6533b86dfe1ef96bd12c9571
RESEARCH PRODUCT
Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation.
W. GroβH. ScharnaglThomas G. OhmM. KircaJürgen BohlW Märzsubject
Apolipoprotein EPathologymedicine.medical_specialtyGenotypeLate onsetBiologyCentral nervous system diseaseDegenerative diseaseApolipoproteins EAlzheimer DiseasemedicineHumansSenile plaquesCognitive declineAllelesAgedAged 80 and overAmyloid beta-PeptidesPolymorphism GeneticGeneral NeuroscienceAge FactorsBrainNeurofibrillary tangleNeurofibrillary TanglesMiddle Agedmedicine.diseaseRegression AnalysisAlzheimer's diseaseChromosomes Human Pair 19description
Only recently, evidence was provided that apolipoprotein E allele epsilon 4 located on Chromosome 19 is associated with late onset (i.e. senile) sporadic Alzheimer's disease. Histologically, Alzheimer's disease is associated with intraneuronal neurofibrillary changes and extraneuronal A4/beta-amyloid deposition. We set out with a histological staging system which considers the gradual development of Alzheimer's disease-related histological changes over time and correlates highly with the cognitive decline ante mortem. Our analysis revealed that both the mean stage for A4/beta-amyloid deposits and the mean stage for neurofibrillary tangles get significantly shifted upwards in epsilon 4-carriers. This represents an earlier onset of the histopathological process of about one decade. The fact that both types of Alzheimer's disease-related changes correlate positively with the prevalence of the epsilon 4-allele suggests for a causal relationship between the apolipoprotein E polymorphism and the development of Alzheimer's disease.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1995-06-01 | Neuroscience |