Nicholas Q Vu1, Howard J Aizenstein. 1. aUniversity of Pittsburgh School of Medicine bDepartment of Psychiatry cDepartment of Bioengineering, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Abstract
PURPOSE OF REVIEW: Late-life depression (LLD) presents in older adults as a heterogeneous mood disorder. Because of the diverse outcomes and symptomatology of LLD, several theories, especially the vascular depression hypothesis, have been proposed to identify its cause. This review outlines the features of LLD and explores the recent advances in characterizing this disorder through studies of brain functioning and cognition, with an emphasis on how vascular changes may mediate this disorder. RECENT FINDINGS: LLD is associated with brain changes, including atrophy of hippocampus, independent of other neurodegenerative states. White matter lesions (WMLs) are frequently found in patients with LLD. Functional imaging has revealed both distinct characteristics of LLD and overlap of some cognitive symptoms with other dementias. Executive dysfunction and impaired processing speeds are at the core of the cognitive deficits in LLD and are associated with the development of WMLs in specific fiber tracts in the brain. SUMMARY: LLD is associated with brain changes in both gray matter and white matter, including cerebrovascular changes, atrophy, and loss of myelin integrity. These brain changes are associated with age of onset of depression, as well as cumulative life-time depression burden, and can explain the increased dementia risk associated with LLD.
PURPOSE OF REVIEW: Late-life depression (LLD) presents in older adults as a heterogeneous mood disorder. Because of the diverse outcomes and symptomatology of LLD, several theories, especially the vascular depression hypothesis, have been proposed to identify its cause. This review outlines the features of LLD and explores the recent advances in characterizing this disorder through studies of brain functioning and cognition, with an emphasis on how vascular changes may mediate this disorder. RECENT FINDINGS: LLD is associated with brain changes, including atrophy of hippocampus, independent of other neurodegenerative states. White matter lesions (WMLs) are frequently found in patients with LLD. Functional imaging has revealed both distinct characteristics of LLD and overlap of some cognitive symptoms with other dementias. Executive dysfunction and impaired processing speeds are at the core of the cognitive deficits in LLD and are associated with the development of WMLs in specific fiber tracts in the brain. SUMMARY: LLD is associated with brain changes in both gray matter and white matter, including cerebrovascular changes, atrophy, and loss of myelin integrity. These brain changes are associated with age of onset of depression, as well as cumulative life-time depression burden, and can explain the increased dementia risk associated with LLD.
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