2012/11/21 by Zhaohui Zhang, Junlin Mu, Jing Li +2 · 1 citation
Medicine · Psychology · #Dementia and Cognitive Impairment Research #Cardiac Health and Mental Health #Stroke Rehabilitation and Recovery #Apolipoprotein E #Internal medicine #Stroke (engine) #Cerebral infarction #Depression (economics) #Medicine #Cognition #Rating scale #Endocrinology #Psychology #Gastroenterology #Cardiology #Disease #Psychiatry #Developmental psychology #Ischemia
paper · doi:10.1089/gtmb.2012.0253
openalex publication_date 2012/11/21 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/28
BACKGROUND: Apolipoprotein E (ApoE) is associated with some diseases with cognitive function defect. AIMS: The purpose of this study was to examine the influence of ApoE on poststroke depression (PSD) risk and to define objective markers for diagnosis. METHODS: The cognitive function, serum ApoE, and peripheral mononuclear blood cell ApoE mRNA expression of patients with PSD were compared to age-matched control patients with stroke and healthy volunteers. Sixty-seven patients with stroke were selected according to the cerebral infarction diagnosis standard of the Fourth National Cerebrovascular Disease Conference and divided into a PSD group (28 patients, 43-76 years old) or a control stroke group (39 patients, 43-78 years old) using the Hamilton Rating Scale for Depression, and compared to 40 healthy volunteers (42-78 years old). Cognitive function was evaluated by analysis of event-related potentials (ERPs), while expression of ApoE mRNA was determined by quantitative reverse transcription-polymerase chain reaction and serum ApoE by ELISA. RESULTS: The latencies of ERP components N2 and P3 were prolonged, and the P3 amplitude was lower in the PSD group compared to the control stroke group and healthy controls (p<0.01). There were no significant group differences in N1 and P2 latencies (all p>0.05). The latency of N2 was positively correlated to the P3 latency in the PSD group (p<0.05). No associations were detected between P3 amplitude, expression of ApoE mRNA, and serum ApoE in the PSD group (all p>0.05). The ERP results indicated that patients with PSD were significantly slower at identifying a target stimulus, suggesting deficits in perception and/or cognitive processing. Peripheral expression of ApoE mRNA was lower in the PSD group than the control stroke group (p<0.701) while serum ApoE was higher than in the control stroke group (p<0.05), possibly reflecting a feedback reduction in expression. CONCLUSION: We suggest that aberrant serum ApoE together with abnormalities in some ERP components may be useful markers for assessment of PSD risk and clinical diagnosis.