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(1) To delineate whether cognitive flexibility and inhibitory ability are neurocognitive markers of passive suicidal ideation (PSI), an early stage of suicide risk in depression and (2) to determine whether PSI is associated with volumetric differences in regions of the prefrontal cortex (PFC) in middle-aged and older adults with depression.
University medical school.
Forty community-dwelling middle-aged and older adults with depression from a larger study of depression and anxiety (NIMH R01 MH091342-05 PI: O’Hara).
Psychiatric measures were assessed for the presence of a DSM-5 depressive disorder and PSI. A neurocognitive battery assessed cognitive flexibility, inhibitory ability, as well as other neurocognitive domains.
The PSI group (n = 18) performed significantly worse on cognitive flexibility and inhibitory ability, but not on other neurocognitive tasks, compared to the group without PSI (n = 22). The group with PSI had larger left mid-frontal gyri (MFG) than the no-PSI group. There was no association between cognitive flexibility/inhibitory ability and left MFG volume.
Findings implicate a neurocognitive signature of PSI: poorer cognitive flexibility and poor inhibitory ability not better accounted for by other domains of cognitive dysfunction and not associated with volumetric differences in the left MFG. This suggests that there are two specific but independent risk factors of PSI in middle- and older-aged adults.
Late life suicide is an international public health crisis, yet the mechanisms underlying late life suicide risk are far less understood compared to younger age groups. Executive dysfunction is widely documented in late life depression (LLD), and cognitive flexibility and inhibition are specifically hypothesized as vulnerabilities for suicide risk. There is some evidence that LLD patients with suicidal ideation or attempt suicide have worse executive dysfunction than LLD patients that do not; however, it is unknown whether these differences exist in Passive Suicidal Ideation (PSI), which may be an important early stage of suicide risk. Delineating the mechanisms of risk for PSI in LLD is a crucial direction for late life suicide research. The purpose of our study was to examine whether cognitive flexibility and inhibitory ability are neurocognitive markers of PSI. The secondary purpose of our study was to determine if neurocognitive differences due to PSI are mediated by volumetric differences in the prefrontal cortex.
Forty community-dwelling middle- and older-aged adults with LLD (18 with PSI, 22 without) completed a neurocognitive battery that assessed cognitive flexibility, inhibitory ability, as well as other neurocognitive domains, and underwent structural neuroimaging.
The PSI group performed significantly worse on cognitive flexibility and inhibitory ability, but not on other neurocognitive tasks which included other measures of executive function. The PSI group had a larger left mid-frontal gyrus (LMFG) than those without PSI, but there was no association between LMFG and cognitive flexibility or inhibitory ability, nor was there statistical evidence of mediation.
Our findings implicate a unique neurocognitive signature in LLD with PSI: poorer cognitive flexibility and poorer inhibitory ability not better accounted for by other domains of cognitive dysfunction and not mediated by volumetric differences in the prefrontal cortex. Volumetric brain differences in the LMFG appear unrelated to differences in cognitive flexibility and inhibitory ability, which suggests two specific but independent risk factors for PSI in middle- and older-aged adults.
Previous studies have identified a number of psychosocial risk factors of dysregulated cortisol (frequently referred to as the “stress hormone”) among older adults with depression. However, these studies have typically only examined a handful of risk factors at a time and have sometimes yielded inconsistent results.
This study aims to address this gap in the literature by simultaneously examining a range of relevant psychosocial predictors of diurnal cortisol among 54 older adults with a depressive disorder. Salivary cortisol was assessed upon awakening, at 5 PM, and at 9 PM across two consecutive days. Participants also completed measures of global psychosocial stress, current psychiatric symptomatology, pervasive distress (e.g. history of past depression), and protective factors (e.g. social support, resiliency, extent to which one has “made sense” of a significant stressor).
High levels of current depressive symptoms, psychiatric comorbidities, past depressive episodes, trait anxiety, and poorer ability to make sense of one's stress were found to be associated with flatter (more abnormal) cortisol slopes. However, when all of these variables were entered simultaneously in a multiple regression analysis, only history of past depression and the degree of sense made of stress emerged as unique predictors of cortisol in the model.
These findings have important implications for identifying depressed elderly individuals with dysregulated cortisol patterns who may be most at risk for health complications. Treatments that aim to limit the chronicity of depression and help to increase the sense made of stress could potentially have a positive impact on health.
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