scholarly journals Late-Onset Alzheimer's Disease: Risk Factors, Clinical Diagnosis and the Search for Biomarkers

10.5772/53775 ◽  
2013 ◽  
Author(s):  
Marisol Herrera-Rivero
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Diagnosis ◽  
Disease Risk ◽  
Late Onset

scholarly journals FMNL2 interacts with cerebrovascular risk factors to alter Alzheimer's disease risk

2020 ◽  
Author(s):  
Neha Raghavan ◽  
Sanjeev Sariya ◽  
Annie Lee ◽  
Yizhe Gao ◽  
Dolly Reyes-Dumeyer ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Risk ◽  
Late Onset ◽  
Major Pathway ◽  
Cerebrovascular Risk Factors ◽  
Interaction Factor ◽  
Gene Level ◽  
Cerebrovascular Risk

INTRODUCTION: Late-onset Alzheimer's disease (AD) frequently co-occurs with cerebrovascular disease. We hypothesized that interactions between genes and cerebrovascular risk factors (CVRFs) contribute to AD risk. METHODS: Participants age 65 years or older from five multi-ethnic cohorts (N=14,669) were included in genome-wide association meta-analyses for AD including an interaction factor for a CVRF score created from body mass index, hypertension, heart disease, and diabetes. Significant gene level results were substantiated using neuropathological and gene expression data. RESULTS: At the gene-level, FMNL2 interacted with the CVRF score to significantly modify AD risk (p= 7.7x10-7). A SNP within FRMD4B, rs1498837, was nominally significant (p=7.95x10-7). Increased FMNL2 expression was significantly associated with brain infarcts and AD. DISCUSSION: FMNL2 is highly expressed in the brain and has been associated with ischemic stroke and failures in endosomal trafficking, a major pathway in AD pathology. The results highlight an interaction between FMNL2 and CVRFs on AD susceptibility.

scholarly journals MAPT H1 Haplotype is Associated with Late-Onset Alzheimer’s Disease Risk in APOE ɛ4 Noncarriers: Results from the Dementia Genetics Spanish Consortium

2015 ◽  
Vol 49 (2) ◽  
pp. 343-352 ◽  
Author(s):  
Pau Pastor ◽  
Fermín Moreno ◽  
Jordi Clarimón ◽  
Agustín Ruiz ◽  
Onofre Combarros ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Risk ◽  
Late Onset

scholarly journals An APOE -independent cis -eSNP on chromosome 19q13.32 influences tau levels and late-onset Alzheimer's disease risk

2018 ◽  
Vol 66 ◽  
pp. 178.e1-178.e8 ◽  
Author(s):  
Shuquan Rao ◽  
Mahdi Ghani ◽  
Zhiyun Guo ◽  
Yuetiva Deming ◽  
Kesheng Wang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Risk ◽  
Late Onset

scholarly journals SRSF1 and PTBP1 Aretrans-Acting Factors That Suppress the Formation of a CD33 Splicing Isoform Linked to Alzheimer’s Disease Risk

2019 ◽  
Vol 39 (18) ◽  
Author(s):  
Petra van Bergeijk ◽  
Uthpala Seneviratne ◽  
Estel Aparicio-Prat ◽  
Robert Stanton ◽  
Samuel A. Hasson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Risk ◽  
Late Onset ◽  
Splice Junction ◽  
Full Length ◽  
Receptor Expression ◽  
Genetic Associations ◽  
Rna Sequences ◽  
Exon 2

ABSTRACTA single nucleotide polymorphism (SNP) in exon 2 of the CD33 gene is associated with reduced susceptibility to late-onset Alzheimer’s disease (AD) and causal for elevated mRNA lacking exon 2. In contrast to full-length CD33, transcripts lacking exon 2 result in CD33 protein unable to suppress activation responses in myeloid cells, including microglia. Currently, little is known about the regulation of CD33 exon 2 splicing. Using functional genomics and proteomic approaches, we found that SRSF1 and PTBP1 act as splicing enhancers to increase CD33 exon 2 inclusion in mRNA. Binding of PTBP1 to RNA sequences proximal to the intron 1-exon 2 splice junction is altered by the SNP and represents a potential mechanism behind the SNP-genotype dependent alternative splicing. Our studies also reveal that binding of SRSF1 to the CD33 RNA is not altered by the SNP genotype. Instead, a putative SRSF1 binding sequence at the 3′ end of exon 2 directs CD33 exon 2 inclusion into the mRNA, indicating that PTBP1 and SRSF1 promote full-length isoform expression through different mechanisms. Our findings shed light on molecular interactions that regulate CD33 exon 2 splicing, ultimately impacting receptor expression on the cell surface. These data aid in the understanding of CD33’s regulation of microglial signaling underpinning the AD genetic associations.

P3-006: Late-onset Alzheimer's disease genetic risk factors in two Canadian cohorts: CSHA and ACCORD

2013 ◽  
Vol 9 ◽  
pp. P551-P552
Author(s):  
Ardeshir Omoumi ◽  
Alice Fok ◽  
Talitha Greenwood ◽  
Dessa Sadovnick ◽  
Howard Feldman ◽  
...  
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genetic Risk ◽  
Late Onset ◽  
Genetic Risk Factors

scholarly journals Microglia in Alzheimer's Disease: Risk Factors and Inflammation

2018 ◽  
Vol 9 ◽  
Author(s):  
Atsuko Katsumoto ◽  
Hideyuki Takeuchi ◽  
Keita Takahashi ◽  
Fumiaki Tanaka
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Risk
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