Thyroid Hormone Signaling and Adult Neurogenesis in Mammals

Remaud, Sylvie; Gothié, Jean-David; Morvan-Dubois, Ghislaine; Demeneix, Barbara

doi:10.3389/fendo.2014.00062

Cited by 102 publications

(89 citation statements)

References 98 publications

(122 reference statements)

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“…As a complement, fT3 levels rose steadily during recovery. The existing literature suggests that thyroid hormones can cross the bloodbrain barrier, promote myelinogenesis, and participate in the secretion of neurotrophic factors, linking thyroid physiology and neurocognitive dysfunction in humans [28]. Thus, it is plausible to take into account whether thyroid hormones play important roles in the pathogenesis of anti-NMDAR encephalitis and that the rise in fT3 levels is conducive to improvement of the condition.…”

Section: Discussionmentioning

confidence: 99%

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Ma¹,

Yin²,

Zeng³

et al. 2018

Neuroimmunomodulation

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Objective: Previous studies have shown that functional abnormalities of the thyroid are associated with the pathogenesis of several neurological diseases. However, their relationship in patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis remains to be defined. Methods: Forty-three patients with anti-NMDAR encephalitis were examined for thyroid function and autoimmune indications, in comparison with 225 healthy controls (CTL). Patients were further classified into 2 subgroups based on their free tri-iodothyronine (fT3) levels. Moreover, fT3 levels were also investigated after at least three months of follow-up. The clinical characteristics of the patients and CTL were described in detail. Results: Serum levels of fT3 and thyroid-stimulating hormone (TSH) were found to be relatively lower in patients with anti-NMDAR encephalitis than in CTL (both p < 0.001). Low T3 syndrome also occurred more frequently in anti- NMDAR encephalitis (25.6 vs. 0.4%, p < 0.001). However, no statistical differences were detected between patients and CTL in terms of the positive rate of thyroid antibodies and other types of thyroid dysfunction. Patients with low T3 levels tended to have a longer hospital stay (p = 0.006), a higher rate of abnormal brain magnetic resonance imaging (MRI) findings (p = 0.033), a higher frequency of consciousness declination (p = 0.029), and a higher modified Rankin scale (mRS) score during hospitalization. Low fT3 levels were also associated with abnormal MRI findings, a decline in consciousness, and the mRS score on admission. In addition, fT3 seemed to gradually return to normal levels upon improvement of the mRS score (r = –0.649, p = 0.002). Conclusions: Low T3 syndrome often copresents in anti-NMDAR encephalitis and indicates a longer hospitalization, abnormal MRI findings, consciousness declination, and a higher clinical severity. However, fT3 levels do not seem to influence the prognosis of anti-NMDAR encephalitis.

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Section: Discussionmentioning

confidence: 99%

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Ma¹,

Yin²,

Zeng³

et al. 2018

Neuroimmunomodulation

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“…Agents used to augment first-line antidepressants, including antipsychotics [50] and thyroid hormone [51], were subsequently shown to increase AHN. Newer antidepressants, such as subanesthetic doses of ketamine, also boost AHN [52].…”

Section: Evidence That Treatments Of Depression and Anxiety Alter Ahnmentioning

confidence: 99%

The current state of the neurogenic theory of depression and anxiety

Miller

Hen

2015

Current Opinion in Neurobiology

335

235

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Newborn neurons are continuously added to the adult hippocampus. Early studies found that adult neurogenesis is impaired in models of depression and anxiety and accelerated by antidepressant treatment. This led to the theory that depression results from impaired adult neurogenesis and restoration of adult neurogenesis leads to recovery. Follow up studies yielded a complex body of often inconsistent results, and the veracity of this theory is uncertain. We propose five criteria for acceptance of this theory, we review the recent evidence for each criterion, and we draw the following conclusions: Diverse animal models of depression and anxiety have impaired neurogenesis. Neurogenesis is consistently boosted by antidepressants in animal models only when animals are stressed. Ablation of neurogenesis in animal models impairs cognitive functions relevant to depression, but only a minority of studies find that ablation causes depression or anxiety. Recent human neuroimaging and postmortem studies are consistent with the neurogenic theory, but they are indirect. Finally, a novel drug developed based on the neurogenic theory is promising in animal models.

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“…Thyroid hormones (THs) are critical for vertebrate growth, development, metabolic balance, and particularly brain organization and functions throughout life (Mullur et al, 2014;Remaud et al, 2014;Yen, 2001). TH (notably T3) actions are predominantly mediated by TH signaling, which involves TH-response gene transcriptional regulation by TH receptors (TRs, TRα and TRβ) (Zhang and Lazar, 2000).…”

Section: Introductionmentioning

confidence: 99%

A screening assay for thyroid hormone signaling disruption based on thyroid hormone-response gene expression analysis in the frog Pelophylax nigromaculatus

Zhang

Qin

et al. 2015

Journal of Environmental Sciences

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Amphibian metamorphosis provides a wonderful model to study the thyroid hormone (TH) signaling disrupting activity of environmental chemicals, with Xenopus laevis as the most commonly used species. This study aimed to establish a rapid and sensitive screening assay based on TH-response gene expression analysis using Pelophylax nigromaculatus, a native frog species distributed widely in East Asia, especially in China. To achieve this, five candidate TH-response genes that were sensitive to T3 induction were chosen as molecular markers, and T3 induction was determined as 0.2 nmol/L T3 exposure for 48 hr. The developed assay can detect the agonistic activity of T3 with a lowest observed effective concentration of 0.001 nmol/L and EC50 at around 0.118-1.229 nmol/L, exhibiting comparable or higher sensitivity than previously reported assays. We further validated the efficiency of the developed assay by detecting the TH signaling disrupting activity of tetrabromobisphenol A (TBBPA), a known TH signaling disruptor. In accordance with previous reports, we found a weak TH agonistic activity for TBBPA in the absence of T3, whereas a TH antagonistic activity was found for TBBPA at higher concentrations in the presence of T3, showing that the P. nigromaculatus assay is effective for detecting TH signaling disrupting activity. Importantly, we observed non-monotonic dose-dependent disrupting activity of TBBPA in the presence of T3, which is difficult to detect with in vitro reporter gene assays. Overall, the developed P. nigromaculatus assay can be used to screen TH signaling disrupting activity of environmental chemicals with high sensitivity.

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Thyroid Hormone Signaling and Adult Neurogenesis in Mammals

Cited by 102 publications

References 98 publications

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Thyroid Function and Autoimmune Indications in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

The current state of the neurogenic theory of depression and anxiety

A screening assay for thyroid hormone signaling disruption based on thyroid hormone-response gene expression analysis in the frog Pelophylax nigromaculatus

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