ArticleBrain, behavior, and immunity2017
Intracranial IL-17A overexpression decreases cerebral amyloid angiopathy by upregulation of ABCA1 in an animal model of Alzheimer's disease.
Article in Brain, behavior, and immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 50 citations in OpenAlex.
- The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.Metabolic brain disease · 2026Review
- A Narrative Review: Do Systemic Drugs Used in the Treatment of Psoriatic Disease Affect Alzheimer's Disease?Dermatology and therapy · 2026Review
- Targeting IL-17 Presents a Promising Strategy for Treating Diseases Related to the Dysregulation of Lipid Homeostasis.Mediators of inflammation · 2026Review
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- MiR-34a deficiency enhances nucleic acid sensing and type I IFN signaling in a mouse model of Alzheimer's disease.Frontiers in immunology · 2026Article
- Article
- Exploratory Analysis of Cerebrospinal Fluid IL-6 and IL-17A Levels in Subcortical Small-Vessel Disease Compared to Alzheimer's Disease: A Pilot Study.Diagnostics (Basel, Switzerland) · 2025Article
- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Unveiling the Therapeutic Potential of Banxia Xiexin Decoction in Alzheimer's Disease: Insights From Network Pharmacology and Experimental Validation.Drug design, development and therapy · 2025Article
- Key actors in neuropathophysiology: The role of γδ T cells.European journal of immunology · 2024Review
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Effects ofFood and waterborne parasitology · 2023Article
- Interleukin-17 as a key player in neuroimmunometabolism.Nature metabolism · 2023Review
- Effects of Biologic Therapy on Laboratory Indicators of Cardiometabolic Diseases in Patients with Psoriasis.Journal of clinical medicine · 2023Article
- Unconventional T cells in brain homeostasis, injury and neurodegeneration.Frontiers in immunology · 2023Review
- Crosstalk between cholesterol metabolism and psoriatic inflammation.Frontiers in immunology · 2023Review
- A glance through the effects of CD4Computational and structural biotechnology journal · 2023Review
- Acquired immunity and Alzheimer's disease.Journal of biomedical research · 2022Article
- The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A.Journal of neuroinflammation · 2022Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Neuroinflammation is a pervasive feature of Alzheimer's disease (AD) and characterized by activated microglia, increased proinflammatory cytokines and/or infiltrating immune cells. T helper 17 (Th17) cells are found in AD brain parenchyma and interleukin-17A (IL-17A) is identified around deposits of aggregated amyloid β protein (Aβ). However, the role of IL-17A in AD pathogenesis remains elusive. We overexpressed IL-17A in an AD mouse model via recombinant adeno-associated virus serotype 5 (rAAV5)-mediated intracranial gene delivery. AD model mice subjected to injection of a vehicle (PBS) or rAAV5 carrying the lacZ gene served as controls. IL-17A did not exacerbate neuroinflammation in IL-17A-overexpressing mice. We found that IL-17A overexpression markedly improved glucose metabolism, decreased soluble Aβ levels in the hippocampus and cerebrospinal fluid, drastically reduced cerebral amyloid angiopathy, and modestly but significantly improved anxiety and learning deficits. Moreover, the ATP-binding cassette subfamily A member 1 (ABCA1), which can transport Aβ from the brain into the blood circulation, significantly increased in IL-17A-overexpressing mice. In vitro treatment of brain endothelial bEnd.3 cells with IL-17A induced a dose-dependent increase in protein expression of ABCA1 through ERK activation. Our study suggests that IL-17A may decrease Aβ levels in the brain by upregulating ABCA1 in blood-brain barrier endothelial cells.
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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.