Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families.
APOE-epsilon 4 gene dose is a major risk factor for late onset AD and, in these families, homozygosity for APOE-epsilon 4 was virtually sufficient to cause AD by age 80.
Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial Alzheimer disease.
- W. Strittmatter, A. Saunders, A. Roses
- BiologyProceedings of the National Academy of Sciences…
- 1 March 1993
It is demonstrated that there was a highly significant association of apolipoprotein E type 4 allele (APOE-epsilon 4) and late-onset familial Alzheimer disease.
Identification of miRNA Changes in Alzheimer's Disease Brain and CSF Yields Putative Biomarkers and Insights into Disease Pathways
Using a sensitive qRT-PCR platform, experimental validation is used to reveal how the deregulated brain microRNAs are biomarkers for known and novel pathways in AD pathogenesis related to amyloid processing, neurogenesis, insulin resistance, and innate immunity.
Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease
A protective effect of the ε2 allele, in addition to the dose effect ofThe ε4 allele in sporadic AD, is demonstrated, which further support the direct involvement of APOE in the pathogenesis of AD.
Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease.
Data support the involvement of ApoE epsilon 4 in the pathogenesis of late-onset familial and sporadic AD and suggest it may operate as a susceptibility gene (risk factor) for the clinical expression of AD.
Binding of human apolipoprotein E to synthetic amyloid beta peptide: isoform-specific effects and implications for late-onset Alzheimer disease.
- W. Strittmatter, K. Weisgraber, A. Roses
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 1 September 1993
Differences in the two isoforms in complexing with the beta/A4 peptide may be involved in the pathogenesis of the intra- and extracellular lesions of Alzheimer disease.
Clinicopathologic studies in cognitively healthy aging and Alzheimer's disease: relation of histologic markers to dementia severity, age, sex, and apolipoprotein E genotype.
Neocortical neurofibrillary tangle densities were substantially correlated with dementia severity, and to a greater degree than was true for senile plaque densities, and the order of the strength of relationships between densities of histologic markers and dementia severity in AD is neuroFibrillary tangles greater than cored senile plaques greater than total senile Plaques.
A TOMM40 variable-length polymorphism predicts the age of late-onset Alzheimer's disease
Using phylogenetic analysis, a polymorphic poly-T variant, rs10524523, in the translocase of outer mitochondrial membrane 40 homolog (TOMM40) gene is identified that provides greatly increased precision in the estimation of age of LOAD onset for APOE ɛ3 carriers.
Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia
- E. Reiman, Kewei Chen, J. Hardy
- Biology, PsychologyProceedings of the National Academy of Sciences…
- 19 December 2003
Young ε4 carriers and noncarriers did not differ significantly in their sex, age, educational level, clinical ratings, or neuropsychological test scores, and an aggregate surface-projection map was generated that compared regional PET measurements in the two groups.
Candidate single-nucleotide polymorphisms from a genomewide association study of Alzheimer disease.
The genomewide association analysis again identified the APOE linkage disequilibrium region as the strongest genetic risk factor for AD.