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Review
. 2018 Apr;55(4):3021-3032.
doi: 10.1007/s12035-017-0533-3. Epub 2017 Apr 29.

Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations

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Review

Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations

Ke Li et al. Mol Neurobiol. .

Abstract

Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory. However, the mechanism underlying these symptoms remains unclear. The best correlation between cognitive decline and pathological changes is in synaptic dysfunction. Histopathological hallmarks of AD are the abnormal aggregation of Aβ and Tau. Evidence suggests that Aβ and Tau oligomers contribute to synaptic loss in AD. Recently, direct links between epigenetic alterations, such as dysfunction in non-coding RNAs (ncRNAs), and synaptic pathologies have emerged, raising interest in exploring the potential roles of ncRNAs in the synaptic deficits in AD. In this paper, we summarize the potential roles of Aβ, Tau, and epigenetic alterations (especially by ncRNAs) in the synaptic dysfunction of AD and discuss the novel findings in this area.

Keywords: Alzheimer’s disease; Epigenetic alterations; Synaptic dysfunction; Tau; miRNA.

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References

    1. BMC Neurosci. 2010 Oct 14;11:130 - PubMed
    1. Sci Rep. 2016 Aug 03;6:30953 - PubMed
    1. Trends Neurosci. 2014 Dec;37(12):721-32 - PubMed
    1. Nat Med. 2008 Jul;14(7):723-30 - PubMed
    1. Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9093-8 - PubMed

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