2018/09/07 by Karen M. Ryan, Ian Patterson, Declan M. McLoughlin · 31 citations
Biochemistry, Genetics and Molecular Biology · Chemistry · Medicine · Neuroscience · Psychology · #Activator (genetics) #Adipose Tissue and Metabolism #Alpha (finance) #Biochemistry #Chemistry #Clinical psychology #Cognition #Electroconvulsive therapy #Endocrinology #Internal medicine #Medicine #Neuroscience #Neurotransmitter Receptor Influence on Behavior #Nuclear receptor #Peroxisome Proliferator-Activated Receptors #Peroxisome proliferator-activated receptor #Peroxisome proliferator-activated receptor alpha #Psychology #Psychometrics #Receptor #Transcription factor
paper · doi:10.1017/s0033291718002556
published in Psychological Medicine 49(11), 1859-1868 (Cambridge University Press)
openalex publication_date 2018/09/07 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/06
BACKGROUND: The transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC-1α), termed the 'master regulator of mitochondrial biogenesis', has been implicated in stress and resilience to stress-induced depressive-like behaviours in animal models. However, there has been no study conducted to date to examine PGC-1α levels in patients with depression or in response to antidepressant treatment. Our aim was to assess PGC-1α mRNA levels in blood from healthy controls and patients with depression pre-/post-electroconvulsive therapy (ECT), and to examine the relationship between blood PGC-1α mRNA levels and clinical symptoms and outcomes with ECT. METHODS: Whole blood PGC-1α mRNA levels were analysed in samples from 67 patients with a major depressive episode and 70 healthy controls, and in patient samples following a course of ECT using quantitative real-time polymerase chain reaction (qRT-PCR). Exploratory subgroup correlational analyses were carried out to determine the relationship between PGC-1α and mood scores. RESULTS: PGC-1α levels were lower in patients with depression compared with healthy controls (p = 0.03). This lower level was predominantly accounted for by patients with psychotic unipolar depression (p = 0.004). ECT did not alter PGC-1α levels in the depressed group as a whole, though exploratory analyses revealed a significant increase in PGC-1α in patients with psychotic unipolar depression post-ECT (p = 0.045). We found no relationship between PGC-1α mRNA levels and depression severity or the clinical response to ECT. CONCLUSIONS: PGC-1α may represent a novel therapeutic target for the treatment of depression, and be a common link between various pathophysiological processes implicated in depression.