Social vulnerability and prefrontal cortical function in elderly people: a report from the Canadian Study of Health and Aging

2010 ◽  
Vol 23 (3) ◽  
pp. 450-458 ◽  
Author(s):  
Melissa K. Andrew ◽  
John D. Fisk ◽  
Kenneth Rockwood

ABSTRACTBackground:Prefrontal cortical lobe function is related to social behavior in humans. We investigated whether performance on tests of prefrontal cortical function was associated with social vulnerability. Associations with non-frontal cognitive function were investigated for comparison.Methods:1216 participants aged 70+ of the Canadian Study of Health and Aging-2 screening examination, who also underwent detailed neuropsychological testing, comprised the study sample. Performance on WAIS-R abstraction, WAIS-R comprehension, Trails B, FAS and category verbal fluency, Block construction, Token Test and Wechsler Memory Scale Information Subset was tested in relation to the participant's level of social vulnerability using regression models adjusted for age, education, sex, frailty, MMSE score, diagnosis of depression, and use of psychoactive medications. Social vulnerability was measured by an index comprising many social problems or “deficits”.Results:The most socially vulnerable group had worse performance on FAS verbal fluency, generating 4.1 fewer words (95% CI: 1.8–6.4, p<0.001) than those in the least socially vulnerable group; those with intermediate social vulnerability generated 2.6 fewer words (95% CI: 0.4–4.8, p = 0.02). Social vulnerability was also associated, though less strongly, with category verbal fluency. The most socially vulnerable people had impaired performance on the Trails B, taking 37 seconds longer (95% CI: 11–63, p = 0.005). These results were independent of age, education, sex, frailty, MMSE score, depression, and psychoactive medications. Social vulnerability was not associated with performance on WAIS-R abstraction, WAIS-R comprehension, Block Design, Token Test or Wechsler Memory Scale testsConclusions:High social vulnerability was associated with impaired performance on verbal fluency and set shifting but not with common sense judgment, abstraction, long-term memory, constructional ability, or language comprehension. The association between social functioning and the cognitive functions subserved by prefrontal cortex warrants further study.

2013 ◽  
Vol 25 (6) ◽  
pp. 334-341 ◽  
Author(s):  
Tina Gooren ◽  
Peter Schlattmann ◽  
Peter Neu

ObjectiveEven though cognitive deficits are well recognised in schizophrenia and depression, direct comparisons between the disorders are scarce in literature. This study aims to assess specificity and degree of cognitive deficits in inpatients with acute schizophrenia and unipolar major depression.MethodsA neuropsychological test battery was administered to 76 schizophrenic patients, 102 patients with unipolar major depression and 85 healthy controls (HCs), assessing verbal learning [Rey Auditory Verbal Learning Test (RAVLT)], processing speed (Trail Making Test), verbal fluency and visual memory (Wechsler Memory Scale-Revised test).ResultsBoth patient groups were significantly impaired compared with HCs with regard to all test outcomes. The schizophrenia group (SG) performed significantly worse in the Wechsler Memory Scale and verbal fluency than the depression group (DG). The DG reached significantly lower scores than the SG in the RAVLT delayed recall subtest. No significant group difference between SG and DG was found for the Trail Making Test and the RAVLT direct recall trails.ConclusionOur results indicate that cognitive impairment is present in both disorders. Schizophrenic patients performed worse than patients with unipolar depression in only two of the administered tests. Differences in cognitive performance between the groups are not as general as often assumed. Therefore, during the acute phase of illness, a diagnostic classification on the grounds of the patients’ neurocognitive performance has to be done with caution.


2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
D.P. Prata ◽  
A. Mechelli ◽  
C. Fu ◽  
M. Picchioni ◽  
F. Kane ◽  
...  

Aims:To examine the effect of a polymorphism in the Dopamine Transporter (DAT) gene on brain activation during executive function and, for the first time:1.determine the extent to which this is altered in schizophrenia and2.use a verbal fluency paradigm.This is relevant since:1.DAT plays a key role in the regulation of dopamine, which modulates cortical activation during cognitive tasks and2.a disruption of dopamine function is a fundamental pathophysiological feature of schizophrenia.Method:Functional magnetic resonance imaging was used to measure whole-brain responses during overt verbal fluency in 85 subjects: 44 healthy volunteers and 41 DSM-IV schizophrenia patients. Main effects of genotype and diagnostic group on activation and their interaction were estimated using an ANOVA in SPM5.Results:The 10-repeat allele of the 3'UTR VNTR was associated with greater activation than the 9-repeat allele in the left (Z=4.8; FWEp=0.005) and right (Z=4.2; FWEp=0.057) anterior insula and with decreased activation in the rostral anterior cingulate (Z=4.3 FWEp=0.04) during word generation (versus baseline). These effects were irrespective of diagnostic group but generally more marked in patients. There were also strong trends for groupxgenotype interactions in the left middle frontal gyrus and the left nucleus accumbens. Analysis was controlled for task performance, IQ, antipsychotic medication, psychopathology and demographics.Conclusion:Cortical function during executive tasks is normally modulated by variation in the DAT gene, effect which is dependent on the brain region. DAT's effect may be altered in schizophrenia patients, which may reflect altered central dopamine function.


2019 ◽  
Vol 144 ◽  
pp. 193-207 ◽  
Author(s):  
Kleanthi Chalkiadaki ◽  
Aggeliki Velli ◽  
Evangelos Kyriazidis ◽  
Vasiliki Stavroulaki ◽  
Vasilis Vouvoutsis ◽  
...  

2019 ◽  
Vol 30 (1) ◽  
pp. 59-71
Author(s):  
Bailey A Kermath ◽  
Amanda M Vanderplow ◽  
Michael E Cahill

Abstract While research has identified alterations in dorsolateral prefrontal cortical function as a key factor to the etiology of bipolar disorder, few studies have uncovered robust changes in protein signal transduction pathways in this disorder. Given the direct relevance of protein-based expressional alterations to cellular functions and because many of the key regulatory mechanisms for the disease pathogenesis likely include alterations in protein activity rather than changes in expression alone, the identification of alterations in discrete signal transduction pathways in bipolar disorder would have broad implications for understanding the disease pathophysiology. As prior microarray data point to a previously unrecognized involvement of the RhoA network in bipolar disorder, here we investigate the protein expression and activity of key components of a RhoA signal transduction pathway in dorsolateral prefrontal cortical homogenates from subjects with bipolar disorder. The results of this investigation implicate overactivation of prefrontal cortical RhoA signaling in specific subtypes of bipolar disorder. The specificity of these findings is demonstrated by a lack of comparable changes in schizophrenia; however, our findings do identify convergence between both disorders at the level of activity-mediated actin cytoskeletal regulation. These findings have implications for understanding the altered cortical synaptic connectivity of bipolar disorder.


2006 ◽  
Vol 30 (5) ◽  
pp. 680-695 ◽  
Author(s):  
Alice Egerton ◽  
Claire Allison ◽  
Ros R. Brett ◽  
Judith A. Pratt

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