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A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
Published on: October 20, 2016
[Apolipoprotein E4 in dementia with Lewy bodies]
F Carrillo García1, E Gil Néciga, R Alberca
1Servicio de Neurología, Hospital Universitario Virgen del Rocío, Sevilla. fatimacarillo@terra.es
The apolipoprotein E4 (APOE4) allele is a risk factor for Alzheimer's disease (AD). This study found APOE4 allele frequency in dementia with Lewy bodies (DLB) patients was similar to controls, unlike AD patients.
Area of Science:
- Neurogenetics
- Neurology
- Molecular Biology
Context:
- The apolipoprotein E (APOE) gene, particularly the e4 allele (APOE4), is a known risk factor for Alzheimer's disease (AD).
- The association between APOE4 and dementia with Lewy bodies (DLB) is less understood, with some studies suggesting a link to increased neuropathological hallmarks.
- This study investigates the prevalence of APOE genotypes in patients with AD and DLB compared to healthy controls.
Purpose:
- To determine the frequency of apolipoprotein E (APOE) genotypes, specifically the e4 allele (APOE4), in patients diagnosed with Alzheimer's disease (AD) and dementia with Lewy bodies (DLB).
- To compare the APOE genotype distribution in AD and DLB patient cohorts with that of a normal control group.
Summary:
- A case-control study analyzed APOE genotypes in 306 probable AD patients, 58 probable DLB patients, and 80 normal controls.
- APOE4 allele frequency was 32% in AD, 16% in DLB, and 12% in controls.
- The APOE4 frequency in DLB was significantly lower than in AD and comparable to normal controls.
Impact:
- Findings suggest that APOE4 may not be a significant risk factor for dementia with Lewy bodies (DLB), differentiating it genetically from Alzheimer's disease (AD).
- This could imply distinct underlying pathophysiological mechanisms in DLB, potentially related to the inverse correlation observed between Alzheimer-type pathology and Parkinsonian signs.
- Further neuropathological confirmation is needed to fully elucidate the genetic and pathological landscape of DLB.
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