The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein
Abstract
A purified protein derived from the twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease has been isolated by Sephadex G-100 column chromatography with 5 M guanidine-HC1 in 1 N acetic acid and by high performance liquid chromatography. Amino acid sequence analysis and a computer search reveals this protein to have no homology with any protein sequenced thus far. This protein may be derived from a unique serum precursor which may provide a diagnostic test for Alzheimer's disease and a means to understand its pathogenesis.
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In the citing paper
“Two pathological hallmarks of AD exist, in terms of senile plaques, which consist of amyloid fibrils composed of the amyloid-beta (Aβ) peptide and neurofibrillary tangles consisting of hyperphosphorylated tau protein [8–10].”
From Clinical trials of new drugs for Alzheimer disease (2020) · cites this paper as [8]
In the citing paper
“Amyloid  protein (A), the principal protein in the senile plaques of Alzheimer's disease (AD), is an ϳ4 kDa secreted polypeptide”
From Age-Dependent Changes in Brain, CSF, and Plasma Amyloid β Protein in the Tg2576 Transgenic Mouse Model of Alzheimer's Disease (2001) · cites this paper as Glenner and Wong, 1984
In the citing paper
“The disease is characterized by key neuropathological features, including extracellular accumulation of beta-amyloid (Aβ) protein in senile plaques (6)”
From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [6]
In the citing paper
“Amyloid β protein (Aβ) is the main component of neuritic plaques in Alzheimer’s disease (AD)”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [1]
In the citing paper
“Aβ peptide is the main component of extracellular plaque pathology in the AD brain [15].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [15]
Citations
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Research works printed but not linked: 3
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- Costa, 1978, 75, 4499
- Glenner, 1972, Prep. Biochem., 2, 39
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“AD pathogenesis begins with APP being cleaved abnormally by a β or G -secretase, producing A β , which later aggregates to form plaques [92–95].”
Metadata
- Authors
- Glenner, G. G., & Wong, C. W.
- Affiliations
- University of California San Diego (US)
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 1984-05
- Volume
- 120
- Issue
- 3
- Pages
- 885-890
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2032920422
- Cited by
- 5,404
- References
- 10
- Citations by year
- 2026: 76 · 2025: 152 · 2024: 163 · 2023: 155 · 2022: 147 · 2021: 141 · 2020: 213 · 2019: 165 · 2018: 150 · 2017: 158 · 2016: 174 · 2015: 160 · 2014: 169 · 2013: 183 · 2012: 176
- FWCI
- 43.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical and Biophysical Research Communications (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of California, San Diego
- 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
- Health Sciences › Medicine › Internal Medicine › Amyloidosis: Diagnosis, Treatment, Outcomes
- Keywords
- Alzheimer's disease, novel proteins, diagnostic testing, pathogenesis, protein characterization
- MeSH terms
- Alzheimer Disease, Amino Acids, Amyloid, Amyloidosis, Brain, Chemistry, Chromatography, High Pressure Liquid, Humans, Amyloid beta-Peptides, Chemical Phenomena
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