ReviewFrontiers in aging neuroscience2018
Clinical PET Imaging of Microglial Activation: Implications for Microglial Therapeutics in Alzheimer's Disease.
Review in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- A multidimensional analysis of neuropsychiatric lupus: clinical, biological and imaging insights from systematic evidence.Frontiers in immunology · 2026Pooled it
- Hypoxia reverses the early anti-inflammatory microglial response to the β-amyloid peptide: mitochondrial involvement and beneficial roles of melatonin and naringenin.Journal of translational medicine · 2025Article
- Role of NLRP3 Inflammasome in Chronic Pain and Alzheimer's Disease-A Review.Journal of biochemical and molecular toxicology · 2025Review
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- Inflammatory Cytokines and Cognition in Alzheimer's Disease and Its Prodrome.Psychiatry investigation · 2024Article
- Oral sub-chronic toxicity of fingerroot (Toxicology reports · 2024Article
- Personalized whole-brain neural mass models reveal combined Aβ and tau hyperexcitable influences in Alzheimer's disease.Communications biology · 2024Article
- Neurological impact of HIV/AIDS and substance use alters brain function and structure.Frontiers in medicine · 2024Review
- In-vivo neuronal dysfunction by Aβ and tau overlaps with brain-wide inflammatory mechanisms in Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Intranasal Drug Delivery by Nanotechnology: Advances in and Challenges for Alzheimer's Disease Management.Pharmaceutics · 2023Review
- The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders.Cells · 2023Review
- Neuroinflammation in the Evolution of Motor Function in Stroke and Trauma Patients: Treatment and Potential Biomarkers.Current issues in molecular biology · 2023Review
- Revealing the combined roles of Aβ and tau in Alzheimer's disease via a pathophysiological activity decoder.bioRxiv : the preprint server for biology · 2023Article
- The effects of low-dose radiation therapy in patients with mild-to-moderate Alzheimer's dementia: an interim analysis of a pilot study.Radiation oncology journal · 2023Article
- Engineered mesenchymal stem cell-derived extracellular vesicles: A state-of-the-art multifunctional weapon against Alzheimer's disease.Theranostics · 2023Review
- Article
- APP Knock-In Mice Produce E22P-Aβ Exhibiting an Alzheimer's Disease-like Phenotype with Dysregulation of Hypoxia-Inducible Factor Expression.International journal of molecular sciences · 2022Article
- Long Non-Coding RNAs, Extracellular Vesicles and Inflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Nitro Capsaicin Suppressed Microglial Activation and TNF-α-Induced Brain Microvascular Endothelial Cell Damage.Biomedicines · 2022Article
- Anti-Inflammatory Activity of Panduratin A against LPS-Induced Microglial Activation.Biomedicines · 2022Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to extracellular β-amyloid plaques and intracellular neurofibrillary tangles, neuroinflammation has been identified as a key pathological characteristic of Alzheimer's disease (AD). Once activated, neuroinflammatory cells called microglia acquire different activation phenotypes. At the early stage of AD, activated microglia are mainly dominated by the neuroprotective and anti-inflammatory M2 phenotype. Conversely, in the later stage of AD, the excessive activation of microglia is considered detrimental and pro-inflammatory, turning into the M1 phenotype. Therapeutic strategies targeting the modulation of microglia may regulate their specific phenotype. Fortunately, with the rapid development of
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.