Changes in expression of discrete VGF fragments have been detected in different neurological and psychiatric conditions. In schizophrenia, one study has shown an increase in the VGF23-62 peptide and a subsequent small study demonstrated that drugs further increase the expression, pointing at a possible ameliorating action of the fragment. A decreased expression of VGF26-62 peptide was found in frontotemporal dementia and the expression of a fragment containing aminoacids 378-398 was found to be changing in amyotrophic lateral sclerosis and Alzheimer's disease. VGF expression has also been shown in damaged peripheral nerves, and it is thought to have a role in neuropathic pain. In Glioblastoma, VGF has been shown to play autocrine and paracrine roles in feedback loops between differentiated glioblastoma cells and glioblastoma-specific cancer stem cells, promoting growth, survival and self-renewal.
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