ArticleNeurochemical research2009
Developmental regulation of TREM2 and DAP12 expression in the murine CNS: implications for Nasu-Hakola disease.
Article in Neurochemical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 101 citations in OpenAlex.
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
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- Trem2 expression in microglia is required to maintain normal neuronal bioenergetics during development.Immunity · 2024Article
- Microglia Colonization Associated with Angiogenesis and Neural Cell Development.Advances in neurobiology · 2024Review
- Letter to the Editor: Novel TREM2 frameshift mutation in a 30-year-old woman with suspected frontotemporal dementia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- Microglial TREM2 at the Intersection of Brain Aging and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2023Review
- The multifaceted roles of embryonic microglia in the developing brain.Frontiers in cellular neuroscience · 2023Review
- The Primary Microglial Leukodystrophies: A Review.International journal of molecular sciences · 2022Review
- Microglial ASD-related genes are involved in oligodendrocyte differentiation.Scientific reports · 2021Article
- Maternal high-fat diet modifies myelin organization, microglial interactions, and results in social memory and sensorimotor gating deficits in adolescent mouse offspring.Brain, behavior, & immunity - health · 2021Article
- SPARC coordinates extracellular matrix remodeling and efficient recruitment to and migration of antigen-specific T cells in the brain following infection.Scientific reports · 2021Article
- Microglial and peripheral immune priming is partially sexually dimorphic in adolescent mouse offspring exposed to maternal high-fat diet.Journal of neuroinflammation · 2020Article
- Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease.Molecular neurodegeneration · 2020Review
- Ocular hypertension suppresses homeostatic gene expression in optic nerve head microglia of DBA/2 J mice.Molecular brain · 2020Article
- Do Alzheimer's Disease Risk Gene Products Actually Act in Microglia?Frontiers in aging neuroscience · 2020Article
- Curcumin restores innate immune Alzheimer's disease risk gene expression to ameliorate Alzheimer pathogenesis.Neurobiology of disease · 2019Article
- TREM2 brain transcript-specific studies in AD and TREM2 mutation carriers.Molecular neurodegeneration · 2019Article
- The cell type resolved mouse transcriptome in neuron-enriched brain tissues from the hippocampus and cerebellum during prion disease.Scientific reports · 2019Article
- Article
- FUS(1-359) transgenic mice as a model of ALS: pathophysiological and molecular aspects of the proteinopathy.Neurogenetics · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Trem2 is an orphan, DAP12 associated receptor constitutively expressed in vivo by subsets of microglia in the healthy adult murine CNS and in vitro by subsets of oligodendrocytes in neonatal mixed glial cultures. Loss of a functional Trem2 signaling pathway is the genetic cause of Nasu-Hakola disease. Whether the early onset cognitive dementia and myelin-pallor associated with this disorder are due to deficits in functional Trem2 signaling in microglia and/or oligodendrocytes is still being debated. Here, we find that Trem2/DAP12 expression is detected in embryonic day 14 CNS mRNA. Using dual immunohistochemistry/in situ hybridization, we find that both Trem2 and DAP12 expression always co-localized with markers of microglia/macrophages. However, Trem2/DAP12 positive microglia are found in very close apposition with CNP+ oligodendrocytes prior to myelination (post-natal day 1). In addition, CNS expression of TREM2 and DAP12 are not detected in PU.1KO which lack microglia and macrophages. Our data provide continuing support for Nasu-Hakola disease being identified as a cognitive disorder caused by a primary dysfunction of CNS microglia.
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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.