ArticleJournal of neuroinflammation2014
IVIg protects the 3xTg-AD mouse model of Alzheimer's disease from memory deficit and Aβ pathology.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.
- Can IVIG Intervene in AD? Insights from Animal Experiments and Clinical Trials-A Systematic Review and Synthesis Without Meta-Analysis.International journal of molecular sciences · 2026Pooled it
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Adaptive immunity in the neuroinflammation of Alzheimer's disease.Chinese medical journal · 2025Review
- Emerging Roles of Adaptive Immune Response in Alzheimer's Disease.Aging and disease · 2024Review
- A Need for Refined Senescence Biomarkers and Measures of Senolytics in the Brain.Journal of Alzheimer's disease : JAD · 2024Article
- Postsynaptic Protein Shank3a Deficiency Synergizes with Alzheimer's Disease Neuropathology to Impair Cognitive Performance in the 3xTg-AD Murine Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Review
- MPC-n (IgG) improves long-term cognitive impairment in the mouse model of repetitive mild traumatic brain injury.BMC medicine · 2023Article
- Riluzole and its prodrugs for the treatment of Alzheimer's disease.Pharmaceutical patent analyst · 2023Article
- Temporal Appearance of Enhanced Innate Anxiety in Alzheimer Model Mice.Biomedicines · 2023Article
- Higher Angiotensin I Converting Enzyme 2 (ACE2) levels in the brain of individuals with Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Co-administration of FVIII with IVIG reduces immune response to FVIII in hemophilia A mice.Scientific reports · 2022Article
- Aducanumab and Its Effects on Tau Pathology: Is This the Turning Point of Amyloid Hypothesis?International journal of molecular sciences · 2022Review
- Insights into T-cell dysfunction in Alzheimer's disease.Aging cell · 2021Review
- Role of Retinoid X Receptors (RXRs) and dietary vitamin A in Alzheimer's disease: Evidence from clinicopathological and preclinical studies.Neurobiology of disease · 2021Article
- Administration of anti-ERMAP antibody ameliorates Alzheimer's disease in mice.Journal of neuroinflammation · 2021Article
- Repurposing beta-3 adrenergic receptor agonists for Alzheimer's disease: beneficial effects in a mouse model.Alzheimer's research & therapy · 2021Article
- Tetrahydrobiopterin Improves Recognition Memory in the Triple-Transgenic Mouse Model of Alzheimer's Disease, Without Altering Amyloid-β and Tau Pathologies.Journal of Alzheimer's disease : JAD · 2021Article
- Administration of Amyloid Precursor Protein Gene Deleted Mouse ESC-Derived Thymic Epithelial Progenitors Attenuates Alzheimer's Pathology.Frontiers in immunology · 2020Article
- Blockade of α4 integrins reduces leukocyte-endothelial interactions in cerebral vessels and improves memory in a mouse model of Alzheimer's disease.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIntravenous immunoglobulin (IVIg) is currently in clinical study for Alzheimer's disease (AD). However, preclinical investigations are required to better understand AD-relevant outcomes of IVIg treatment and develop replacement therapies in case of unsustainable supply.
methodsWe investigated the effects of IVIg in the 3xTg-AD mouse model, which reproduces both Aβ and tau pathologies. Mice were injected twice weekly with 1.5 g/kg IVIg for 1 or 3 months.
resultsIVIg induced a modest but significant improvement in memory in the novel object recognition test and attenuated anxiety-like behavior in 3xTg-AD mice. We observed a correction of immunologic defects present in 3xTg-AD mice (-22% CD4/CD8 blood ratio; -17% IL-5/IL-10 ratio in the cortex) and a modulation of CX3CR1+ cell population (-13% in the bone marrow). IVIg treatment led to limited effects on tau pathology but resulted in a 22% reduction of the soluble Aβ42/Aβ40 ratio and a 60% decrease in concentrations of 56 kDa Aβ oligomers (Aβ*56).
conclusionThe memory-enhancing effect of IVIg reported here suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD.
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