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

  • Keeps some sensory neurons and the nerves of taste alive during development 3
  • Protects motor neurons and retinal ganglion cells in animal models of injury
  • Mice without it are nearly normal, so BDNF, which shares its receptor, appears to cover for it 3

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

  1. Pasutto et al., Heterozygous NTF4 mutations impairing neurotrophin-4 signalling in primary open-angle glaucoma, American Journal of Human Genetics 2009
  2. Rao et al., Variations in NTF4, VAV2 and VAV3 are not involved with primary open-angle glaucoma, Investigative Ophthalmology and Visual Science 2010
  3. 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.