ArticleAlzheimer's research & therapy2020
APOE ε4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer's disease.
Article in Alzheimer's research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- Oral health, genetic susceptibility, and risk of dementia: a prospective cohort study of UK Biobank.GeroScience · 2026Article
- Aging, Rather than Genotype, Is the Principal Contributor to Differential Gene Expression Within Targeted Replacement APOE2, APOE3, and APOE4 Mouse Brain.Brain sciences · 2025Article
- Cerebrospinal fluid proteomic signatures in cognitively normal individuals identify distinct clusters linked to neurodegeneration.Nature aging · 2025Article
- Cerebrospinal fluid proteomic associations of APOE genotypes reveal distinct protective and risk mechanisms for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The effect of APOE4 on Alzheimer's plasma biomarkers among Mexican Americans in the HABS-HD cohort.Alzheimer's research & therapy · 2025Article
- Mendelian randomization identifies proteins involved in neurodegenerative diseases.Brain : a journal of neurology · 2025Article
- Proteome profiling of cerebrospinal fluid using machine learning shows a unique protein signature associated with APOE4 genotype.Aging cell · 2025Article
- Proteome profiling of cerebrospinal fluid using machine learning shows a unique protein signature associated with APOE4 genotype.bioRxiv : the preprint server for biology · 2024Article
- Atypical intrinsic neural timescale in the left angular gyrus in Alzheimer's disease.Brain communications · 2024Article
- APOE and immunity: Research highlights.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Replacement of leisure-time sedentary behavior with various physical activities and the risk of dementia incidence and mortality: A prospective cohort study.Journal of sport and health science · 2023Article
- Article
- APOE modulates microglial immunometabolism in response to age, amyloid pathology, and inflammatory challenge.Cell reports · 2023Article
- Association ofFrontiers in aging neuroscience · 2023Article
- ApoE in Alzheimer's disease: pathophysiology and therapeutic strategies.Molecular neurodegeneration · 2022Review
- CSF proteome profiling across the Alzheimer's disease spectrum reflects the multifactorial nature of the disease and identifies specific biomarker panels.Nature aging · 2022Article
- Biofluid-based biomarkers for Alzheimer's disease-related pathologies: An update and synthesis of the literature.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Review
- Don't forget about tau: the effects of ApoE4 genotype on Alzheimer's disease cerebrospinal fluid biomarkers in subjects with mild cognitive impairment-data from the Dementia Competence Network.Journal of neural transmission (Vienna, Austria : 1996) · 2022Article
- Effects of age, amyloid, sex, andAlzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
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Authors and funding
23 authors at 12 institutions in 9 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAggregation of amyloid β into plaques in the brain is one of the earliest pathological events in Alzheimer's disease (AD). The exact pathophysiology leading to dementia is still uncertain, but the apolipoprotein E (APOE) ε4 genotype plays a major role. We aimed to identify the molecular pathways associated with amyloid β aggregation using cerebrospinal fluid (CSF) proteomics and to study the potential modifying effects of APOE ε4 genotype.
methodsWe tested 243 proteins and protein fragments in CSF comparing 193 subjects with AD across the cognitive spectrum (65% APOE ε4 carriers, average age 75 ± 7 years) against 60 controls with normal CSF amyloid β, normal cognition, and no APOE ε4 allele (average age 75 ± 6 years).
resultsOne hundred twenty-nine proteins (53%) were associated with aggregated amyloid β. APOE ε4 carriers with AD showed altered concentrations of proteins involved in the complement pathway and glycolysis when cognition was normal and lower concentrations of proteins involved in synapse structure and function when cognitive impairment was moderately severe. APOE ε4 non-carriers with AD showed lower expression of proteins involved in synapse structure and function when cognition was normal and lower concentrations of proteins that were associated with complement and other inflammatory processes when cognitive impairment was mild. Repeating analyses for 114 proteins that were available in an independent EMIF-AD MBD dataset (n = 275) showed that 80% of the proteins showed group differences in a similar direction, but overall, 28% effects reached statistical significance (ranging between 6 and 87% depending on the disease stage and genotype), suggesting variable reproducibility.
conclusionsThese results imply that AD pathophysiology depends on APOE genotype and that treatment for AD may need to be tailored according to APOE genotype and severity of the cognitive impairment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.