{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T06:05:15Z","timestamp":1784009115591,"version":"3.55.0"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>\n                    Anorexia nervosa (AN) carries the highest mortality of any psychiatric disorder, yet no pharmacological agent has received regulatory approval for its treatment in adults. Multimodal neuroimaging has now revealed a coherent neurobiological architecture: functional MRI documents blunted ventral striatal and amygdalar responses to food, alongside excessive prefrontal\u2013cingulate engagement; PET corroborates trait-level reductions in 5-HT2A binding, elevations in 5-HT1A binding across cingulate, frontal, parietal, temporal, and dorsal raphe regions, and compensatory upregulation of D2\/D3 receptors in the anteroventral striatum; SPECT identifies persistent temporal and cingulate hypoperfusion; and EEG reveals attenuated P300 amplitudes, delayed N2 latencies, and parieto-occipital theta hyperarousal. We propose that cariprazine\u2014a dopamine D3-preferring D3\/D2 receptor partial agonist with 5-HT1A partial agonism and 5-HT2A\/2B antagonism\u2014confers a uniquely matched pharmacological toolkit for this disorder. Cariprazine\u2019s D3 partial agonism is predicted to restore mesolimbic dopamine signaling, thereby reinstating incentive salience to food cues; its 5-HT1A stabilizer property attenuates the trait-amplified corticolimbic inhibitory tone underlying harm avoidance and anxiety; its prefrontal glutamate-modulating action attenuates excessive cognitive control over eating, and chronic administration confers substrate-dependent set-point recalibration of the upregulated mesolimbic D3 receptor pool. Furthermore, cariprazine\u2019s favorable metabolic profile (number needed to harm for clinically significant weight gain of 34\n                    <jats:italic>versus<\/jats:italic>\n                    6 for olanzapine) renders its safety burden meaningfully lower than that of currently used agents. In summary, the receptor pharmacology of cariprazine maps with notable specificity onto the neuroimaging-defined substrate of AN, providing a mechanistically grounded rationale for prospective clinical investigation of cariprazine as a candidate pharmacotherapy for this otherwise intractable disorder.\n                  <\/jats:p>","DOI":"10.3389\/fphar.2026.1877615","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T05:40:03Z","timestamp":1784007603000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Cariprazine as a candidate for drug repurposing in anorexia nervosa: a mechanistic hypothesis grounded in neuroimaging evidence"],"prefix":"10.3389","volume":"17","author":[{"given":"Attila","family":"Kovacs","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Krisztina","family":"Csapo","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabor","family":"Andrassy","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Csaba","family":"Papp","sequence":"additional","affiliation":[{"name":"Institute for Primary Care and Health Promotion of Debrecen, Clinical Center, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rudolf","family":"Gesztelyi","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judit","family":"Zsuga","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, Faculty of Medicine, University of Debrecen","place":["Debrecen, Hungary"]},{"name":"Centre for Translational Neuropsychiatry, Clinical Center, University of Debrecen","place":["Debrecen, Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,14]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"661973","DOI":"10.3389\/fnbeh.2021.661973","article-title":"Where dopaminergic and cholinergic systems interact: a gateway for tuning neurodegenerative disorders","volume":"15","author":"Amalric","year":"2021","journal-title":"Front. 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