ArticleIntractable & rare diseases research2019
Microglia express TMEM119 in the brains of Nasu-Hakola disease.
Article in Intractable & rare diseases research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The lung-brain axis in neurodegeneration: inflammatory, immune, and vascular mechanisms with therapeutic implications.Inflammopharmacology · 2026Review
- Anti-VEGF vascular remodeling drives germinal center B cell-rich tertiary lymphoid structures during antibody-toxin and anti-CD40 combination therapy in glioblastoma.Research square · 2026Article
- Primary Human Reactive Microglia Display Mitochondrial Dysfunction and Metabolic Imbalance Upon Lipopolysaccharide Exposure.Neurochemical research · 2026Article
- Detection of disease-associated microglia among various microglia phenotypes induced by West Nile virus infection in mice.Journal of neurovirology · 2023Article
- A New Understanding of TMEM119 as a Marker of Microglia.Frontiers in cellular neuroscience · 2022Article
- Chronic exposure to IL-6 induces a desensitized phenotype of the microglia.Journal of neuroinflammation · 2021Article
- Increased transmembrane protein 119 (TMEM119) levels in the cerebrospinal fluid of patients with mild cognitive impairment due to Alzheimer's disease suggest early microglial involvement.Alzheimer's & dementia (Amsterdam, Netherlands)Article
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Authors and funding
5 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
We previously identified an evolutionarily conserved protein named transmembrane protein 119 (TMEM119) as the most reliable maker for human microglia. Recent studies showed that under homeostatic conditions, microglia intensely express TMEM119, whereas the expression levels are greatly reduced in disease-associated microglia (DAM) activated at the site of neurodegeneration. Nasu-Hakola disease (NHD) is a rare autosomal recessive disorder, pathologically characterized by leukoencephalopathy, astrogliosis, axonal spheroids, and accumulation of microglia. However, it remains unknown whether microglia are homeostatic or activated in NHD brains. In the present study, we identified TMEM119 on microglia in NHD brains by immunohistochemistry. TMEM119 was expressed on microglia in NHD brains as well as in the brains of non-neurological controls (NC) and Alzheimer's disease (AD) patients, although TMEM119-immunolabeled areas exhibited great variability from case to case without significant differences among the study population. These results suggest that TMEM119 expression on microglia might play a key role in steady-state brain maintenance in NHD, AD and controls.
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