ReviewJournal of neuroinflammation2019
Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease.
Review in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
116 citing papers in PubMed, 181 citations in OpenAlex.
- Targeting glial PD-1/PD-L1 restores microglial homeostasis and reduces neuronal hyperactivity in an Alzheimer's disease model.Science advances · 2026Article
- Article
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Targeted nanomedicine strategies for Alzheimer's disease therapy.Discover nano · 2026Review
- Brain Aging Mediating Heart Imaging-Derived Phenotypes and Mental and Nervous System Disorders.Aging cell · 2026Article
- The Crossroads of Neurodegeneration: Exploring the Overlap Between Alzheimer's Disease and Depression.Cureus · 2026Review
- Neuroinflammation and Oxidative Stress in Parkinson's Disease, Alzheimer's Disease, and COVID-19: Microglia-Neutrophil Interaction.ACS omega · 2026Review
- Chronic methanol exposure induces cognitive impairment and Alzheimer's-like pathology in rhesus monkeys.Animal models and experimental medicine · 2026Article
- Bitter Compounds as Multifunctional Agents against Diabetes-associated Cognitive Dysfunction: Bridging Metabolic Regulation and Neuroprotection.Mini reviews in medicinal chemistry · 2026Review
- Prenatal immune activation and adult Poly(I:C) re-challenge promote neuroimmune priming and AD-related behavioural, cellular and molecular alterations in wild-type mice.Frontiers in immunology · 2026Article
- Interplay between Peripheral and Central Nervous System Myeloid Cells during Aging: Impact for Lade-Life Depression and Alzheimer's Disease.Neuroimmunomodulation · 2026Review
- Autoimmune signatures in neurodegenerative dementias: from peripheral immune activation to CNS pathology.Frontiers in immunology · 2026Review
- Targeted Nanoparticles for Drug Delivery Across the Blood-Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review.Molecular neurobiology · 2025Review
- AI-orchestrated microglial sculptors: pioneering neural homeostasis restoration in 2025.Annals of medicine and surgery (2012) · 2025Article
- Genome-wide pleiotropy analysis of longitudinal blood pressure and harmonized cognitive performance measures.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Antigen-Specifically Activated CD8+ and Double-Negative T Cells Accumulate in the Brain of Alzheimer's Disease Mice.Aging and disease · 2025Article
- Adaptive Immune Dyshomeostasis as a Mediator of Vascular Cognitive Decline: Unraveling Neurovascular Crosstalk.Aging and disease · 2025Review
- Microbiome Engineering for Biotherapeutic in Alzheimer's Disease Through the Gut-Brain Axis: Potentials and Limitations.International journal of molecular sciences · 2025Review
- Immune cells in Alzheimer's disease: insights into pathogenesis and potential therapeutic targets.Medical review (2021) · 2025Review
- Effect of neuroinflammation on the progression of Alzheimer's disease and its significant ramifications for novel anti-inflammatory treatments.IBRO neuroscience reports · 2025Review
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD). Neuritic plaques composed of amyloid β and neurofibrillary tangle-laden neurons are surrounded by reactive astrocytes and microglia. Exposure of microglia, the resident myeloid cell of the CNS, to amyloid β causes these cells to acquire an inflammatory phenotype. While these reactive microglia are important to contain and phagocytose amyloid plaques, their activated phenotype impacts CNS homeostasis. In rodent models, increased neuroinflammation promoted by overexpression of proinflammatory cytokines can cause an increase in hyperphosphorylated tau and a decrease in hippocampal function. The peripheral immune system can also play a detrimental or beneficial role in CNS inflammation. Systemic inflammation can increase the risk of developing AD dementia, and chemokines released directly by microglia or indirectly by endothelial cells can attract monocytes and T lymphocytes to the CNS. These peripheral immune cells can aid in amyloid β clearance or modulate microglia responses, depending on the cell type. As such, several groups have targeted the peripheral immune system to modulate chronic neuroinflammation. In this review, we focus on the interplay of immunomodulating factors and cell types that are being investigated as possible therapeutic targets for the treatment or prevention of AD.
Indexed as
Identifiers
What OpenQuestion holds
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.