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| http://dx.doi.org/10.1161/CIRCULATIONAHA.123.066034 | DOI Listing |
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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Apolipoprotein E (ApoE) exists in three protein isoforms: E2, E3, and E4, which differ by only one or two amino acids. These slight differences profoundly effect protein structure and function, allowing each isoform to differentially impact Alzheimer's Disease (AD) risk. Relative to the most common E3 isoform, E4 dramatically increases risk, while E2 confers a substantial decrease in risk.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Rensselaer Polytechnic Institute, Troy, NY, USA.
Background: Heparan sulfate (HS) interacts with many important proteins. These interactions are primarily driven by electrostatics, with specificity determined by sulfation patterns. Although 3-O-sulfation is a rare modification in HS, several genome-wide association studies (GWAS) revealed that the Hs3st1 gene, encoding HS-3-O-sulfotransferase-1, is significantly linked to late onset AD risk.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Compared with the E3 allele of Apolipoprotein E (APOE), E4 increases late-onset Alzheimer's Disease (AD) risk up to 15-fold, while the E2 allele substantially decreases risk. In the CNS, ApoE is predominantly synthesized by astrocytes and microglia, making these two cell types promising targets for ApoE-directed therapeutic approaches. Our lab has generated an inducible "switch" mouse model (APOE4s2) in which we can conditionally replace E4 with the protective E2 in a cell-specific manner.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Robarts Research Institute, London, ON, Canada.
Background: ApoE4 is the strongest genetic risk factor for late onset Alzheimer's Disease (AD). However, ApoE4 has also been suggested to exhibit antagonistic pleiotropy, a phenomenon by which some allelic variations of a gene promote fitness during certain periods of life but may be detrimental in others. Previous work suggests that ApoE4 carriers exhibit superior performance on executive function tasks in early and middle age, while later in life (>70 years) ApoE4 carriers experience greater cognitive decline across multiple domains.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is heterogeneous in both its clinical and neuropathologic course. Age at onset and distribution of corticolimbic tangles can vary widely among individuals. Genetic risk factors APOE ε4 and MAPT H1 increase AD risk.
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