Frontiers in Cellular Neuroscience · 2 authors, 3 centres
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This narrative review synthesizes evidence for and against the adenosine hypofunction hypothesis of schizophrenia, integrating data from neurochemistry, animal models, and human clinical studies. It concludes that current support for the hypothesis is limited, with existing adenosine-based therapies showing only modest efficacy for positive symptoms.
This narrative review evaluates the adenosine hypofunction hypothesis of schizophrenia, which posits that reduced adenosine signaling contributes to the disorder's pathology. The authors synthesize preclinical data from rodent models (e.g., knockout studies showing behavioral deficits), human neuroimaging (PET studies failing to confirm consistent receptor alterations), and clinical trials of adenosine-augmenting drugs (allopurinol, dipyridamole, propentofylline). Central findings indicate that while some small trials reported benefits for positive symptoms, a larger trial failed to replicate results, and overall evidence for therapeutic efficacy is limited and inconsistent.
