Genetic discoveries and advances in late‐onset Alzheimer's disease. Issue 10 (20th February 2019)

• Record Type: Journal Article
• Authors: Rezazadeh, Maryam; Hosseinzadeh, Hassan; Moradi, Mohsen; Salek Esfahani, Behnaz; Talebian, Shahrzad; Parvin, Shaho; Gharesouran, Jalal
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 10(2019:Oct.)
• Page Start: 16873
• Page End: 16884
• Publication Date: 2019-02-20
• Subjects: Alzheimer's disease -- amyloid‐β -- candidate gene -- neurodegeneration; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28372
• Languages: English
• ISSNs: 0021-9541

Abstract

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. 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. These discoveries showed that there should be additional genetic risk factors for both early‐onset AD and late‐onset AD to help fully explain the leading molecular mechanisms in a single pathophysiological entity.