This BDNF SNP may serve to moderate the links between psychosocial factors and depressive symptoms, but such links are nuanced, being gender-dependent and varying with the nature of the social interactions experienced.
The aim of this study was to investigate the effects of zinc, vitamin D, and their co-supplementation versus placebo on changes in the Beck Depression Inventory II (BDI-II) score, serum cortisol level, and brain-derived neurotrophic factor (BDNF) in obese/overweight patients with depressive symptoms.
Changes of BDNF levels inversely correlated with change in depressive symptoms assessed using the Calgary Depression Rating Scale in Schizophrenia (Pearson's r = - 0.195; p = 0.018).
BDNF mRNA was measured in plasma using standardised procedures.<b>Results:</b> Patients with ≥90 min of physical activity per week had fewer depressive symptoms (<i>P</i> ˂0.001, Cohen's <i>d</i> = 0.48) and performed significantly better on working memory (<i>P</i> ˂ 0.001, <i>d</i> = 0.44) and executive functioning tasks (<i>P</i> ˂ 0.001, <i>d</i> = 0.50) compared to the ˂90-min group.
In conclusion, greater circulating copper concentrations and higher copper/zinc ratios were associated with lower depressive symptoms (but not cognition), with copper also positively associated with BDNF concentration, in a sample of community-dwelling older adults.
Furthermore, at D2 just patients treated with ayahuasca (<i>N</i> = 14), and not with placebo (<i>N</i> = 14), presented a significant negative correlation between serum BDNF levels and depressive symptoms.
Further, the finding of significantly greater (p = ≤ 0.0001) depression scores among the insomnia group suggested that BDNF is an important factor in the development of depressive symptoms.
And the regression analysis showed that negative symptoms and general psychopathology in PANSS, attention and delayed memory in RBANS, BDNF and SIRT1 were independent risk factors for depressive symptoms in schizophrenia.
These results reveal an endogenous mechanism to explain how physical exercise leads to the induction of BDNF, and identify lactate as a potential endogenous molecule that may have therapeutic value for CNS diseases in which BDNF signaling is disrupted.<b>SIGNIFICANCE STATEMENT</b> It is established that exercise promotes learning and memory formation and alleviates the symptoms of depression.
Self-Reported Mild Traumatic Brain Injuries in Relation to Rumination and Depressive Symptoms: Moderating Role of Sex Differences and a Brain-Derived Neurotrophic Factor Gene Polymorphism.
The absence of an association between changes in sBDNF levels and depressive symptoms challenges the proposed concept of sBDNF/pBDNF as key markers of the effects of ECT.
Overall, 12 weeks of synbiotic supplementation resulted in greater improvement in depression symptoms and serum BDNF level compared to the probiotic supplementation in HD patients especially in the subgroup of patients with depression symptoms.
The objective was to investigate if high cadence cycling altered non-motor cognition and depression symptoms in individuals with Parkinson's disease (PD) and whether exercise responses were influenced by brain-derived neurotrophic factor (BDNF) Val66Met polymorphism.
The relationship between IR and BDNF levels (F = 6.199, P = 0.00) was controlled for the effects of depressive symptoms ( <i>β</i> = 2.73, P = 0.00) and psychiatric treatments, including selective serotonin reuptake inhibitors (SSRIs) (<i>β</i> = 0.17, P = 0.08), serotonin and norepinephrine reuptake inhibitors (SNRIs) ( <i>β</i> = -0.23, P = 0.02), tricyclic antidepressants (TCAs) ( <i>β</i> = -0.17, P = 0.10), lithium ( <i>β</i> = 0.29, P = 0.00), anticonvulsants ( <i>β</i> = 0.22, P = 0.03), antipsychotics ( <i>β</i> = -0.05, P = 0.61), and electroconvulsive therapy ( <i>β</i> = 0.00, P = 0.98).
A BDNFVal66Met × Harsh Parenting interaction predicted the rise in depressive symptoms across a 3-year period, whereas a 5-HTTLPR × Harsh Parenting interaction predicted greater frequency in elevated depressive symptoms.
Activation of the mechanistic target of rapamycin (mTOR), as well as increased levels of BDNF, may increase long-term potentiation and result in an improvement in the symptoms of depression.
The heterogeneity of participant recruitment criteria and the lack of control of variables that influence circulating BDNF levels regardless of dementia (depressive symptoms, medications, lifestyle, lack of overlap between serum and plasma, and experimental aspects) are likely to bias result and prevent study comparability.