Where it comes from
- Made in
- Muscle, prostate, thymus, placenta, and a little in brain
- Sent out by
- Muscle activity raises it
- Acts on
- Motor neurons
- Sensory neurons of touch
- Taste buds
- Retinal ganglion cells
What it does
In medicine
- No medicine and no clinical assay; anything aimed at TrkB would act on BDNF as well, so NT-4 has never been a target on its own
- Its only clinical lead was in glaucoma, and that remains unsettled 1
Beyond the body’s own use
- There is no NT-4 product and no human trial; it is the least studied of the four neurotrophins
- A 2009 study reported NTF4 mutations that impair TrkB signalling in families with primary open-angle glaucoma 1
- Attempts to find the same variants in Indian and Chinese cohorts were negative, so the glaucoma link is unconfirmed rather than disproved 2
- What is genuinely unknown is whether NT-4 does anything BDNF cannot. The knockout mice differ sharply: losing NT-4 costs some touch and taste neurons, losing BDNF is severe 3
Sources
- Pasutto et al., Heterozygous NTF4 mutations impairing neurotrophin-4 signalling in primary open-angle glaucoma, American Journal of Human Genetics 2009
- Rao et al., Variations in NTF4, VAV2 and VAV3 are not involved with primary open-angle glaucoma, Investigative Ophthalmology and Visual Science 2010
- Erickson et al., Mice lacking BDNF show sensory losses distinct from mice lacking NT4, Journal of Neuroscience 1996
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.