A review in Nature Neuroscience refines the 'neurotrophin hypothesis of depression' by examining the complex biology of Brain-Derived Neurotrophic Factor (BDNF). It highlights that while BDNF signaling is necessary for antidepressants to work, genetic disruption of these pathways does not inherently cause depression. The authors emphasize the opposing roles of the precursor proBDNF and mature mBDNF, suggesting that the balance between these peptides, rather than BDNF levels alone, is critical for understanding mood disorders.
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