Aberrant apolipoprotein E expression and cognitive dysfunction in patients with poststroke depression
- PMID: 23171142
- PMCID: PMC3525887
- DOI: 10.1089/gtmb.2012.0253
Aberrant apolipoprotein E expression and cognitive dysfunction in patients with poststroke depression
Abstract
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.
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