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Genome-wide Association Study to Identify Variants Associated with Alzheimer's Disease And Cognitive Impairment
Başlık:
Genome-wide Association Study to Identify Variants Associated with Alzheimer's Disease And Cognitive Impairment
Yazar:
Lee, Jong Seo, author.
ISBN:
9780355913088
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (34 pages)
Genel Not:
Source: Masters Abstracts International, Volume: 57-06M(E).
Advisors: Andrew T. DeWan Committee members: Janghoo Lim.
Özet:
Alzheimer’s disease (AD) is a progressive neurodegenerative disease, affecting millions of people around the world. The study of familial and sporadic AD over the past decades has led to discovery of hallmark pathological features and major biological pathways involved in the disease. However, the disease etiology of late-onset AD (LOAD) remains unclear, and there are currently no effective therapeutic or preventive measures available for AD patients. Previous genome-wide association studies (GWAS) have identified and validated 20 novel risk variants in addition to APOE-ε4 allele, known to be the strongest genetic risk factor for LOAD. Outside of the APOE genotypes, few AD risk genes are directly involved in the AD pathogenesis, and there is still a large portion of the AD genetics that remains unexplained. In the present study, we conducted a GWAS on the Alzheimer’s Disease Neuroimaging Initiative cohort. We identified 36 single nucleotide polymorphisms (SNPs) that display suggestive association with AD risk in 122 AD cases compared to 142 cognitively normal controls (p < 1.0E-04). Seven risk alleles at FRMD4A were associated with AD risk independent of its association with the severity of cognitive decline and AD-related biomarkers, including Tau, pTau181p, and Aβ42 levels in the cerebrospinal fluid. In addition, we detected four variants at 11q25, upstream of NTM, to be nominally associated with risk for mild cognitive impairment and AD. These variants also displayed strong ties to the AD related biological parameters, which significantly correlated with different stages of cognitive impairment. Our GWAS findings warrant further investigation of the role and mechanisms by which these FRMD4A and NTM variants are involved in AD pathobiology.
Notlar:
School code: 0265
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
---|---|---|---|
XX(692080.1) | 692080-1001 | Proquest E-Tez Koleksiyonu | Arıyor... |
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