ArticleAging cell2021
Neuronal loss and microgliosis are restricted to the core of Aβ deposits in mouse models of Alzheimer's disease.
Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Six promising drug repurposing candidates for Alzheimer's disease and their sex-specific mechanisms and efficacy.Neural regeneration research · 2026Article
- Expression of GPR34 in microglia remains stable in human Alzheimer's disease.Acta neuropathologica · 2026Article
- SLC38A9 Regulation Affects Hippocampal Neuronal Autophagy: A Potential Alzheimer's Therapeutic Approach by Suppressing Alzheimer's Disease-Related Protein Deposition.CNS neuroscience & therapeutics · 2026Article
- Interferon signaling modulates Down syndrome-associated Alzheimer's disease pathology in a mouse model.iScience · 2025Article
- Selegiline Improves Cognitive Impairment in the Rat Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Detection of sex-specific glutamate changes in subregions of hippocampus in an early-stage Alzheimer's disease mouse model using GluCEST MRI.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Sex-specific hypothalamic neuropathology and glucose metabolism in an amyloidosis transgenic mouse model of Alzheimer's disease.Cell & bioscience · 2024Article
- Loss of Cholinergic and Monoaminergic Afferents inInternational journal of molecular sciences · 2024Article
- Gallic Acid Alleviates Cognitive Impairment by Promoting Neurogenesis via the GSK3β-Nrf2 Signaling Pathway in an APP/PS1 Mouse Model.Journal of Alzheimer's disease reports · 2024Article
- Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- Cacao Ameliorates Amyloid Beta-Induced Cognitive and Non-Cognitive Disturbances.Neuroscience insights · 2024Article
- Astrocyte-specific knockout of YKL-40/Chi3l1 reduces Aβ burden and restores memory functions in 5xFAD mice.Journal of neuroinflammation · 2023Article
- mTOR-dependent TFEB activation and TFEB overexpression enhance autophagy-lysosome pathway and ameliorate Alzheimer's disease-like pathology in diabetic encephalopathy.Cell communication and signaling : CCS · 2023Article
- MRI and fluid biomarkers reveal determinants of myelin and axonal loss with aging.Annals of clinical and translational neurology · 2023Article
- Is Drp1 a link between mitochondrial dysfunction and inflammation in Alzheimer's disease?Frontiers in molecular neuroscience · 2023Review
- Myelin repair in Alzheimer's disease: a review of biological pathways and potential therapeutics.Translational neurodegeneration · 2022Review
- MicroRNA-22-3p ameliorates Alzheimer's disease by targeting SOX9 through the NF-κB signaling pathway in the hippocampus.Journal of neuroinflammation · 2022Article
- Therapeutic Effects of High-Intensity Interval Training Exercise Alone and Its Combination with Ecdysterone Against Amyloid Beta-Induced Rat Model of Alzheimer's Disease: A Behavioral, Biochemical, and Histological Study.Neurochemical research · 2022Article
- Bezafibrate Exerts Neuroprotective Effects in a Rat Model of Sporadic Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-β (Aβ) deposits, pathologic tau, and neurodegeneration are major pathological hallmarks of Alzheimer's disease (AD). The relationship between neuronal loss and Aβ deposits is one of the fundamental questions in the pathogenesis of AD. However, this relationship is controversial. One main reason for the conflicting results may be the confounding effects of pathologic tau, which often coexists with Aβ deposits in the brains of AD patients. To clarify the relationship between neuronal loss and Aβ deposits, mouse models of AD, which develop abundant Aβ deposits in the aged brain without pathologic tau, were used to examine the co-localization of NeuN-positive neurons, NF-H-positive axons, MBP-positive myelin sheaths, and Aβ deposits. Neuronal loss, as measured by decreased staining of the neuronal cell body, axon, and myelin sheath, as well as the IBA-1-positive microglia, was significantly increased in the core area of cerebral Aβ deposits, but not in adjacent areas. Furthermore, neuronal loss in the core area of cerebral Aβ deposits was correlated with Aβ deposit size. These results clearly indicate that neuronal loss is restricted to the core of Aβ deposits, and this restricted loss probably occurs because the Aβ deposit attracts microglia, which cluster in the core area where Aβ toxicity and neuroinflammation toxicity are restrained. These findings may contribute to our understanding of the relationship between neuronal loss and Aβ deposits in the absence of pathologic tau.
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