Cognitive deficits in depression: Possible implications for functional neuropathology

Cognitive deficits in depression: Possible implications for functional neuropathology

2001 | MARIE-PAULE AUSTIN, PHILIP MITCHELL and GUY M. GOODWIN
Depression is associated with cognitive deficits, including memory and executive function impairments, which are not merely secondary to the disorder but may reflect underlying neurobiological changes. Recent studies show that these deficits are consistent across various depression subtypes and are not solely influenced by age, severity, or task difficulty. Executive impairments, particularly in set-shifting tasks, are common in depression and persist even after clinical recovery. These deficits suggest a disruption in the interaction between motivation, affect, and cognitive function, potentially involving the prefrontal cortex. Cognitive impairments in depression may also be linked to microvascular disease, especially in older patients, and may contribute to persistent cognitive deficits even after recovery. The relationship between depression and cognitive function is complex, with some deficits being more sensitive to motivational and affective factors. While some studies suggest that cognitive impairments in depression are secondary to motivational deficits, others indicate that they may reflect direct neurobiological changes. The findings highlight the importance of understanding the neurobiological basis of cognitive deficits in depression to better understand the disorder's pathogenesis and develop targeted treatments.Depression is associated with cognitive deficits, including memory and executive function impairments, which are not merely secondary to the disorder but may reflect underlying neurobiological changes. Recent studies show that these deficits are consistent across various depression subtypes and are not solely influenced by age, severity, or task difficulty. Executive impairments, particularly in set-shifting tasks, are common in depression and persist even after clinical recovery. These deficits suggest a disruption in the interaction between motivation, affect, and cognitive function, potentially involving the prefrontal cortex. Cognitive impairments in depression may also be linked to microvascular disease, especially in older patients, and may contribute to persistent cognitive deficits even after recovery. The relationship between depression and cognitive function is complex, with some deficits being more sensitive to motivational and affective factors. While some studies suggest that cognitive impairments in depression are secondary to motivational deficits, others indicate that they may reflect direct neurobiological changes. The findings highlight the importance of understanding the neurobiological basis of cognitive deficits in depression to better understand the disorder's pathogenesis and develop targeted treatments.
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