Genetic research into Alzheimer's Disease: a European focus group study on ethical issues

2007 ◽  
Vol 23 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Anco van der Vorm ◽  
Marcel Olde Rikkert ◽  
Myrra Vernooij-Dassen ◽  
Wim Dekkers ◽  
2010 ◽  
Vol 77 (4) ◽  
pp. 382-388 ◽  
Author(s):  
A van der Vorm ◽  
AL van der Laan ◽  
G Borm ◽  
M Vernooij-Dassen ◽  
M Olde Rikkert ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Lidia Lopez-Gutierrez ◽  
José María García-Alberca ◽  
Silvia Mendoza ◽  
Esther Gris ◽  
María Paz De la Guía ◽  
...  

Alzheimer’s disease is the most common cause of dementia worldwide, and longitudinal studies are crucial to find the factors affecting disease development. Here, we describe a novel initiative from southern Spain designed to contribute in the identification of the genetic component of the cognitive decline of Alzheimer’s disease patients. The germline variant rs9320913 is a C>A substitution mapping within a gene desert. Although it has been previously associated to a higher educational achievement and increased fluid intelligence, its role on Alzheimer’s disease risk and progression remains elusive. A total of 407 subjects were included in the study, comprising 153 Alzheimer disease patients and 254 healthy controls. We have explored the rs9320913 contribution to both Alzheimer disease risk and progression according to the Mini-Mental State Exams. We found that rs9320913 maps within a central nervous system lincRNA AL589740.1. eQTL results show that rs9320913 correlated with the brain-frontal cortex ( beta = − 0.15 , p value = 0.057) and brain-spinal cord (beta of -0.23, p value = 0.037). We did not find rs9320913 to be associated to AD risk, although AA patients seemed to exhibit a less pronounced Mini-Mental State Exam score decline.


2017 ◽  
Vol 29 (1) ◽  
pp. 21-38 ◽  
Author(s):  
Ahmed A. Moustafa ◽  
Mubashir Hassan ◽  
Doaa H. Hewedi ◽  
Iman Hewedi ◽  
Julia K. Garami ◽  
...  

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.


2012 ◽  
Vol 12 (5) ◽  
pp. 557-567 ◽  
Author(s):  
Antoine Leuzy ◽  
Serge Gauthier

2004 ◽  
Vol 7 (1) ◽  
pp. 44-54 ◽  
Author(s):  
Mee Lian Wong ◽  
Kee Seng Chia ◽  
Sharon Wee ◽  
Sin Eng Chia ◽  
Jeannette Lee ◽  
...  

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