ReviewFrontiers in human neuroscience2016
Microglial Priming and Alzheimer's Disease: A Possible Role for (Early) Immune Challenges and Epigenetics?
Review in Frontiers in human neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- Arsenic attenuates responsiveness to inflammatory stimuli in the SIM-A9 microglial cell line.Neurotoxicology · 2026Article
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- Maternal Stress Primes Adolescent Stress Susceptibility via Microglial Complement-Dependent Synaptic Phagocytosis.Research (Washington, D.C.) · 2026Article
- Early antiviral treatment following gammaherpesvirus-68 infection of the central nervous system prevents subsequent multiple sclerosis-like disease.Journal of neuroinflammation · 2025Article
- Perinatal asphyxia and Alzheimer's disease: is there a correlation?Frontiers in pediatrics · 2025Review
- Aging Microglia and Their Impact in the Nervous System.Advances in neurobiology · 2024Review
- The dynamic influence of nutrition on prolonged cognitive healthspan across the life course: A perspective review.Neuroscience applied · 2024Review
- Transcriptional and epigenetic decoding of the microglial aging process.Nature aging · 2023Article
- Systemic Inflammation Causes Microglial Dysfunction With a Vascular AD phenotype.Brain, behavior, & immunity - health · 2023Article
- Neuroimmune contributions to Alzheimer's disease: a focus on human data.Molecular psychiatry · 2022Review
- Connecting aging biology and inflammation in the omics era.The Journal of clinical investigation · 2022Review
- Delirium and the risk of developing dementia: a cohort study of 12 949 patients.Journal of neurology, neurosurgery, and psychiatry · 2022Article
- Autism Spectrum Disorder Initiation by Inflammation-Facilitated Neurotoxin Transport.Neurochemical research · 2022Review
- ENT-A010, a Novel Steroid Derivative, Displays Neuroprotective Functions and Modulates Microglial Responses.Biomolecules · 2022Article
- An Alternative Explanation for Alzheimer's Disease and Parkinson's Disease Initiation from Specific Antibiotics, Gut Microbiota Dysbiosis and Neurotoxins.Neurochemical research · 2022Review
- Neuronal cell death mechanisms in Alzheimer's disease: An insight.Frontiers in molecular neuroscience · 2022Review
- Adolescent Binge Alcohol Enhances Early Alzheimer's Disease Pathology in Adulthood Through Proinflammatory Neuroimmune Activation.Frontiers in pharmacology · 2022Article
- Neuroimmune multi-hit perspective of coronaviral infection.Journal of neuroinflammation · 2021Review
- Gut Microbiota Composition and Epigenetic Molecular Changes Connected to the Pathogenesis of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2021Review
- The Impact of Obesity on Microglial Function: Immune, Metabolic and Endocrine Perspectives.Cells · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is thought to contribute to Alzheimer's disease (AD) pathogenesis that is, to a large extent, mediated by microglia. Given the tight interaction between the immune system and the brain, peripheral immune challenges can profoundly affect brain function. Indeed, both preclinical and clinical studies have indicated that an aberrant inflammatory response can elicit behavioral impairments and cognitive deficits, especially when the brain is in a vulnerable state, e.g., during early development, as a result of aging, or under disease conditions like AD. However, how exactly peripheral immune challenges affect brain function and whether this is mediated by aberrant microglial functioning remains largely elusive. In this review, we hypothesize that: (1) systemic immune challenges occurring during vulnerable periods of life can increase the propensity to induce later cognitive dysfunction and accelerate AD pathology; and (2) that "priming" of microglial cells is instrumental in mediating this vulnerability. We highlight how microglia can be primed by both neonatal infections as well as by aging, two periods of life during which microglial activity is known to be specifically upregulated. Lasting changes in (the ratios of) specific microglial phenotypes can result in an exaggerated pro-inflammatory cytokine response to subsequent inflammatory challenges. While the resulting changes in brain function are initially transient, a continued and/or excess release of such pro-inflammatory cytokines can activate various downstream cellular cascades known to be relevant for AD. Finally, we discuss microglial priming and the aberrant microglial response as potential target for treatment strategies for AD.
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