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VGF and VGF-derived peptides have been repeatedly identified in well-powered and well-designed multi-omic studies as dysregulated in neurodegenerative and psychiatric diseases. New therapeutics is urgently needed for these devastating and costly diseases, as are new biomarkers to improve disease diagnosis and mechanistic understanding. From a list of 537 genes involved in Alzheimer\u2019s disease pathogenesis, VGF was highlighted by the Accelerating Medicines Partnership in Alzheimer\u2019s disease as the potential therapeutic target of greatest interest. VGF levels are consistently decreased in brain tissue and CSF samples from patients with Alzheimer\u2019s disease compared to controls, and its levels correlate with disease severity and Alzheimer\u2019s disease pathology. In the brain, VGF exists as multiple functional VGF-derived peptides. Full-length human VGF1\u2013615 undergoes proteolytic processing by prohormone convertases and other proteases in the regulated secretory pathway to produce at least 12 active VGF-derived peptides. In cell and animal models, these VGF-derived peptides have been linked to energy balance regulation, neurogenesis, synaptogenesis, learning and memory, and depression-related behaviours throughout development and adulthood. The C-terminal VGF-derived peptides, TLQP-62 (VGF554\u2013615) and TLQP-21 (VGF554\u2013574) have differential effects on Alzheimer\u2019s disease pathogenesis, neuronal and microglial activity, and learning and memory. TLQP-62 activates neuronal cell-surface receptors and regulates long-term hippocampal memory formation. TLQP-62 also prevents immune-mediated memory impairment, depression-like and anxiety-like behaviours in mice. TLQP-21 binds to microglial cell-surface receptors, triggering microglial chemotaxis and phagocytosis. These actions were reported to reduce amyloid-\u03b2 plaques and decrease neuritic dystrophy in a transgenic mouse model of familial Alzheimer\u2019s disease. Expression differences of VGF-derived peptides have also been associated with frontotemporal lobar dementias, amyotrophic lateral sclerosis, Lewy body diseases, Huntington\u2019s disease, pain, schizophrenia, bipolar disorder, depression and antidepressant response. This review summarizes current knowledge and highlights questions for future investigation regarding the roles of VGF and its dysregulation in neurodegenerative and psychiatric disease. Finally, the potential of VGF and VGF-derived peptides as biomarkers and novel therapeutic targets for neurodegenerative and psychiatric diseases is highlighted.<\/jats:p>","DOI":"10.1093\/braincomms\/fcab261","type":"journal-article","created":{"date-parts":[[2021,10,25]],"date-time":"2021-10-25T19:13:50Z","timestamp":1635189230000},"source":"Crossref","is-referenced-by-count":125,"title":["VGF as a biomarker and therapeutic target in neurodegenerative and psychiatric diseases"],"prefix":"10.1093","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7015-5409","authenticated-orcid":false,"given":"James P","family":"Quinn","sequence":"first","affiliation":[{"name":"Department of Neurology, Alzheimer's Clinical & Translational Research Unit, Massachusetts General Hospital, Charlestown, MA 02129, USA"},{"name":"Department of Neurology, Harvard Medical School, Boston, MA 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Savannah 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