ArticleNature metabolism2023
Alleviating symptoms of neurodegenerative disorders by astrocyte-specific overexpression of TMEM164 in mice.
Article in Nature metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- HDAC7 acts as an astrocytic mediator of Aβ pathology that directly engages IKK to drive astrocyte neurotoxicity and neurodegeneration in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Allosteric drugs in biomolecular condensates: ways forward.Drug discovery today · 2026Review
- Cryo-EM structure of TMEM164 reveals distinct phospholipid remodeling mechanisms with anti-ferroptotic potential.Nature communications · 2025Article
- Fibroblast Growth Factor 8 Suppresses Neurotoxic Astrocytes and Alleviates Neuropathic Pain via Spinal FGFR3 Signaling.Neuroscience bulletin · 2025Article
- TMEM164 enhances radioresistance of GBM cells by inhibiting the FASN-NADPH-ROS axis.Journal of neuro-oncology · 2025Article
- Inhibition of astrocyte BMP signaling alleviates neuroinflammation in experimental models of Parkinson's disease.Cell death discovery · 2025Article
- Astrocyte FGF7/FGFR2 autocrine signaling mediates neuroinflammation and promotes MPTP-induced degeneration of dopaminergic neurons.Acta pharmaceutica Sinica. B · 2025Article
- Modulating mTOR-dependent astrocyte substate transitions to alleviate neurodegeneration.Nature aging · 2025Article
- Innate and adaptive immunity in neurodegenerative disease.Cellular and molecular life sciences : CMLS · 2025Review
- Advancements in Immunity and Dementia Research: Highlights from the 2023 AAIC Advancements: Immunity Conference.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Sepsis-associated encephalopathy: Mechanisms, Diagnosis, and Treatments update.International journal of biological sciences · 2025Review
- (Re)building the nervous system: A review of neuron-glia interactions from development to disease.Journal of neurochemistry · 2025Review
- Pharmacological effects, molecular mechanisms and strategies to improve bioavailability of curcumin in the treatment of neurodegenerative diseases.Frontiers in pharmacology · 2025Review
- Advances in the study of phencyclidine-induced schizophrenia-like animal models and the underlying neural mechanisms.Schizophrenia (Heidelberg, Germany) · 2024Review
- Astrocyte-Neuron Interactions in Alzheimer's Disease.Advances in neurobiology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammatory microglia secrete cytokines to induce neurotoxic reactive astrocytes, which are one of the major causes of neuronal death. However, the intrinsic key regulators underlying neurotoxic reactive astrocytes induction are unknown. Here we show that the transmembrane protein 164 (TMEM164) is an early-response intrinsic factor that regulates neurotoxic astrocyte reactivity. TMEM164 overexpression inhibits the induction of neurotoxic reactive astrocytes, maintains normal astrocytic functions and suppresses neurotoxic reactive astrocyte-mediated neuronal death by decreasing the secretion of neurotoxic saturated lipids. Adeno-associated virus-mediated, astrocyte-specific TMEM164 overexpression in male and female mice prevents the induction of neurotoxic reactive astrocytes, dopaminergic neuronal loss and motor deficits in a Parkinson's disease model. Notably, brain-wide astrocyte-specific TMEM164 overexpression prevents the induction of neurotoxic reactive astrocytes, amyloid β deposition, neurodegeneration and memory decline in the 5XFAD Alzheimer's disease mouse model, suggesting that TMEM164 could serve as a potential therapeutic target for neurodegenerative disorders.
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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.