ReviewNeurochemical research2019
Understanding the Role of ApoE Fragments in Alzheimer's Disease.
Review in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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
52 citing papers in PubMed, 85 citations in OpenAlex.
- Ontological Analysis of Brain Proteostasis Highlights the Sex-Dependent Trajectory of ApoE Isoform-Specific Regulation.bioRxiv : the preprint server for biology · 2026Article
- In Vivo 4D Oxy-Wavelet MRI as a Non-Invasive Biomarker of Brain Mitochondrial Function across the Lifespan.bioRxiv : the preprint server for biology · 2026Article
- APOE4 exacerbates glucocorticoid stress hormone-induced tau pathology via mitochondrial dysfunction.Cell death & disease · 2026Article
- Article
- The connection between autophagy and Alzheimer's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- An interpretable generative multimodal neuroimaging-genomics framework for decoding Alzheimer's disease.Journal of neural engineering · 2025Article
- Proteomic Analysis of the Low Molecular Mass Fraction of Newly Diagnosed and Recurrent Glioblastoma CUSA Fluid: A Pilot Investigation of the Peptidomic Profile.International journal of molecular sciences · 2025Article
- The Role of N6-Methyladenosine in Mitochondrial Dysfunction and Pathology.International journal of molecular sciences · 2025Review
- EnSCAN: ENsemble Scoring for prioritizing CAusative variaNts across multiplatform GWASs for late-onset alzheimer's disease.BioData mining · 2025Article
- Apolipoprotein E in Alzheimer's Disease: Focus on Synaptic Function and Therapeutic Strategy.Molecular neurobiology · 2025Review
- Oral Diseases Are Associated with Cognitive Decline and Dementia.Advances in experimental medicine and biology · 2025Review
- Association of liver function markers and apolipoprotein E ε4 with pathogenesis and cognitive decline in Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Alzheimer's disease phenotype based upon the carrier status of the apolipoprotein E ɛ4 allele.Brain pathology (Zurich, Switzerland) · 2024Review
- Apolipoprotein ε in Brain and Retinal Neurodegenerative Diseases.Aging and disease · 2023Review
- APOE Gene Associated with Dementia-Related Traits, Depression, and Anxiety in the Hispanic Population.Genes · 2023Article
- Apolipoprotein-E deficiency leads to brain network alteration characterized by diffusion MRI and graph theory.Frontiers in neuroscience · 2023Article
- Article
- Linking the Amyloid, Tau, and Mitochondrial Hypotheses of Alzheimer's Disease and Identifying Promising Drug Targets.Biomolecules · 2022Review
- COR388 (atuzaginstat): an investigational gingipain inhibitor for the treatment of Alzheimer disease.Expert opinion on investigational drugs · 2022Article
- Functional diversity of apolipoprotein E: from subcellular localization to mitochondrial function.Cellular and molecular life sciences : CMLS · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is one of the most devastating neurodegenerative diseases. It has been known for decades that the APOE ɛ4 allele is the most significant genetic risk factor for late-onset AD and yet its precise role in the disease remains unclear. The APOE gene encodes apolipoprotein E (apoE), a 35 kDa glycoprotein highly expressed in the brain. There are three different isoforms: apoE3 is the most common allele in the population, whilst apoE2 decreases, and apoE4 increases AD risk. ApoE has numerous functions that affect neuronal and non-neuronal cells, thus how it contributes to disease onset and progression is hotly debated. The apoE4 isoform has been linked to the accumulation of both of the major pathological hallmarks of AD, amyloid plaques containing amyloid β peptides, and neurofibrillary tangles containing hyperphosphorylated tau protein, as well as other hallmarks of the disease, including inflammation and oxidative stress. Numerous studies have shown that apoE undergoes fragmentation in the human brain, and that the fragmentation pattern varies between isoforms. It was previously shown that apoE4 has neurotoxic functions, however recent data has also identified a neuroprotective role for the apoE N-terminal 25 kDa fragment, which is more prevalent in apoE3 individuals. The ability of the apoE 25 kDa fragment to promote neurite outgrowth was recently demonstrated and this suggests there is a potential loss of neuroprotection in apoE4 individuals in addition to the previously described gain of toxic function for specific apoE4 fragments. Here we review the enzymes proposed to be responsible for apoE fragmentation, the specific functions of different apoE fragments and their possible links with 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.