ArticleJournal of neural transmission (Vienna, Austria : 1996)2009
ApoE4-dependent Abeta-mediated neurodegeneration is associated with inflammatory activation in the hippocampus but not the septum.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Age- and ApoE Genotype-Dependent Transcriptomic Responses to OInternational journal of molecular sciences · 2025Article
- Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.European review for medical and pharmacological sciences · 2022Review
- Defective Lysosomal Lipid Catabolism as a Common Pathogenic Mechanism for Dementia.Neuromolecular medicine · 2021Review
- Cancer Chemotherapy Related Cognitive Impairment and the Impact of the Alzheimer's Disease Risk FactorCancers · 2020Review
- ApoE4 Exacerbates Hippocampal Pathology Following Acute Brain Penetration Injury in Female Mice.Journal of molecular neuroscience : MN · 2020Article
- Cyclic ONeurobiology of aging · 2019Article
- Invited Review: APOE at the interface of inflammation, neurodegeneration and pathological protein spread in Alzheimer's disease.Neuropathology and applied neurobiology · 2019Review
- The Effects of APOE4 on Mitochondrial Dynamics and Proteins in vivo.Journal of Alzheimer's disease : JAD · 2019Article
- Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities.Frontiers in aging neuroscience · 2019Review
- Glial Contribution to Excitatory and Inhibitory Synapse Loss in Neurodegeneration.Frontiers in cellular neuroscience · 2019Review
- Interactions between inflammation, sex steroids, and Alzheimer's disease risk factors.Frontiers in neuroendocrinology · 2016Review
- Obesity and sex interact in the regulation of Alzheimer's disease.Neuroscience and biobehavioral reviews · 2016Review
- Differential Effects of apoE4 and Activation of ABCA1 on Brain and Plasma Lipoproteins.PloS one · 2016Article
- Behavioral testing affects the phenotypic expression of APOE ε3 and APOE ε4 in targeted replacement mice and reduces the differences between them.Alzheimer's & dementia (Amsterdam, Netherlands) · 2015Article
- APOE-modulated Aβ-induced neuroinflammation in Alzheimer's disease: current landscape, novel data, and future perspective.Journal of neurochemistry · 2015Review
- Reversal of apoE4-driven brain pathology and behavioral deficits by bexarotene.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Apolipoprotein E, amyloid-beta, and neuroinflammation in Alzheimer's disease.Neuroscience bulletin · 2014Review
- Involvement of the Apoer2 and Lrp1 receptors in mediating the pathological effects of ApoE4 in vivo.Current Alzheimer research · 2014Article
- ApoE4 induces Aβ42, tau, and neuronal pathology in the hippocampus of young targeted replacement apoE4 mice.Molecular neurodegeneration · 2013Article
- Effects of apoE deficiency and occlusal disharmony on amyloid-beta production and spatial memory in rats.PloS one · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein E4 (ApoE4), the most prevalent genetic risk factor for Alzheimer's disease, is histopathologically associated with increased deposition of amyloid-beta and brain inflammation and with impaired neuronal plasticity and repair. We have recently shown that the activation of the amyloid cascade by inhibition of the Abeta-degrading enzyme, neprilysin, stimulates the isoform-specific degeneration of hippocampal CA1 neurons and septal neurons in apoE4 transgenic mice and that this effect is accompanied by the accumulation of intracellular Abeta in the affected neurons. We presently examined the extent to which this apoE4-dependent Abeta-mediated neurodegeneration is associated with brain area specific inflammatory activation. This revealed that the activation of the amyloid cascade in apoE transgenic mice results in the activation of microgliosis and astrogliosis in the hippocampus of apoE4, but not in apoE3 transgenic mice. The effect was most pronounced in the hippocampal CA1 subfield and its initial kinetics followed that of the accumulation of Abeta in CA1 neurons. In contrast, the corresponding apoE4-dependent Abeta degeneration of septal neurons was not associated with the activation of either gliosis or astrogliosis in this brain area. These animal model findings, that the association between brain inflammation and neurodegeneration is brain area specific, suggest that neuropathological inflammatory interactions in AD may also be brain area specific and that consequently the efficacy of putative anti-inflammatory intervention may also be brain area selective.
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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.