Translational Psychiatry· 2019Q1
Mechanisms and treatment of late-life depression
- 569citations
- Q1SCImago
- 2019year
Short summary
Late-life depression accelerates biological aging and increases medical illness risk, with reciprocal relationships suggesting shared targets for prevention and treatment.
AI-generated from the title and abstract; the full text is not read.
Key points
- Late-life depression is associated with biological aging markers like shorter telomeres and advanced epigenetic aging.
- Medical illnesses increase the risk of late-life depression, and depression, in turn, predisposes to medical illnesses.
- Targeting mid-life vascular disease risk factors may prevent vascular depression.
- Depression increases the risk of dementia, though antidepressants are less effective for depression in demented patients.
AI-generated from the title and abstract; the full text is not read.
Abstract
Abstract Depression predisposes to medical illnesses and advances biological aging indicated by shorter telomere length, accelerated brain aging and advanced epigenetic aging. Medical illnesses also increase the risk of late-life depression. The reciprocal relationships of depression with aging-related and disease-related processes have generated pathogenetic hypotheses and provided treatment targets. Targeting risk factors of vascular disease in mid-life is a logical approach in prevention of vascular depression. The depression-executive dysfunction and the vascular depression syndromes have clinical presentations and neuroimaging findings consistent with frontostriatal abnormalities. Dopamine D 2/3 agonists are effective in depression of Parkinson’s disease and their efficacy needs to be assessed in these two syndromes. Computerized cognitive remediation targeting functions of the cognitive control network may improve both executive functions and depressive symptoms of late-life major depression. Significant progress has been made in neurostimulation treatments in depressed younger adults. TMS targeting deep structures responsible for mood regulation is well tolerated by older adults and its efficacy in syndromes of late-life depression needs to be studied. Efficacious psychotherapies for late-life depression exist, but are underutilized in part because of their complexity. Streamlined, stepped psychotherapies targeting behaviors assumed to result from dysfunction of brain networks implicated in late-life depression can be easy to learn and have potential for dissemination. However, their effectiveness needs further investigation. Depression increases the risk of dementing disorders. Antidepressants are rather ineffective in treating depression of demented patients, but long-term use of antidepressants may reduce the risk of dementia. However, confirmation studies are needed.
The authors' abstract, as published at the source. Translational Psychiatry, 2019 · DOI ↗
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Field: Biological Psychiatry
Biological PsychiatryNeuroscience