Polymorphisms in genes related to the hypothalamic-pituitary-adrenal axis and antidepressant response – Systematic review

Fischer, Susanne; Gardini, Elena; Haas, Florence; Cleare, Anthony J.

doi:10.1016/j.neubiorev.2018.11.009

Cited by 13 publications

(7 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our series, the only factor that entered the model was USN, but the exclusion of patients with a relevant history of pre-depression probably ruled out some of the potential non-responder cases (65). A recent study found that in major depressive disorder and in persistent depressive disorder, specific single nucleotide polymorphisms and haplotypes in genes related to the corticotrophin-releasing hormone (CRHBP, CRHR1) and melanocortins (POMC) predicted the non-responder status (66). Therefore, it is also important to perform these studies in PSD patients.…”

Section: Discussionmentioning

confidence: 99%

Post-stroke Depression Increases Disability More Than 15% in Ischemic Stroke Survivors: A Case-Control Study

et al. 2019

View full text Add to dashboard Cite

We performed a retrospective, case-control study in consecutive ischemic stroke patients admitted to our stroke rehabilitation unit. Patients were matched for severity of neurological impairment (evaluated with the Canadian Neurological Scale, CNS), age (difference within 1 year), and onset admission interval (difference within 3 days). Participants were divided into two subgroups according to the presence or absence of PSD. Aim was to assess the specific influence of post-stroke depression (PSD) and antidepressant treatment on both basal functional status and rehabilitation outcomes. All PSD patients were treated primarily with serotoninergic antidepressants (AD). The final sample included 280 patients with depression (out of 320 found in a whole case series of 993 ischemic patients, i.e., 32.25%) and 280 without depression. Forty patients with depression were excluded because they had a history of severe psychiatric illness or aphasia, with a severe comprehension deficit. On one hand, PSD patients obtained lower Barthel Index (BI) and Rivermead Mobility Index (RMI) scores at both admission and discharge, with minor effectiveness of rehabilitative treatment and longer length of stay; on the other hand, this group had a lower percentage of dropouts. Lastly, PSD patients showed a different functional outcome, based on their response to antidepressant therapy, that was significantly better in responders than in non-responders (13.13%). Our results confirm the unfavorable influence of PSD on functional outcome, despite pharmacological treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Post-stroke Depression Increases Disability More Than 15% in Ischemic Stroke Survivors: A Case-Control Study

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Another mechanism is based on a dysfunction in the hypothalamic-pituitary-adrenal (HPA) axis. Research found that a disturbance might be secondary to gene polymorphism ( 49 ), exposure to maternal depression in childhood ( 50 ) or experience of early life stress ( 51 ) ( Figure 1 ). In general, studies share a view that depressive patients presented hypercortisolemia ( 52 – 54 ), unless they had an atypical depression ( 55 ).…”

Section: Mechanism Of Impaired Cognition In Depressionmentioning

confidence: 99%

Mechanisms of Cognitive Impairment in Depression. May Probiotics Help?

Dobielska

Bartosik²,

Zyzik³

et al. 2022

Front. Psychiatry

View full text Add to dashboard Cite

Depression is the major cause of disability globally. Apart from lowered mood and accompanying symptoms, it leads to cognitive impairment that altogether predicts disadvantaged social functioning. Reduced cognitive function in depression appears a bit neglected in the field of clinical and molecular psychiatry, while it is estimated to occur in two-thirds of depressed patients and persist in at least one third of remitted patients. This problem, therefore, requires elucidation at the biomolecular and system levels and calls for improvement in therapeutic approach. In this review study, we address the above-mentioned issues by discussing putative mechanisms of cognitive decline in depression: (1) increased oxidative stress and (2) inflammation, (3) disturbed hypothalamus-pituitary-adrenals axis, and (4) reduced monoamines functionality. Moreover, we acknowledge additional underpinnings of cognitive impairment in depressed elderly: (5) vascular-originated brain ischemia and (6) amyloid-beta plaque accumulation. Additionally, by reviewing molecular, pre-clinical and clinical evidence, we propose gut microbiota-targeted strategies as potential adjuvant therapeutics. The study provides a consolidated source of knowledge regarding mechanisms of cognitive impairment in depression and may path the way toward improved treatment options.

show abstract

“…Moreover, normalization of HPA axis activity in patients with depressive disorders has shown improved clinical outcomes (Min et al, 2012 ). In some animal models of depression, antidepressants, anxiolytics, and mood stabilizers have been shown to reduce the overall responsiveness of the HPA axis (Fernandez et al, 2013 ; Valvassori et al, 2017 ; Fischer et al, 2019 ). Hence, it is inferred that aberrant activation of the HPA axis may play a possible role in the pathophysiology of depression.…”

Section: Introductionmentioning

confidence: 99%

Daidzein Alleviates Hypothalamic-Pituitary-Adrenal Axis Hyperactivity, Ameliorates Depression-Like Behavior, and Partly Rectifies Circulating Cytokine Imbalance in Two Rodent Models of Depression

Chen

Wang

Zhang

et al. 2021

Front. Behav. Neurosci.

View full text Add to dashboard Cite

Depression is one very common mental health disorder which can cause morbidity and mortality if not addressed. Recent studies have provided strong evidence that depression may be accompanied by immune activation, secondary inflammatory reaction, and hyperactivity of the Hypothalamic Pituitary Adrenal (HPA) axis. It is well-known that it takes at least 2 weeks for conventional antidepressants, especially SSRIs (Selective serotonin reuptake inhibitors) to produce effects. To better understand the mechanism of antidepressant effects on depression and subsequently further elucidate the pathogenesis of depression, we selected phytestrogen daidzein (DD) to observe its effects on the depression-like and anxiety-like behavior in two different rodent models of depression which were induced by learned helplessness and chronic mild stress (CMS) and then simultaneous evaluation of the depression-like behavior, the activity of HPA axis, and circulatory cytokines. Our results showed that daidzein attenuated depression-like behaviors through alleviating HPA axis hyperactivity, decreasing the levels of stress-related hormones, and partly rectifying some inflammatory cytokines imbalance in both the rodent models of depression.

show abstract

Polymorphisms in genes related to the hypothalamic-pituitary-adrenal axis and antidepressant response – Systematic review

Cited by 13 publications

References 39 publications

Post-stroke Depression Increases Disability More Than 15% in Ischemic Stroke Survivors: A Case-Control Study

Post-stroke Depression Increases Disability More Than 15% in Ischemic Stroke Survivors: A Case-Control Study

Mechanisms of Cognitive Impairment in Depression. May Probiotics Help?

Daidzein Alleviates Hypothalamic-Pituitary-Adrenal Axis Hyperactivity, Ameliorates Depression-Like Behavior, and Partly Rectifies Circulating Cytokine Imbalance in Two Rodent Models of Depression

Contact Info

Product

Resources

About