Chronobiological hypothalamic–pituitary–thyroid axis status and antidepressant outcome in major depression

Duval, Fabrice; Mokrani, Marie‐Claude; Erb, Alexis; Lopera, Felix Gonzalez; Alexa, C.; Proudnikova, Xenia; Butucaru, Iuliana

doi:10.1016/j.psyneuen.2015.05.005

Cited by 30 publications

(27 citation statements)

References 38 publications

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“…Accumulating evidence indicates that angiotensin receptor signaling within the brain can promote susceptibility or resiliency to stress-related disease Pavlatou et al, 2008;Saavedra et al, 2011;Khoury et al, 2012;Saavedra, 2012;Hurt et al, 2015;Nylocks et al, 2015;Wang et al, 2016a,b). Angiotensin-II (Ang-II) is the effector peptide of the renin-angiotensin system (RAS), an endocrine system best known for its role in hydromineral balance and cardiovascular function.…”

Section: Introductionmentioning

confidence: 99%

A Unique “Angiotensin-Sensitive” Neuronal Population Coordinates Neuroendocrine, Cardiovascular, and Behavioral Responses to Stress

et al. 2017

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Stress elicits neuroendocrine, autonomic, and behavioral responses that mitigate homeostatic imbalance and ensure survival. However, chronic engagement of such responses promotes psychological, cardiovascular, and metabolic impairments. In recent years, the renin-angiotensin system has emerged as a key mediator of stress responding and its related pathologies, but the neuronal circuits that orchestrate these interactions are not known. These studies combine the use of the Cre-recombinase/loxP system in mice with optogenetics to structurally and functionally characterize angiotensin type-1a receptor-containing neurons of the paraventricular nucleus of the hypothalamus, the goal being to determine the extent of their involvement in the regulation of stress responses. Initial studies use neuroanatomical techniques to reveal that angiotensin type-1a receptors are localized predominantly to the parvocellular neurosecretory neurons of the paraventricular nucleus of the hypothalamus. These neurons are almost exclusively glutamatergic and send dense projections to the exterior portion of the median eminence. Furthermore, these neurons largely express corticotrophin-releasing hormone or thyrotropin-releasing hormone and do not express arginine vasopressin or oxytocin. Functionally, optogenetic stimulation of these neurons promotes the activation of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes, as well as a rise in systolic blood pressure. When these neurons are optogenetically inhibited, the activity of these neuroendocrine axes are suppressed and anxiety-like behavior in the elevated plus maze is dampened. Collectively, these studies implicate this neuronal population in the integration and coordination of the physiological responses to stress and may therefore serve as a potential target for therapeutic intervention for stress-related pathology. Chronic stress leads to an array of physiological responses that ultimately rouse psychological, cardiovascular, and metabolic impairments. As a consequence, there is an urgent need for the development of novel therapeutic approaches to prevent or dampen deleterious aspects of "stress." While the renin-angiotensin system has received some attention in this regard, the neural mechanisms by which this endocrine system may impact stress-related pathologies and consequently serve as targets for therapeutic intervention are not clear. The present studies provide substantial insight in this regard. That is, they reveal that a distinct population of angiotensin-sensitive neurons is integral to the coordination of stress responses. The implication is that this neuronal phenotype may serve as a target for stress-related disease.

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Section: Introductionmentioning

confidence: 99%

A Unique “Angiotensin-Sensitive” Neuronal Population Coordinates Neuroendocrine, Cardiovascular, and Behavioral Responses to Stress

et al. 2017

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“…110 Furthermore, thyroid responses can normalize with successful treatment for depression. 111 Within the above, it is important also to consider signaling pathways across systems, such as glycogen synthase kinase-3, mitogen-activated protein kinase and cyclic adenosine 3′,5′-monophosphate, involved in synaptic plasticity 112 and modified by antidepressants. 113 Further potential biomarker candidates that span biologic systems particularly are measured using neuroimaging or genetics.…”

Section: Neuroendocrine Findings In Depressionmentioning

confidence: 99%

Biomarkers for Depression: Recent Insights, Current Challenges and Future Prospects

Strawbridge¹,

Young

Cleare³

2018

FOC

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A plethora of research has implicated hundreds of putative biomarkers for depression, but has not yet fully elucidated their roles in depressive illness or established what is abnormal in which patients and how biologic information can be used to enhance diagnosis, treatment and prognosis. This lack of progress is partially due to the nature and heterogeneity of depression, in conjunction with methodological heterogeneity within the research literature and the large array of biomarkers with potential, the expression of which often varies according to many factors. We review the available literature, which indicates that markers involved in inflammatory, neurotrophic and metabolic processes, as well as neurotransmitter and neuroendocrine system components, represent highly promising candidates. These may be measured through genetic and epigenetic, transcriptomic and proteomic, metabolomic and neuroimaging assessments. The use of novel approaches and systematic research programs is now required to determine whether, and which, biomarkers can be used to predict response to treatment, stratify patients to specific treatments and develop targets for new interventions. We conclude that there is much promise for reducing the burden of depression through further developing and expanding these research avenues.

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“…hastaların tek terapötik ajan olarak TH ile tedavisini bildiren çalışmalar da vardır (15). Ulusal Klinik Biyokimya Akademisi Elkitabı'na göre hipotiroidizm için önerilen tedavi şekli; 1.6 iu/kg/gün levotiroksin (LT4) ile monoterapi ve bunun sonucu olarak TSH'nin ortalama değerinin 0.5-2.0 iU/ml olarak elde edilmesidir (16).…”

Section: Sayfa 1022unclassified

Can Sleeping Disorder Continue Despite Hypothyroidism Levothyroxine Therapy Be a Marker for Depression?

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et al. 2018

Adıyaman Üniversitesi Sağlık Bilimleri Dergisi

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Amaç: Bu araştırmanın amacı, primer hipotiroidizmi olan hastalarda depresif semptomların sıklığını araştırmak, bu semptomların levotiroksin (LT4) tedavisi sonrası iyileşme düzeyini belirlemek ve öngörücü semptomların varlığını değerlendirmektir.Yöntemler: 140 primer hipotiroidizmi olan kadın hasta Beck Depresyon Envanteri (BDÖ) ile değerlendirildi. Hepsi sadece LT4 ile tedavi edildi. Tiroid stimüle edici hormon (TSH) değeri tedaviden sonra test edildi ve daha önce depresif belirtiler gösteren hastalar BDÖ ile tekrar değerlendirildi.Bulgular: Çalışmamızda 72 (%51.4) hastada (BDÖ=22.8±1.1, TSH=19.1±3.7 iU/ml, yaş (yıl)=44.0±2.0) depresif belirti olduğu ve 68 hastada (%48.6) ise olmadığı gösterildi. (BDÖ=8.7±0.6, TSH=12.0±1.2 iU/ml, yaş (yıl)=45.0± 2.2). Primer hipotiroidizmin tedavisinden sonra, çalışmanın ilk bölümünde depresif belirtiler gösteren 72 hastada (TSH sonrası 1.54 iU/ml ±0.31) BDÖ tekrar uygulandı ve 54 hastanın (%75) depresif belirtilerinin ortadan kalktığı görüldü (BDÖ=9.0±1.0, TSH=1.59±0.31 iU/ml, yaş (yıl)=45.0±2.0). Hastaların 18'inde (%25) depresif semptomların devam ettiği görüldü (BDÖ=23.0±2.0, TSH=1.28±0.31 iU/ml, yaş (yıl)=42.0±2.0). Uyku bozukluğu, madde 16, tedaviden sonra belirgin kalıcılığı olan tek faktördür (p > 0.045).Sonuçlar: Hipotiroidizmli hastaların %51.4'ü depresif belirtiler gösterdi. Hipotiroidizm tedavisi tüm olgularda TSH değerlerini normal seviyesine getirmek ve %75'inde depresif belirtileri tersine çevirmek için yeterliydi. Kalan %25'lik grupta uyku bozukluğunun devam etmesi, öngörücü, yanıtsız bir semptom olarak düşünülebilir ve tanıyı tekrar değerlendirmek ve başka bir tedavinin eklenmesini göz önünde bulundurmak gerektiğine işaret eder. Anahtar kelimeler: Major depresif bozukluk, hipotiroidizm, levotiroksin, uyku bozuklukları Doi:Abstract Aim: The aim of this study was to investigate the frequency of depressive symptoms in patients with primary hypothyroidism, to determine the degree of recovery of these symptoms after levothyroxine (LT4) treatment, and to assess the presence of predictive symptoms.Methods: 140 women with primary hypothyroidism were evaluated with the Beck Depression Inventory (BDI). All were treated with LT4 alone. Thyroid stimulating hormone (TSH) value was tested after treatment and patients with previous depressive symptoms were reevaluated with BDI.Results: In our study, it was shown that 72 (51.4%) patients had depressive symptoms and 68 patients (48.6%) did not have depressive symptoms (BDI=22.8±1.1, TSH=19.1±3.7 iU/ml, (BDI=8.7±0.6, TSH=12.0±1.2 iU/ml, age (year)=45.0±2.2). After the treatment of primary hypothyroidism, BDI was reapplied in 72 patients with depressive symptoms (1.54 iU/ml±0.31 after TSH) in the first part of the study and depressive symptoms of 54 patients (75%) were found to be absent (BDI=9.0±1.0, TSH=1.59±0.31 iU/ml, age (years)=45.0±2.0). Depressive symptoms persisted in 18 (25%) of the patients (BDI=23.0±2.0, TSH=1.28±0.31 iU/ml, age (year)=42.0±2.0). Sleep disturbance, item 16, is the only persistent persistence after treat...

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Chronobiological hypothalamic–pituitary–thyroid axis status and antidepressant outcome in major depression

Cited by 30 publications

References 38 publications

A Unique “Angiotensin-Sensitive” Neuronal Population Coordinates Neuroendocrine, Cardiovascular, and Behavioral Responses to Stress

A Unique “Angiotensin-Sensitive” Neuronal Population Coordinates Neuroendocrine, Cardiovascular, and Behavioral Responses to Stress

Biomarkers for Depression: Recent Insights, Current Challenges and Future Prospects

Can Sleeping Disorder Continue Despite Hypothyroidism Levothyroxine Therapy Be a Marker for Depression?

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