Etiology and pathogenesis of alzheimer's disease
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Cited by (5)
Blood-brain barrier leakage in Alzheimer's disease: From discovery to clinical relevance
2022, Pharmacology and TherapeuticsCitation Excerpt :Electron microscopy and diffraction studies in the 1960s demonstrated that plaques and NFTs are large, organized structures of β-pleated and paired helical filaments (Eanes & Glenner, 1968; Terry, 1963; Terry, Gonatas, & Weiss, 1964). By the 1980s, multiple biochemical studies found that amyloid-beta (Aβ, 4 kDa) accumulates in these plaques as oligomers, protofibrils, and fibrillar sheets (Fig. 1A) (Glenner & Wong, 1984; Masters, 1984; Masters et al., 1985; Roher et al., 1996). Aβ is a 36-43 amino acid peptide that forms when amyloid precursor protein (APP) is cleaved by alpha- and gamma-secretases within the transmembrane region (Esch et al., 1990; Sisodia, Koo, Beyreuther, Unterbeck, & Price, 1990).
The genetics of alzheimer's disease: A review and a discussion of the implications
1986, Neurobiology of AgingDisplay of AD Related Genes Based on GSE118553
2021, ACM International Conference Proceeding SeriesInconsistencies and Controversies Surrounding the Amyloid Hypothesis of Alzheimer's Disease
2014, Acta Neuropathologica CommunicationsEtiologic theories of Alzheimer's disease
1986, American Journal of Alzheimer's Disease and Other Dementias
Copyright © 1984 Royal College of Pathologists of Australasia. Published by Elsevier B.V. All rights reserved.