Anxiety, depression and comorbidity: a comparison of cognitive function in young adults

Quinn, Zane (2017) Anxiety, depression and comorbidity: a comparison of cognitive function in young adults. PhD thesis, James Cook University.

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The holy grail of depression cognition research is to identify cognitive deficits that are not only associated with depression but which may precede depression and play a role in depression onset. Currently, research to identify cognitive deficits for young to middle-aged adults with depression has been mixed, although some studies have shown significant differences between depression and healthy control groups in the executive function (EF) domains of inhibition, updating, set-shifting, planning and verbal learning and memory. The significant relationships between EF and depression are reflected in biological evidence, with biological abnormalities in EF-associated brain areas, such as the dorsal lateral prefrontal cortex (dlPFC) and the orbital frontal cortex (OFC), being found in depression patients. This thesis presents a series of investigations aimed at advancing understanding of the complex relationships among depression, anxiety and cognitive deficits.

Study participants were primarily recruited from first- and second-year psychology classes at James Cook University, Townsville, Australia. The participants were aged between 17 and 35 years and had experienced depressive and or anxiety symptoms. The participants performed a battery of cognitive tests that included social cognition, inhibition, updating, set-shifting, planning and verbal learning and memory. They underwent a series of structured interviews to determine disorder classification and severity. Other information, such as medical history, school subject history and an intelligence measure, was collected. A small group of participants completed a secondary study investigating correlations between cognition and plasma gamma-aminobutyric acid (GABA). These participants also gave a blood sample.

Study 1 compared the cognitive functioning of the depression (including comorbid depression), anxiety disorder only and healthy control groups. No significant cognitive differences were found among the three groups. It was noted that approximately one-third of the healthy control group had a high susceptibility to future depressive episodes owing to familial depression diagnosis or subclinical symptoms.

Study 2 investigated depression comorbid with anxiety, focusing on the way anxiety interacted with depression. Participants classified as primary depression, in which depression onset was not due to an anxiety disorder or medical condition, were compared to participants termed secondary depression, whose depression was most probably caused by an anxiety disorder. The healthy control group from Study 1 was included in this comparison. The results showed that those with secondary depression committed significantly fewer errors in the set-shifting task than the primary and healthy control groups; however, there were no significant differences between the primary and healthy control groups. In the rationale for comparing primary and secondary depression, it was suggested that as depression onset for secondary depression is due to a non-depressive disorder, there was a higher probability of biological abnormalities playing a role in primary depression than in secondary depression, which may have been reflected in the results.

Study 3 compared measures of cognition between young adults who had experienced only one or two episodes of depression and then no more episodes (i.e., non-recurrent depression) to those who had experienced three or more episodes (recurrent depression). The recurrent group was found to commit significantly more errors in prosody tasks when the statement was read in a sarcastic tone compared to the non-recurrent group.

In depression cognition studies, it is important to have a measure of intelligence to ensure that outliers do not confound the experiment. Intelligence measures based on literacy are more common in depression experiments than numeracy measures. Study 4 investigated the impact of mathematical ability on cognition, comparing students who had achieved at least a grade of 'B' in either advanced mathematics or physics at high school to those who had studied ordinary mathematics. The results showed that the advanced mathematics group committed fewer errors in the set-shifting task and remembered more words in the initial trial of the verbal learning and memory task than the ordinary mathematics group.

Study 5 investigated the relationship between plasma GABA concentration and EF. Plasma GABA concentration, which has been proposed as a biomarker for depression, has been shown to be lower in depression patients, especially those with primary depression. The results showed that for the subgroup primary depression, there was a significant correlation between plasma GABA concentration and the EF tasks of updating and verbal learning and memory, both of which have significant working memory components. This result was replicated with the ordinary mathematics subgroup (from Study 4). Post hoc analysis has suggested that deficits in EF in the primary depression subgroup and ordinary mathematics subgroup have a biological basis, because of their significant relationship with plasma GABA concentration.

In conclusion, while no significant differences were found between the disorder groups, depression and anxiety, and the healthy control groups, significant differences were found in the subgroups of depression. Young adults with primary depression made significantly more errors in set-shifting than those with secondary depression, while young adults with recurrent depression made significantly more errors in prosody than those with non-recurrent depression. Young adults in the ordinary mathematics group made significantly more errors in set-shifting than those in the advanced mathematics group. In the GABA cognition study, for the subgroups primary depression and ordinary mathematics, plasma GABA concentration significantly correlated with updating and verbal learning and memory.

From these results, two depression pathways were proposed. The Prosodic Pathway proposed that deficits in prosody mediate the pathway from anxiety to depression, while the EF Pathway proposed a link between biological abnormalities in the PFC to depression onset. Both pathways were recommended as models for future research.

Item ID: 51514
Item Type: Thesis (PhD)
Keywords: depression cognition, young adults, anxiety, comorbidity, comorbid depression, intelligence measures
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Appendix C (publication) is not available through this repository.

Date Deposited: 13 Nov 2017 04:06
FoR Codes: 17 PSYCHOLOGY AND COGNITIVE SCIENCES > 1701 Psychology > 170106 Health, Clinical and Counselling Psychology @ 50%
17 PSYCHOLOGY AND COGNITIVE SCIENCES > 1702 Cognitive Science > 170299 Cognitive Science not elsewhere classified @ 50%
SEO Codes: 92 HEALTH > 9204 Public Health (excl. Specific Population Health) > 920410 Mental Health @ 100%
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