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Genome-wide Analysis Suggests the Importance of Vascular Processes and Neuroinflammation in Late-life Antidepressant Response by Marshe, Victoria S. (author);Maciukiewicz, Malgorzata (author);Hauschild, Anne-Christin (author);Islam, Farhana (author);Qin, Li (author);Tiwari, Arun K. (author);Sibille, Etienne (author);Blumberger, Daniel M. (author);Karp, Jordan F. (author);Flint, Alastair J. (author);Turecki, Gustavo (author);Lam, Raymond W. (author);Milev, Roumen V. (author);Frey, Benicio N. (author);Rotzinger, Susan (author);Foster, Jane A. (author);Kennedy, Sidney H. (author);Kennedy, James L. (author);Mulsant, Benoit H. (author);Reynolds, Charles F. (author);Lenze, Eric J. (author);Müller, Daniel J. (author) is a Neuroscience article available to read on EtoBox.
What is Genome-wide Analysis Suggests the Importance of Vascular Processes and Neuroinflammation in Late-life Antidepressant Response about?
## Abstract Antidepressant outcomes in older adults with depression is poor, possibly because of comorbidities such as cerebrovascular disease. Therefore, we leveraged multiple genome-wide approaches to understand the genetic architecture of antidepressant response. Our sample included 307 older adults (≥60 years) with current major depression, treated with venlafaxine extended-release for 12 weeks. A standard genome-wide association study (GWAS) was conducted for post-treatment remission status, followed by in silico biological characterization of associated genes, as well as polygenic risk scoring for depression, neurodegenerative and cerebrovascular disease. The top-associated variants for remission status and percentage symptom improvement were PIEZO1 rs12597726 (OR = 0.33 [0.21, 0.51], p = 1.42 × 10^−6^) and intergenic rs6916777 (Beta = 14.03 [8.47, 19.59], p = 1.25 × 10^−6^), respectively. Pathway analysis revealed significant contributions from genes involved in the ubiquitin-proteasome system, which regulates intracellular protein degradation with has implications for inflammation, as well as atherosclerotic cardiovascular disease (n = 25 of 190 genes, p = 8.03 × 10^−6^, FD
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- Author
- Marshe, Victoria S. (author);Maciukiewicz, Malgorzata (author);Hauschild, Anne-Christin (author);Islam, Farhana (author);Qin, Li (author);Tiwari, Arun K. (author);Sibille, Etienne (author);Blumberger, Daniel M. (author);Karp, Jordan F. (author);Flint, Alastair J. (author);Turecki, Gustavo (author);Lam, Raymond W. (author);Milev, Roumen V. (author);Frey, Benicio N. (author);Rotzinger, Susan (author);Foster, Jane A. (author);Kennedy, Sidney H. (author);Kennedy, James L. (author);Mulsant, Benoit H. (author);Reynolds, Charles F. (author);Lenze, Eric J. (author);Müller, Daniel J. (author)
- Publisher
- Springer Science and Business Media LLC
- Published
- 2021
- Language
- EN
- Field
- Neuroscience (Life Sciences)