ReviewInternational journal of molecular sciences2022
Alzheimer's Disease: From Immune Homeostasis to Neuroinflammatory Condition.
Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Plasma proteomics mediate the association between degenerative joint diseases and dementia risk.Journal of advanced research · 2026Article
- The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.Metabolic brain disease · 2026Review
- Navigating the Ethereal Tightrope: The Nanogenerator Manipulates Neurons for Immune Equilibrium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Increased risk of incident dementia associated with vitamin D deficiency in glaucoma patients: a TriNetX cohort study.Frontiers in nutrition · 2026Article
- A Review of Cutaneous Viral Infections and Their Potential Role in Neurologic Diseases.Journal of clinical medicine · 2025Review
- Integration of multi-omics quantitative trait loci evidence reveals novel susceptibility genes for Alzheimer's disease.Scientific reports · 2025Article
- Mozart's rhythm influence on Alzheimer's disease progression via modulation of pathological damage and cognition.iScience · 2025Article
- Microbiome Engineering for Biotherapeutic in Alzheimer's Disease Through the Gut-Brain Axis: Potentials and Limitations.International journal of molecular sciences · 2025Review
- CD28BMC neurology · 2025Article
- Identification and Exploration of Immunity-Related Genes and Natural Products for Alzheimer's Disease Based on Bioinformatics, Molecular Docking, and Molecular Dynamics.Immunity, inflammation and disease · 2025Article
- Exposure to autoimmune disorders is associated with increased Alzheimer's disease risk in a multi-site electronic health record analysis.Cell reports. Medicine · 2025Observational
- A subcellular sampling instrument allows spatial resolution of amyloid deposit-derived organelle-specific effects in microglia.Communications biology · 2025Article
- Integrative bioinformatics and machine learning identify iron metabolism genes MAP4, GPT, and HIRIP3 as diagnostic biomarkers and therapeutic targets in Alzheimer's disease.Frontiers in cellular neuroscience · 2025Article
- The role of peripheral innate immune cells in Alzheimer's disease progression.Frontiers in immunology · 2025Review
- Prenatal Stress Increases the Risk of the FPR2-related Dysfunction in the Brain's Resolution of Inflammation: A Study on the Humanized APPCurrent neuropharmacology · 2025Article
- Bifurcations in coupled amyloid-β aggregation-inflammation systems.NPJ systems biology and applications · 2024Article
- Causal relationships between peripheral immune cells and Alzheimer's disease: a two-sample Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Article
- Comprehensive analysis of genetic risk loci uncovers novel candidate genes and pathways in the comorbidity between depression and Alzheimer's disease.Translational psychiatry · 2024Article
- The protective effect of Astaxanthin on scopolamine - induced Alzheimer's model in mice.Neurosciences (Riyadh, Saudi Arabia) · 2024Article
- Risk Factors and Diagnostic Model Construction of Chronic Pain with Cognitive Impairment.Journal of pain research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's Disease is the most common cause in the world of progressive cognitive decline. Although many modifiable and non-modifiable risk factors have been proposed, in recent years, neuroinflammation has been hypothesized to be an important contributing factor of Alzheimer's Disease pathogenesis. Neuroinflammation can occur through the combined action of the Central Nervous System resident immune cells and adaptive peripheral immune system. In the past years, immunotherapies for neurodegenerative diseases have focused wrongly on targeting protein aggregates Aβ plaques and NFT treatment. The role of both innate and adaptive immune cells has not been fully clarified, but several data suggest that immune system dysregulation plays a key role in neuroinflammation. Recent studies have focused especially on the role of the adaptive immune system and have shown that inflammatory markers are characterized by increased CD4+ Teff cells' activities and reduced circulating CD4+ Treg cells. In this review, we discuss the key role of both innate and adaptive immune systems in the degeneration and regeneration mechanisms in the pathogenesis of Alzheimer's Disease, with a focus on how the crosstalk between these two systems is able to sustain brain homeostasis or shift it to a neurodegenerative condition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.