ReviewNeuropathology and applied neurobiology2019
Invited Review: APOE at the interface of inflammation, neurodegeneration and pathological protein spread in Alzheimer's disease.
Review in Neuropathology and applied neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Dissecting the genetic and proteomic risk factors for delirium.Nature aging · 2026Pooled it
- Does sex moderate health and Alzheimer's disease risk tied to early educational experiences? The reducing inequities through social and educational change follow-up in early adulthood extension study protocol.Brain, behavior, & immunity - health · 2026Article
- The influence of blood lipids on cerebral perfusion by apolipoprotein E status.Journal of lipid research · 2026Article
- APOE4-Expressing Astrocytes Exhibit Parkinson's Disease-Related Pathology.Molecular neurobiology · 2026Article
- PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.Experimental neurobiology · 2026Article
- The utility of aqueous and serum apolipoprotein E and galectin-3 as biomarkers of neuroinflammation in glaucoma.Scientific reports · 2026Article
- Molecular characterization of humanized APOE mouse models reveals source and genotype dependent differences.Molecular neurodegeneration · 2026Article
- The metabolic roots of memory loss: interlinking the Diabetes-Alzheimer's hypothesis.Metabolic brain disease · 2026Review
- The Amyloid Plaque Proteomes of Alzheimer's Disease and Mild Cognitive Impairment.Research square · 2026Article
- Walking to protect against cognitive decline: the role of APOE genotype and sex.Biology of sex differences · 2026Article
- The 2024 NIA-AA biological definition of Alzheimer's disease: linking biomarkers to clinical practice.Frontiers in dementia · 2026Review
- Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction.Autophagy · 2025Article
- Intervention Role of APOE in CNS Diseases: APOE Actions and APOE Neurogenesis Capability.Molecular neurobiology · 2025Review
- Altered gut microbiota mediates the association between APOE genotype and amyloid-β accumulation in middle-aged adults.Journal of neurology · 2025Article
- Huang-Lian-Jie-Du decoction alleviates cognitive deficits in Alzheimer's disease model 5xFAD mice by inhibiting Trem2/Dap12 signaling pathway.Chinese medicine · 2025Article
- Lysosomal proteomics reveals mechanisms of neuronal apoE4-associated lysosomal dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Inflammatory biomarkers profiles and cognition among older adults.Scientific reports · 2025Article
- Free-water imaging of the nucleus basalis of Meynert in apolipoprotein E4 carriers.Frontiers in aging neuroscience · 2025Article
- Endothelial progenitor cells and cerebral small vessel disease inCerebral circulation - cognition and behavior · 2025Article
- Identifying network state-based Parkinson's disease subtypes using clustering and support vector machine models.Frontiers in psychiatry · 2025Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Despite more than a century of research, the aetiology of sporadic Alzheimer's disease (AD) remains unclear and finding disease modifying treatments for AD presents one of the biggest medical challenges of our time. AD pathology is characterized by deposits of aggregated amyloid beta (Aβ) in amyloid plaques and aggregated tau in neurofibrillary tangles. These aggregates begin in distinct brain regions and spread throughout the brain in stereotypical patterns. Neurodegeneration, comprising loss of synapses and neurons, occurs in brain regions with high tangle pathology, and an inflammatory response of glial cells appears in brain regions with pathological aggregates. Inheriting an apolipoprotein E ε4 (APOE4) allele strongly increases the risk of developing AD for reasons that are not yet entirely clear. Substantial amounts of evidence support a role for APOE in modulating the aggregation and clearance of Aβ, and data have been accumulating recently implicating APOE4 in exacerbating neurodegeneration, tau pathology and inflammation. We hypothesize that APOE4 influences all the pathological hallmarks of AD and may sit at the interface between neurodegeneration, inflammation and the spread of pathologies through the brain. Here, we conducted a systematic search of the literature and review evidence supporting a role for APOE4 in neurodegeneration and inflammation. While there is no direct evidence yet for APOE4 influencing the spread of pathology, we postulate that this may be found in future based on the literature reviewed here. In conclusion, this review highlights the importance of understanding the role of APOE in multiple important pathological mechanisms in AD.
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Registered trials
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.