ArticleFrontiers in aging neuroscience2018
Microglia in Alzheimer's Disease: Activated, Dysfunctional or Degenerative.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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Who cites it
128 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- iDCF: Interpretable deconvolution of cell fractions via biologically-informed deep learning using scRNA-seq data.PLoS computational biology · 2026Article
- PGK1 Drives Glial Glycolytic Reprogramming to Mediate Isoflurane-Induced Cognitive Impairment in Aged Mice.Journal of cellular and molecular medicine · 2026Article
- Expression of GPR34 in microglia remains stable in human Alzheimer's disease.Acta neuropathologica · 2026Article
- EGR2 affects mixed stroke repair through BNIP3L-mediated microglial mitophagy.IBRO neuroscience reports · 2026Article
- Visceral adipose tissue differentially affects tau and Aβ pathology in 3xTg-AD mice.Cell communication and signaling : CCS · 2026Article
- Multiscale Approximations to Understand the Complex Role of Microglia in Alzheimer's Disease.The European journal of neuroscience · 2026Review
- Structural changes in gray matter and white matter across the Alzheimer's disease continuum.Frontiers in neuroscience · 2026Article
- Boosting angiotensin-converting enzyme (ACE) in microglia protects against Alzheimer's disease in 5xFAD mice.Nature aging · 2025Article
- Isoliensinine confers neuroprotection and alleviates LPS-induced neuroinflammation in microglia by regulating the MAPK/NF-κB signaling.Frontiers in pharmacology · 2025Article
- Research progress on resistance exercise therapy for improving cognitive function in patients with AD and muscle atrophy.Frontiers in aging neuroscience · 2025Review
- Molecular Modeling Insights on the Pharmaceuticals and Hypotheses of Alzheimer's Disease.Current medicinal chemistry · 2025Review
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- Extracellular vesicles from human-induced pluripotent stem cell-derived neural stem cells alleviate proinflammatory cascades within disease-associated microglia in Alzheimer's disease.Journal of extracellular vesicles · 2024Article
- Exploring the potential therapeutic benefits of 7-methoxy coumarin for neuropathy pain: an in vivo, in vitro, and in silico approach.Molecular biology reports · 2024Article
- Simple and highly specific targeting of resident microglia with adeno-associated virus.iScience · 2024Article
- The roles of long non-coding RNAs in Alzheimer's disease diagnosis, treatment, and their involvement in Alzheimer's disease immune responses.Non-coding RNA research · 2024Review
- Microglial modulation as a therapeutic strategy in Alzheimer's disease: Focus on microglial preconditioning approaches.Journal of cellular and molecular medicine · 2024Review
- Review
- Microglia measured by TSPO PET are associated with Alzheimer's disease pathology and mediate key steps in a disease progression model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglial activation has been considered a crucial player in the pathological process of multiple human neurodegenerative diseases. In some of these pathologies, such as Amyotrophic Lateral Sclerosis or Multiple Sclerosis, the immune system and microglial cells (as part of the cerebral immunity) play a central role. In other degenerative processes, such as Alzheimer's disease (AD), the role of microglia is far to be elucidated. In this "mini-review" article, we briefly highlight our recent data comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients. Since the AD pathology could display regional heterogeneity, we focus our work at the hippocampal formation. In APP based models a prominent microglial response is triggered around amyloid-beta (Aβ) plaques. These strongly activated microglial cells could drive the AD pathology and, in consequence, could be implicated in the neurodegenerative process observed in models. On the contrary, the microglial response in human samples is, at least, partial or attenuated. This patent difference could simply reflect the lower and probably slower Aβ production observed in human hippocampal samples, in comparison with models, or could reflect the consequence of a chronic long-standing microglial activation. Beside this differential response, we also observed microglial degeneration in Braak V-VI individuals that, indeed, could compromise their normal role of surveying the brain environment and respond to the damage. This microglial degeneration, particularly relevant at the dentate gyrus, might be mediated by the accumulation of toxic soluble phospho-tau species. The consequences of this probably deficient immunological protection, observed in AD patients, are unknown.
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