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Title: Alzheimer’s disease : a panorama glimpse
Authors: Zhao, Li Na
Mu, Yuguang
Lu, Lanyuan
Chew, Lock Yue
Keywords: DRNTU::Science::Biological sciences
Issue Date: 2014
Source: Zhao, L. N., Lu, L., Chew, L. Y., & Mu, Y. (2014). Alzheimer’s Disease—A Panorama Glimpse. International Journal of Molecular Sciences, 15(7), 12631-12650.
Series/Report no.: International Journal of Molecular Sciences
Abstract: The single-mutation of genes associated with Alzheimer’s disease (AD) increases the production of Aβ peptides. An elevated concentration of Aβ peptides is prone to aggregation into oligomers and further deposition as plaque. Aβ plaques and neurofibrillary tangles are two hallmarks of AD. In this review, we provide a broad overview of the diverses sources that could lead to AD, which include genetic origins, Aβ peptides and tau protein. We shall discuss on tau protein and tau accumulation, which result in neurofibrillary tangles. We detail the mechanisms of Aβ aggregation, fibril formation and its polymorphism. We then show the possible links between Aβ and tau pathology. Furthermore, we summarize the structural data of Aβ and its precursor protein obtained via Nuclear Magnetic Resonance (NMR) or X-ray crystallography. At the end, we go through the C-terminal and N-terminal truncated Aβ variants. We wish to draw reader’s attention to two predominant and toxic Aβ species, namely Aβ4-42 and pyroglutamate amyloid-beta peptides, which have been neglected for more than a decade and may be crucial in Aβ pathogenesis due to their dominant presence in the AD brain.
ISSN: 1422-0067
DOI: 10.3390/ijms150712631
Rights: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles
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