Deficiency in Mitochondrial Aldehyde Dehydrogenase Increases the Risk for Late-Onset Alzheimer's Disease in the Japanese Population

2000 ◽  
Vol 273 (1) ◽  
pp. 192-196 ◽  
Author(s):  
Kouzin Kamino ◽  
Keiko Nagasaka ◽  
Masaki Imagawa ◽  
Hideki Yamamoto ◽  
Hiroshi Yoneda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Aldehyde Dehydrogenase ◽  
Japanese Population ◽  
Late Onset

Association study of susceptibility genes for late-onset Alzheimer’s disease in the Japanese population

2012 ◽  
Vol 22 (6) ◽  
pp. 290-293 ◽  
Author(s):  
Tomoyuki Ohara ◽  
Toshiharu Ninomiya ◽  
Yoichiro Hirakawa ◽  
Kyota Ashikawa ◽  
Akira Monji ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Japanese Population ◽  
Late Onset ◽  
Susceptibility Genes

scholarly journals Polygenic analysis of late‐onset Alzheimer’s disease in a Japanese population

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Masataka Kikuchi ◽  
Akinori Miyashita ◽  
Norikazu Hara ◽  
Daichi Shigemizu ◽  
Kouichi Ozaki ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Japanese Population ◽  
Late Onset ◽  
Polygenic Analysis

A genome-wide association study of late-onset Alzheimer’s disease in a Japanese population

2015 ◽  
Vol 25 (4) ◽  
pp. 139-146 ◽  
Author(s):  
Atsushi Hirano ◽  
Tomoyuki Ohara ◽  
Atsushi Takahashi ◽  
Masayuki Aoki ◽  
Yuta Fuyuno ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Association Study ◽  
Japanese Population ◽  
Genome Wide Association Study ◽  
Late Onset ◽  
Genome Wide Association ◽  
Genome Wide ◽  
A Genome

Lack of Genetic Association Between TREM2 and Late-Onset Alzheimer's Disease in a Japanese Population

2014 ◽  
Vol 41 (4) ◽  
pp. 1031-1038 ◽  
Author(s):  
Akinori Miyashita ◽  
Yanan Wen ◽  
Nobutaka Kitamura ◽  
Etsuro Matsubara ◽  
Takeshi Kawarabayashi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Association ◽  
Japanese Population ◽  
Late Onset

T/G polymorphism at intron 9 of presenilin 1 gene is associated with, but not responsible for sporadic late-onset Alzheimer's disease in Japanese population

1997 ◽  
Vol 227 (2) ◽  
pp. 123-126 ◽  
Author(s):  
Yumiko Nishiwaki ◽  
Kouzin Kamino ◽  
Aoi Yoshiiwa ◽  
Naoyuki Sato ◽  
Kyoko Tateishi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Japanese Population ◽  
Late Onset ◽  
Presenilin 1

Familial Patterns of Risk in Very Late-Onset Alzheimer's Disease

2003 ◽  
Author(s):  
J. M. Silverman ◽  
C. J. Smith ◽  
D. B. Marin ◽  
R. C. Mohs ◽  
C. B. Propper
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Familial Patterns

Exploring the Role of Aggregated Proteomes in the Pathogenesis of Alzheimer’s Disease

2020 ◽  
Vol 21 (12) ◽  
pp. 1164-1173
Author(s):  
Siju Ellickal Narayanan ◽  
Nikhila Sekhar ◽  
Rajalakshmi Ganesan Rajamma ◽  
Akash Marathakam ◽  
Abdullah Al Mamun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Precursor Protein ◽  
Early Onset ◽  
Late Onset ◽  
Precursor Protein ◽  
Brain Disorder ◽  
Amyloid Aβ ◽  
T Tau

: Alzheimer’s disease (AD) is a progressive brain disorder and one of the most common causes of dementia and death. AD can be of two types; early-onset and late-onset, where late-onset AD occurs sporadically while early-onset AD results from a mutation in any of the three genes that include amyloid precursor protein (APP), presenilin 1 (PSEN 1) and presenilin 2 (PSEN 2). Biologically, AD is defined by the presence of the distinct neuropathological profile that consists of the extracellular β-amyloid (Aβ) deposition in the form of diffuse neuritic plaques, intraneuronal neurofibrillary tangles (NFTs) and neuropil threads; in dystrophic neuritis, consisting of aggregated hyperphosphorylated tau protein. Elevated levels of (Aβ), total tau (t-tau) and phosphorylated tau (ptau) in cerebrospinal fluid (CSF) have become an important biomarker for the identification of this neurodegenerative disease. The aggregation of Aβ peptide derived from amyloid precursor protein initiates a series of events that involve inflammation, tau hyperphosphorylation and its deposition, in addition to synaptic dysfunction and neurodegeneration, ultimately resulting in dementia. The current review focuses on the role of proteomes in the pathogenesis of AD.

Molecular Genetics of Early- and Late-Onset Alzheimer’s Disease

2020 ◽  
Vol 20 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Sharifa Hasana ◽  
Md. Farhad Hossain ◽  
Md. Siddiqul Islam ◽  
Tapan Behl ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Massively Parallel Sequencing ◽  
Late Onset ◽  
Current Knowledge ◽  
The Elderly ◽  
Apoe Ε4 ◽  
Sequencing Technologies ◽  
Genetic Components ◽  
Ε4 Allele

: Alzheimer’s disease (AD) is the most common form of dementia in the elderly and this complex disorder is associated with environmental as well as genetic components. Early-onset AD (EOAD) and late-onset AD (LOAD, more common) are major identified types of AD. The genetics of EOAD is extensively understood with three genes variants such as APP, PSEN1, and PSEN2 leading to disease. On the other hand, some common alleles including APOE are effectively associated with LOAD identified but the genetics of LOAD is not clear to date. It has been accounted that about 5% to 10% of EOAD patients can be explained through mutations in the three familiar genes of EOAD. The APOE ε4 allele augmented the severity of EOAD risk in carriers, and APOE ε4 allele was considered as a hallmark of EOAD. A great number of EOAD patients, who are not genetically explained, indicate that it is not possible to identify disease- triggering genes yet. Although several genes have been identified through using the technology of next-generation sequencing in EOAD families including SORL1, TYROBP, and NOTCH3. A number of TYROBP variants were identified through exome sequencing in EOAD patients and these TYROBP variants may increase the pathogenesis of EOAD. The existence of ε4 allele is responsible for increasing the severity of EOAD. However, several ε4 allele carriers live into their 90s that propose the presence of other LOAD genetic as well as environmental risk factors that are not identified yet. It is urgent to find out missing genetics of EOAD and LOAD etiology to discover new potential genetics facets which will assist to understand the pathological mechanism of AD. These investigations should contribute to developing a new therapeutic candidate for alleviating, reversing and preventing AD. This article based on current knowledge represents the overview of the susceptible genes of EOAD, and LOAD. Next, we represent the probable molecular mechanism which might elucidate the genetic etiology of AD and highlight the role of massively parallel sequencing technologies for novel gene discoveries.

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