Genome-wide linkage disequilibrium mapping of late-onset Alzheimer's disease in Finland

Neurology ◽  
2001 ◽  
Vol 57 (9) ◽  
pp. 1663-1668 ◽  
Author(s):  
M. Hiltunen ◽  
A. Mannermaa ◽  
D. Thompson ◽  
D. Easton ◽  
M. Pirskanen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Linkage Disequilibrium ◽  
Late Onset ◽  
Linkage Disequilibrium Mapping ◽  
Genome Wide ◽  
Genome Wide Linkage Disequilibrium

Genome-wide linkage disequilibrium mapping of late onset Alzheimer's disease in Finland

2000 ◽  
Vol 21 ◽  
pp. 12
Author(s):  
Mikko J. Hiltunen ◽  
Arto Mannermaa ◽  
Mia Pirskanen ◽  
Anne Koivisto ◽  
Seppo Helisalmi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Linkage Disequilibrium ◽  
Late Onset ◽  
Linkage Disequilibrium Mapping ◽  
Genome Wide ◽  
Genome Wide Linkage Disequilibrium

Substantial linkage disequilibrium across the insulin-degrading enzyme locus but no association with late-onset Alzheimer's disease

2001 ◽  
Vol 109 (6) ◽  
pp. 646-652 ◽  
Author(s):  
Richard Abraham ◽  
Amanda Myers ◽  
Fabienne Wavrant-DeVrieze ◽  
Marian L. Hamshere ◽  
Hollie V. Thomas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Linkage Disequilibrium ◽  
Late Onset ◽  
Enzyme Locus ◽  
Insulin Degrading Enzyme ◽  
Degrading Enzyme

scholarly journals Genes, pathways and risk prediction in Alzheimer’s disease

2019 ◽  
Author(s):  
John Hardy ◽  
Valentina Escott-Price
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Membrane Damage ◽  
Disease Process ◽  
Complete Understanding ◽  
Induced Membrane ◽  
Genome Wide ◽  
Key Factor ◽  
Risk Of Disease

Abstract The failure of recent clinical trials in Alzheimer's disease has highlighted the need for the development of a more complete understanding of the pathogenesis of the disorder and also a belief that therapies may only work if given very early in the disease process before overt symptoms occur. The rare, early onset forms of the disease are all caused by mutations which make amyloid deposition a more likely event. Here we discuss the recent data showing that, in contrast, much of the risk of late onset disease is encoded by loci involved in lipid metabolism and/or encoded by microglia. We discuss these finding and suggest that amyloid induced membrane damage may be a key factor in disease and also review the evidence that genome wide genetic analysis can substantially help in the prediction of those individuals at high risk of disease in the general population.

scholarly journals Association Study of Genetic Variants inCDKN2A/CDKN2BGenes/Loci with Late-Onset Alzheimer's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-4
Author(s):  
Andrea Tedde ◽  
Irene Piaceri ◽  
Silvia Bagnoli ◽  
Ersilia Lucenteforte ◽  
Uwe Ueberham ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Variants ◽  
Genetic Variant ◽  
Case Control Study ◽  
Late Onset ◽  
Common Genetic Variant ◽  
Genome Wide ◽  
Control Study

Alzheimer's disease (AD) is the most common form of dementia clinically characterized by progressive impairment of memory and other cognitive functions. Many genetic researches in AD identified one common genetic variant (ε4) in Apolipoprotein E (APOE) gene as a risk factor for the disease. Two independent genome-wide studies demonstrated a new locus on chromosome 9p21.3 implicated in Late-Onset Alzheimer's Disease (LOAD) susceptibility in Caucasians. In the present study, we investigated the role of three SNP's in theCDKN2Agene (rs15515, rs3731246, and rs3731211) and one in theCDKN2Bgene (rs598664) located in 9p21.3 using an association case-control study carried out in a group of Caucasian subjects including 238 LOAD cases and 250 controls. The role ofCDKN2AandCDKN2Bgenetic variants in AD is not confirmed in our LOAD patients, and further studies are needed to elucidate the role of these genes in the susceptibility of AD.

scholarly journals Genetic underpinnings in Alzheimer’s disease – a review

2017 ◽  
Vol 29 (1) ◽  
pp. 21-38 ◽  
Author(s):  
Ahmed A. Moustafa ◽  
Mubashir Hassan ◽  
Doaa H. Hewedi ◽  
Iman Hewedi ◽  
Julia K. Garami ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Late Onset ◽  
Genetic Research ◽  
Twin Studies ◽  
Pedigree Analysis ◽  
Protein Signaling ◽  
Genetic Components ◽  
Genome Wide ◽  
Pharmacological Targets

AbstractIn this review, we discuss the genetic etiologies of Alzheimer’s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein (APP) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2,PSEN1/2andAPP) and late-onset (apolipoprotein E,ApoE) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.

scholarly journals Linkage disequilibrium in the 13q12 region in Finnish late onset Alzheimer's disease patients

1999 ◽  
Vol 7 (6) ◽  
pp. 652-658 ◽  
Author(s):  
Mikko Hiltunen ◽  
Arto Mannermaa ◽  
Anne Maria Koivisto ◽  
Maarit Lehtovirta ◽  
Seppo Helisalmi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Linkage Disequilibrium ◽  
Late Onset

scholarly journals Predicting late-onset Alzheimer’s disease from genomic data using deep neural networks

2019 ◽  
Author(s):  
Javier de Velasco Oriol ◽  
Edgar E. Vallejo ◽  
Karol Estrada ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Neural Networks ◽  
Alzheimer's Disease ◽  
Genetic Variants ◽  
Deep Neural Networks ◽  
Late Onset ◽  
Association Studies ◽  
Genome Wide Association Studies ◽  
Clinical Markers ◽  
Genome Wide

AbstractAlzheimer’s disease (AD) is the leading form of dementia. Over 25 million cases have been estimated worldwide and this number is predicted to increase two-fold every 20 years. Even though there is a variety of clinical markers available for the diagnosis of AD, the accurate and timely diagnosis of this disease remains elusive. Recently, over a dozen of genetic variants predisposing to the disease have been identified by genome-wide association studies. However, these genetic variants only explain a small fraction of the estimated genetic component of the disease. Therefore, useful predictions of AD from genetic data could not rely on these markers exclusively as they are not sufficiently informative predictors. In this study, we propose the use of deep neural networks for the prediction of late-onset Alzheimer’s disease from a large number of genetic variants. Experimental results indicate that the proposed model holds promise to produce useful predictions for clinical diagnosis of AD.

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