PMID- 24994553 OWN - NLM STAT- MEDLINE DCOM- 20151016 LR - 20211021 IS - 1432-2072 (Electronic) IS - 0033-3158 (Linking) VI - 232 IP - 1 DP - 2015 Jan TI - Altered BDNF is correlated to cognition impairment in schizophrenia patients with tardive dyskinesia. PG - 223-32 LID - 10.1007/s00213-014-3660-9 [doi] AB - BACKGROUND: Long-term antipsychotic treatment for schizophrenia is often associated with the emergence of tardive dyskinesia (TD), which is linked to greater cognitive impairment. Brain-derived neurotrophic factor (BDNF) plays a critical role in cognitive function, and schizophrenia patients with TD have lower BDNF levels than those without TD. OBJECTIVE: This study examines the BDNF levels, the cognitive function, and the association of BDNF with cognitive function in schizophrenia patients with or without TD. METHODS: We recruited 83 male chronic patients with (n=35) and without TD (n=48) meeting DSM-IV criteria for schizophrenia and 52 male control subjects. We examined the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and BDNF levels for all subjects. Positive and Negative Symptom Scale (PANSS) and the Abnormal Involuntary Movement Scale (AIMS) were assessed in patients. RESULTS: BDNF levels were lower in patients with than those without TD (p<0.05). RBANS total score (p<0.01) and subscales of immediate memory, visuospatial/constructional performance, and attention were lower in patients with than those without TD (all p<0.05). BDNF levels were positively associated with immediate memory in patients without TD, but negatively in TD patients (both p<0.05). Multiple regression analysis confirmed that in either TD or non-TD group, BDNF was an independent contributor to immediate memory (both p<0.05). CONCLUSIONS: BDNF may be involved in the pathophysiology of TD. While the associations between BDNF and cognition in both TD and non-TD patients suggest a close relationship between BDNF and cognition, the different directions may implicate distinct mechanisms between TD and non-TD patients. FAU - Wu, Jing Qin AU - Wu JQ AD - School of Biomedical Sciences and Pharmacy, Faculty of Health, The University of Newcastle, University Drive, Callaghan, NSW, 2308, Australia. FAU - Chen, Da Chun AU - Chen DC FAU - Tan, Yun Long AU - Tan YL FAU - Tan, Shu Ping AU - Tan SP FAU - Hui, Li AU - Hui L FAU - Lv, Men Han AU - Lv MH FAU - Soares, Jair C AU - Soares JC FAU - Zhang, Xiang Yang AU - Zhang XY LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20140704 PL - Germany TA - Psychopharmacology (Berl) JT - Psychopharmacology JID - 7608025 RN - 0 (Antipsychotic Agents) RN - 0 (Biomarkers) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 7171WSG8A2 (BDNF protein, human) SB - IM MH - Adult MH - Aged MH - Antipsychotic Agents/adverse effects/therapeutic use MH - Biomarkers/blood MH - Brain-Derived Neurotrophic Factor/*blood MH - Cognition Disorders/*blood/epidemiology MH - Humans MH - Male MH - Middle Aged MH - Movement Disorders/*blood/epidemiology MH - Neuropsychological Tests MH - Schizophrenia/*blood/drug therapy/epidemiology EDAT- 2014/07/06 06:00 MHDA- 2015/10/17 06:00 CRDT- 2014/07/05 06:00 PHST- 2014/04/05 00:00 [received] PHST- 2014/06/03 00:00 [accepted] PHST- 2014/07/05 06:00 [entrez] PHST- 2014/07/06 06:00 [pubmed] PHST- 2015/10/17 06:00 [medline] AID - 10.1007/s00213-014-3660-9 [doi] PST - ppublish SO - Psychopharmacology (Berl). 2015 Jan;232(1):223-32. doi: 10.1007/s00213-014-3660-9. Epub 2014 Jul 4.