ArticleiScience2023
INPP5D modulates TREM2 loss-of-function phenotypes in a β-amyloidosis mouse model.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Pooled it
- Immunotherapy with B28, an antibody to Aβ oligomers, potently decreases amyloid plaques, microgliosis, and memory decline in APP knock-in mice.Cell reports · 2026Article
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.Molecular neurodegeneration · 2026Article
- Article
- Article
- INPP5D Upregulation by Minocycline Mitigates Sepsis-Associated Neuroinflammation and Neuronal Dysfunction Via Microglial Autophagy and Antioxidant Pathways.Inflammation · 2026Article
- Inflammatory mechanisms underlying early Alzheimer's disease pathology: evidence from the aging rhesus macaque brain.Frontiers in cellular neuroscience · 2026Review
- Astrocyte activation persists one year after TBI: a dynamic shift from inflammation to neurodegeneration.Communications biology · 2025Article
- High throughput identification of genetic regulators of microglial inflammatory processes in Alzheimer's disease.Journal of neuroinflammation · 2025Article
- Selective agonism of GPR34 stimulates microglial uptake and clearance of amyloid β fibrils.Alzheimer's research & therapy · 2025Article
- INPP5D/SHIP1 is a dual regulator of endo-lysosome function and selective phagocytosis in human microglia.bioRxiv : the preprint server for biology · 2025Article
- LEGEND: Identifying Co-expressed Genes in Multimodal Transcriptomic Sequencing Data.Genomics, proteomics & bioinformatics · 2025Article
- Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer's knock-in mouse phenotypes.bioRxiv : the preprint server for biology · 2025Article
- A common Iba1 antibody labels vasopressin neurons in mice.bioRxiv : the preprint server for biology · 2025Article
- Unraveling the complex role of microglia in Alzheimer's disease: amyloid β metabolism and plaque formation.Inflammation and regeneration · 2025Review
- Discovery and evaluation of novel SHIP-1 inhibitors.Bioorganic & medicinal chemistry · 2024Article
- Emerging roles for ITAM and ITIM receptor signaling in microglial biology and Alzheimer's disease-related amyloidosis.Journal of neurochemistry · 2024Review
- Loss of Inpp5d has disease-relevant and sex-specific effects on glial transcriptomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Neutral or Detrimental Effects of TREM2 Agonist Antibodies in Preclinical Models of Alzheimer's Disease and Multiple Sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
The genetic associations of TREM2 loss-of-function variants with Alzheimer disease (AD) indicate the protective roles of microglia in AD pathogenesis. Functional deficiencies of TREM2 disrupt microglial clustering around amyloid β (Aβ) plaques, impair their transcriptional response to Aβ, and worsen neuritic dystrophy. However, the molecular mechanism underlying these phenotypes remains unclear. In this study, we investigated the pathological role of another AD risk gene,
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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.