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Finasteride‐induced depression: new insights into possible pathomechanisms
Author(s) -
Römer Benedikt,
Gass Peter
Publication year - 2010
Publication title -
journal of cosmetic dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.626
H-Index - 44
eISSN - 1473-2165
pISSN - 1473-2130
DOI - 10.1111/j.1473-2165.2010.00533.x
Subject(s) - finasteride , allopregnanolone , neurogenesis , neuroactive steroid , anxiolytic , 5 alpha reductase inhibitor , dihydrotestosterone , medicine , hippocampal formation , neuroprotection , pharmacology , endocrinology , psychology , neuroscience , gabaa receptor , androgen , receptor , prostate , hormone , cancer
Summary 5‐alpha‐reductase is involved as a rate‐imitating enzyme in the metabolism of steroids. Several 5‐alpha‐reduced steroids such as dihydrotestosterone, allopregnanolone or tetrahydrocorticosterone have neurotrophic, neuroprotective, and anxiolytic properties. Reduced 5‐alpha‐reductase activity has been observed during depressive illness in humans. Finasteride inhibits 5‐alpha‐reductase and can robustly induce anxious and depressive behaviors in rodents. In humans finasteride treatment has been linked to an increase of depressive symptoms. A recent study reported that finasteride treatment inhibits hippocampal neurogenesis in mice. As hippocampal neurogenesis has been linked to emotional behavior, this could be of possible relevance for the pathophysiology of affective disorders. Further studies are needed to evaluate potential neuropsychiatric side effects of finasteride treatment in humans.