Ntrk1 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Ntrk1 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
NTKR1 is a gene/protein encoding a key neuronal protein involved in synaptic function, signal transduction, and cellular homeostasis. Dysfunction of NTKR1 is associated with neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and related disorders.
Function
NTRK1 encodes TrkA (Tropomyosin receptor kinase A), the primary receptor for nerve growth factor (NGF). TrkA is a receptor tyrosine kinase that plays critical roles in neuronal development, survival, and function. In the adult nervous system, TrkA signaling promotes the survival of specific neuronal populations including nociceptors, thermoreceptors, and cholinergic [neurons](/entities/neurons) in the basal forebrain. In Alzheimer's disease, NGF/TrkA signaling is impaired, and restoring this pathway has been explored as a therapeutic strategy.
High expression in regions undergoing neurodegeneration in AD makes it a therapeutic target.
Key Publications
Hempstead BL, et al. (1991). "TrkA: a receptor for nerve growth factor." Cold Spring Harb Symp Quant Biol. PMID: 1669073(https://pubmed.ncbi.nlm.nih.gov/1669073/)
Chao MV, et al. (2006). "Neurotrophins: roles in neuronal development and function." Annu Rev Neurosci. PMID: 16719985(https://pubmed.ncbi.nlm.nih.gov/16719985/)
Longo FM, et al. (2013). "Small molecule neurotrophin receptor agonists for Alzheimer's disease." J Alzheimers Dis. PMID: 23948871(https://pubmed.ncbi.nlm.nih.gov/23948871/)
The study of Ntrk1 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
External Links
[PubMed](https://pubmed.ncbi.nlm.nih.gov/) - Biomedical literature
[Alzheimer's Disease Neuroimaging Initiative](https://adni.loni.usc.edu/) - Research data
[Allen Brain Atlas](https://brain-map.org/) - Brain gene expression data
References
[Doebele RC et al., "Entrectinib in patients with advanced or metastatic NTRK fusion-positive solid tumours: integrated analysis of three phase 1-2 trials." *The Lancet (2020)](https://doi.org/10.1016/S1470-2045(19)
[Obeidat AM et al., "Piezo2 expressing nociceptors mediate mechanical sensitization in experimental osteoarthritis." Nature communications (2023) (2023)](https://doi.org/10.1038/s41467-023-38241-x)
[Jiang T et al., "Development of small-molecule tropomyosin receptor kinase (TRK) inhibitors for NTRK fusion cancers." *Acta pharmaceutica Sinica (2021)](https://doi.org/10.1016/j.apsb.2020.05.004)
[Gianno F et al., "Paediatric-type diffuse high-grade gliomas in the 5th CNS WHO Classification." Pathologica (2022) (2022)](https://doi.org/10.32074/1591-951X-830)
[Megarbane A et al., "A 20-year Clinical and Genetic Neuromuscular Cohort Analysis in Lebanon: An International Effort." Journal of neuromuscular diseases (2022) (2022)](https://doi.org/10.3233/JND-210652)
[Clarke M et al., "Infant High-Grade Gliomas Comprise Multiple Subgroups Characterized by Novel Targetable Gene Fusions and Favorable Outcomes." Cancer discovery (2020) (2020)](https://doi.org/10.1158/2159-8290.CD-19-1030)
[Yang K et al., "NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway." Cell death discovery (2023) (2023)](https://doi.org/10.1038/s41420-023-01685-7)
[Bogumil H et al., "Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA): a molecularly distinct brain tumor type with recurrent NTRK gene fusions." Acta neuropathologica (2023) (2023)](https://doi.org/10.1007/s00401-023-02558-0)