ReviewFrontiers in neuroscience2015
Does neuroinflammation turn on the flame in Alzheimer's disease? Focus on astrocytes.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Cognitive Stimulation Modulates Platelet Total Phospholipases A2 Activity in Subjects with Mild Cognitive Impairment.Journal of Alzheimer's disease : JAD · 2016Trial
- Dysregulation of Immune Mediators and Synaptic Plasticity in Central Nervous System Disorders.Cells · 2026Review
- Neuroinflammation-mediated YKL-40 correlates with tau pathology and predicts longitudinal cognitive impairment and brain atrophy in Alzheimer's disease, with hypertensive dependency.Frontiers in aging neuroscience · 2025Article
- Astrocyte biomarkers GFAP and YKL-40 mediate early Alzheimer's disease progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- A sex-stratified analysis of neuroimmune gene expression signatures in Alzheimer's disease brains.GeroScience · 2023Article
- Effects of Ultramicronized Palmitoylethanolamide (um-PEA) in COVID-19 Early Stages: A Case-Control Study.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The Role of PPAR Alpha in the Modulation of Innate Immunity.International journal of molecular sciences · 2021Review
- Successful and Unsuccessful Brain Aging in Pets: Pathophysiological Mechanisms behind Clinical Signs and Potential Benefits from Palmitoylethanolamide Nutritional Intervention.Animals : an open access journal from MDPI · 2021Review
- Methylation factor MRPL15 identified as a potential biological target in Alzheimer's disease.Aging · 2021Article
- Alternative Targets to Fight Alzheimer's Disease: Focus on Astrocytes.Biomolecules · 2021Review
- Ultramicronized Palmitoylethanolamide (um-PEA): A New Possible Adjuvant Treatment in COVID-19 patients.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Randomized Cross Over Study Assessing the Efficacy of Non-invasive Stimulation of the Vagus Nerve in Patients With Axial Spondyloarthritis Resistant to Biotherapies: The ESNV-SPA Study Protocol.Frontiers in human neuroscience · 2021Article
- Cerebrospinal Fluid C18 Ceramide Associates with Markers of Alzheimer's Disease and Inflammation at the Pre- and Early Stages of Dementia.Journal of Alzheimer's disease : JAD · 2021Article
- Do the Bugs in Your Gut Eat Your Memories? Relationship between Gut Microbiota and Alzheimer's Disease.Brain sciences · 2020Review
- Association of glial and neuronal degeneration markers with Alzheimer's disease cerebrospinal fluid profile and cognitive functions.Alzheimer's research & therapy · 2020Article
- Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice.Brain and behavior · 2020Article
- Changes in Inflammatory Response, Redox Status and NaNeurotoxicity research · 2020Article
- Chronic sleep fragmentation shares similar pathogenesis with neurodegenerative diseases: Endosome-autophagosome-lysosome pathway dysfunction and microglia-mediated neuroinflammation.CNS neuroscience & therapeutics · 2020Article
- Traditional Chinese medicine for anti-Alzheimer's disease: berberine and evodiamine fromChinese medicine · 2020Review
- Potential Bidirectional Relationship Between Periodontitis and Alzheimer's Disease.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Data from animal models and Alzheimer's disease (AD) subjects provide clear evidence for an activation of inflammatory pathways during the pathogenetic course of such illness. Biochemical and neuropathological studies highlighted an important cause/effect relationship between inflammation and AD progression, revealing a wide range of genetic, cellular, and molecular changes associated with the pathology. In this context, glial cells have been proved to exert a crucial role. These cells, in fact, undergo important morphological and functional changes and are now considered to be involved in the onset and progression of AD. In particular, astrocytes respond quickly to pathology with changes that have been increasingly recognized as a continuum, with potentially beneficial and/or negative consequences. Although it is now clear that activated astrocytes trigger the neuroinflammatory process, however, the precise mechanisms have not been completely elucidated. Neuroinflammation is certainly a multi-faceted and complex phenomenon and, especially in the early stages, exerts a reparative intent. However, for reasons not yet all well known, this process goes beyond the physiologic control and contributes to the exacerbation of the damage. Here we scrutinize some evidence supporting the role of astrocytes in the neuroinflammatory process and the possibility that these cells could be considered a promising target for future AD therapies.
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