The role of neuroinflammation in neurodegenerative diseases: current understanding and future therapeutic targets
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Neuroinflammation refers to a highly complicated reaction of the central nervous system (CNS) to certain stimuli such as trauma, infection, and neurodegenerative diseases. This is a cellular immune response whereby glial cells are activated, inflammatory mediators are liberated and reactive oxygen and nitrogen species are synthesized. Neuroinflammation is a key process that helps protect the brain from pathogens, but inappropriate, or protracted inflammation yields pathological states such as Parkinson’s disease, Alzheimer’s, Multiple Sclerosis, and other neurodegenerative disorders that showcase various pathways of neurodegeneration distributed in various parts of the CNS. This review reveals the major neuroinflammatory signaling pathways associated with neurodegeneration. Additionally, it explores promising therapeutic avenues, such as stem cell therapy, genetic intervention, and nanoparticles, aiming to regulate neuroinflammation and potentially impede or decelerate the advancement of these conditions. A comprehensive understanding of the intricate connection between neuroinflammation and these diseases is pivotal for the development of future treatment strategies that can alleviate the burden imposed by these devastating disorders.
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In early AD stages, microglia and astrocytes exert protective effects by phagocytosing Aβ and secreting trophic factors that support neuronal survival.
“During the early stages, microglia and astrocytes exert protective effects by phagocytosing Aβ and secreting trophic factors that support neuronal survival [88].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [88]
Section 4.1 (page unavailable) says activated microglia promote neuronal survival and help degrade Aβ oligomers. Sections 3.1 and 3.2 describe microglial growth-factor secretion and protective astrocyte activity, but they do not establish that both cell types phagocytose Aβ and secrete trophic factors during early AD. (LLM, conf=0.86)
Experimental — accuracy not yet measuredWhen glial activation becomes chronic or dysregulated, glial cells shift toward a maladaptive proinflammatory phenotype that fuels oxidative and nitrosative stress, perturbs synaptic plasticity, and promotes neuronal death.
“However, when activation becomes chronic or dysregulated, glial cells shift toward a maladaptive proinflammatory phenotype that fuels oxidative and nitrosative stress, perturbs synaptic plasticity, and promotes neuronal death [88].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [88]
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- Authors
- Adamu, A., Li, S., Gao, F., & Xue, G.
- Affiliations
- Shanxi Medical University (CN)
- Corresponding author
- Xue, Guofang
- ORCID
- Xue, Guofang
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2024-04-12
- Volume
- 16
- Pages
- 1347987-1347987
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC11045904
- OpenAlex
- W4394757778
- Cited by
- 564
- References
- 14
- Citations by year
- 2026: 292 · 2025: 226 · 2024: 46
- FWCI
- 27.18
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- neuroinflammation, neurodegenerative diseases, glial activation, reactive oxygen species, reactive nitrogen species, Parkinson's disease, Alzheimer's disease, multiple sclerosis, stem cell therapy, genetic interventions, nanoparticles
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