| Literature DB >> 30790294 |
Maryam Rezazadeh1,2, Hassan Hosseinzadeh3, Mohsen Moradi1, Behnaz Salek Esfahani1, Shahrzad Talebian1, Shaho Parvin1, Jalal Gharesouran1,2.
Abstract
Alzheimer's disease (AD) is a heterogeneous disorder with multiple patterns of clinical manifestations. Recently, due to the advance of linkage studies, next-generation sequencing and genome-wide association studies, a large number of putative risk genes for AD have been identified using acquired genome mega data. The genetic association between three causal genes, including amyloid precursor protein, presenilin1, and presenilin2 in early-onset AD (EOAD), was discovered over the past few decades. These discoveries showed that there should be additional genetic risk factors for both EOAD and late-onset AD (LOAD) to help fully explain the leading molecular mechanisms in a single pathophysiological entity. This study reviews the clinical features and genetic etiology of LOAD and discusses a variety of AD-mediated genes that are involved in cholesterol and lipid metabolism, endocytosis, and immune response according to their mutations for more efficient selection of functional candidate genes for LOAD. New mechanisms and pathways have been identified as a result.Entities:
Keywords: Alzheimer’s disease; amyloid-β; candidate gene; neurodegeneration
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Year: 2019 PMID: 30790294 DOI: 10.1002/jcp.28372
Source DB: PubMed Journal: J Cell Physiol ISSN: 0021-9541 Impact factor: 6.384