ArticleMolecular brain2017
ApoE isoforms differentially regulates cleavage and secretion of BDNF.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Trial
- The Role of Brain-Derived Neurotrophic Factor (BDNF) in Neural Development and Cognitive Behavior in Pigeons: Advances and Future Perspectives.Current issues in molecular biology · 2026Review
- The prognostic potential of circulating BDNF levels and its polymorphisms in age-related cognitive impairment and neurodegeneration.Frontiers in aging neuroscience · 2026Review
- Intervention Role of APOE in CNS Diseases: APOE Actions and APOE Neurogenesis Capability.Molecular neurobiology · 2025Review
- BDNF/proBDNF Interplay in the Mediation of Neuronal Apoptotic Mechanisms in Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Comprehensive characterization of the neurogenic and neuroprotective action of a novel TrkB agonist using mouse and human stem cell models of Alzheimer's disease.Stem cell research & therapy · 2024Article
- Potential role ofFrontiers in aging neuroscience · 2024Article
- Aerobic Exercise, Training Dose, and Cardiorespiratory Fitness: Effects and Relationships with Resting Plasma Neurotrophic Factors in Alzheimer's Dementia.Journal of vascular diseases · 2023Article
- Exercise modulates APOE expression in brain cortex of female APOE3 and APOE4 targeted replacement mice.Neuropeptides · 2023Article
- How does apolipoprotein E genotype influence the relationship between physical activity and Alzheimer's disease risk? A novel integrative model.Alzheimer's research & therapy · 2023Review
- Linking Diabetes to Alzheimer's Disease: Potential Roles of Glucose Metabolism and Alpha-Glucosidase.Current neuropharmacology · 2023Review
- Serum brain-derived neurotrophic factor as diagnosis clue for Alzheimer's disease: A cross-sectional observational study in the elderly.Frontiers in psychiatry · 2023Article
- Longterm Increased S100B Enhances Hippocampal Progenitor Cell Proliferation in a Transgenic Mouse Model.International journal of molecular sciences · 2022Article
- Human-Induced Pluripotent Stem Cell-Based Models for Studying Sex-Specific Differences in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2022Review
- Single nuclei RNA sequencing investigation of the Purkinje cell and glial changes in the cerebellum of transgenic Spinocerebellar ataxia type 1 mice.Frontiers in cellular neuroscience · 2022Article
- Peptides Derived from Growth Factors to Treat Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Isoform-Specific Effects of Apolipoprotein E on Markers of Inflammation and Toxicity in Brain Glia and Neuronal Cells In Vitro.Current issues in molecular biology · 2021Article
- APOE4 genetic polymorphism results in impaired recovery in a repeated mild traumatic brain injury model and treatment with Bryostatin-1 improves outcomes.Scientific reports · 2020Article
- Effects of Sevoflurane Exposure During Late Pregnancy on Brain Development and Beneficial Effects of Enriched Environment on Offspring Cognition.Cellular and molecular neurobiology · 2020Article
- The physiology of regulated BDNF release.Cell and tissue research · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein E4 (ApoE4) is a major genetic risk factor for sporadic or late onset Alzheimer's disease (AD). Brain-derived neurotrophic factor (BDNF) is decreased by 3 to 4-fold in the brains of AD patients at autopsy. ApoE4 mice also have reduced BDNF levels. However, there have been no reports relating the different ApoE isoforms or AD to differential regulation of BDNF. Here we report that in the hippocampal regions of AD patients both prepro-BDNF and pro-BDNF expression showed a 40 and 60% decrease respectively compared to that expression in the hippocampi of age-matched control patients. We further report that ApoE isoforms differentially regulate maturation and secretion of BDNF from primary human astrocytes. After 24 h, ApoE3 treated astrocytes secreted 1.75- fold higher pro-BDNF than ApoE2-treated astrocytes, and ApoE2-treated astrocytes secreted 3-fold more mature-BDNF (m-BDNF) than ApoE3-treated astrocytes. In contrast, ApoE4-treated cells secreted negligible amounts of m-BDNF or pro-BDNF. ApoE2 increased the level of intracellular pre-pro BDNF by 19.04 ± 6.68%, while ApoE4 reduced the pre-pro BDNF by 21.61 ± 5.9% compared to untreated cells. Similar results were also seen in ApoE2, ApoE3 or ApoE4 treated cells at 4 h. Together, these results indicate that an ApoE2 or ApoE3 mediated positive regulation of BDNF may be protective while ApoE4 related defects in BDNF processing could lead to AD pathophysiology. These interactions of the ApoE isoforms with BDNF may help explain the increased risk of AD associated with the ApoE4 isoform.
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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.