The hypothalamus in anxiety disorders

Fischer, Susanne

doi:10.1016/b978-0-12-820107-7.00009-4

Cited by 13 publications

(6 citation statements)

References 84 publications

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“…In particular, our results highlight that a prominent differential role on anxiety-like behaviours is exerted by neuropeptides in hypothalamus, as also underlined by significant time percentage spent in open arms and neuropeptide levels associations, which is especially evident in females. The hypothalamus is reported to be a critical structure in the neurobiological modulation of fear conditioning and extinction, thus acting as a crucial determinant in anxiety-related disorders (Fischer, 2021). In addition to confirming previous data about the critical relevance of hypothalamic HPA axis hormones in anxiety-like behaviours, the present findings demonstrate that NKA and neurotensin may also provide a contribution which was not formerly recognised.…”

Section: Discussionsupporting

confidence: 89%

Neuropeptide Y, calcitonin gene-related peptide, and neurokinin A in brain regions of HAB rats correlate with anxiety-like behaviours

Carboni

Khoury

Beiderbeck

et al. 2022

European Neuropsychopharmacology

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Section: Discussionsupporting

confidence: 89%

Neuropeptide Y, calcitonin gene-related peptide, and neurokinin A in brain regions of HAB rats correlate with anxiety-like behaviours

Carboni

Khoury

Beiderbeck

et al. 2022

European Neuropsychopharmacology

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“…Studies have shown that patients with PD have changes in peripheral hypothalamic-pituitary-adrenal (HPA) axis markers, which may indicate abnormal functioning of the central corticotropin-releasing hormone system [35]. In a sample of mostly women hospitalized with panic disorder, abnormal expression of N-methyl-Daspartate receptors (NMDARs) is closely related to anxiety disorder with thyroid lesions, NMDAR subunits may have various activities and exert diverse effects in thyroid nodules, and the NR2A subunit may be an important regulator in anxiety disorder with thyroid nodules [36].…”

Section: Discussionmentioning

confidence: 99%

Assessment of the relationship between thyroid function and panic disorder: A mendelian randomization study

Yu,

Shen,

Zhu

2023

Preprint

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Background Multiple observational studies have indicated a correlation between thyroid function and the risk of panic disorder (PD). Nevertheless, the causality surrounding this association remains unclear. Our objective was to evaluate the causality between thyroid function and the risk of PD by employing Mendelian randomization (MR). Methods We employed publicly available genome-wide association studies (GWAS) to select single nucleotide polymorphisms (SNPs) that are associated with various aspects of thyroid function (hyperthyroidism, hypothyroidism, FT4, TSH, TPOAb, and thyroid nodules). The statistical data on panic disorder were obtained from the FinnGen consortium. To assess causality, we utilized the inverse variance weighted (IVW) method, MR-Egger method and weighted median (WM) method for the MR estimates. Sensitivity analyses were conducted using Cochran’s Q test, MR-Egger intercept, MR-Pleiotropy Residual Sum and Outlier method, leave-one-out analysis, and funnel plot. Results The genetically predicted presence of hyperthyroidism showed an inverse association with PD as evident from the IVW OR of 0.93 (95% CI: 0.87–0.98; P = 0.01).However, our findings did not indicate any causal effects of variation in FT4 (OR: 0.78, 95%CI: 0.78–1.27; P = 1)、TSH (OR: 1.03, 95%CI: 0.83–1.28; P = 0.77)、TPOAb (OR: 0.9, 95%CI: 0.47–1.72; P = 0.75)、hypothyroidism (OR: 0.57, 95%CI: 0.01–50.54; P = 0.81) and thyroid nodules (OR: 1.02, 95%CI: 0.91–1.14; P = 0.76) on PD risk. Conclusions In summary, Our findings indicated a significant inverse correlation between hyperthyroidism and PD risk, with no discernible causal impacts of alterations in FT4、TSH、TPOAb、hypothyroidism and thyroid nodules on PD risk. It may suggest that most thyroid function may not be the etiological factor of PD, further studies are needed to verify our results in the real world.

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“…This accumulation of 4EPS was associated with a significant increase in glucose uptake (i.e., activity) in the subregions of the hypothalamus, amygdala, the bed nucleus of stria terminalis and the paraventricular nucleus of the thalamus ( Needham et al, 2022 ). Notably, these brain regions have inter-related functions that include controlling anxiety behaviours and responses to stress stimuli ( Goode et al, 2019 ; Forster et al, 2012 ; Fischer, 2021 ; Barson, Mack, and Gao, 2020 ).…”

Section: How Does 4eps Affect the Brain?mentioning

confidence: 99%

4-Ethylphenol—fluxes, metabolism and excretion of a gut microbiome derived neuromodulator implicated in autism

Day,

O’Sullivan,

Pook

2023

Front. Mol. Biosci.

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Gut-microbiome-derived metabolites, such as 4-Ethylphenol [4EP], have been shown to modulate neurological health and function. Although the source of such metabolites is becoming better understood, knowledge gaps remain as to the mechanisms by which they enter host circulation, how they are transported in the body, how they are metabolised and excreted, and the way they exert their effects. High blood concentrations of host-modified 4EP, 4-ethylphenol sulfate [4EPS], are associated with an anxiety phenotype in autistic individuals. We have reviewed the existing literature and discuss mechanisms that are proposed to contribute influx from the gut microbiome, metabolism, and excretion of 4EP. We note that increased intestinal permeability is common in autistic individuals, potentially explaining increased flux of 4EP and/or 4EPS across the gut epithelium and the Blood Brain Barrier [BBB]. Similarly, kidney dysfunction, another complication observed in autistic individuals, impacts clearance of 4EP and its derivatives from circulation. Evidence indicates that accumulation of 4EPS in the brain of mice affects connectivity between subregions, particularly those linked to anxiety. However, we found no data on the presence or quantity of 4EP and/or 4EPS in human brains, irrespective of neurological status, likely due to challenges sampling this organ. We argue that the penetrative ability of 4EP is dependent on its form at the BBB and its physicochemical similarity to endogenous metabolites with dedicated active transport mechanisms across the BBB. We conclude that future research should focus on physical (e.g., ingestion of sorbents) or metabolic mechanisms (e.g., conversion to 4EP-glucuronide) that are capable of being used as interventions to reduce the flux of 4EP from the gut into the body, increase the efflux of 4EP and/or 4EPS from the brain, or increase excretion from the kidneys as a means of addressing the neurological impacts of 4EP.

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The hypothalamus in anxiety disorders

Cited by 13 publications

References 84 publications

Neuropeptide Y, calcitonin gene-related peptide, and neurokinin A in brain regions of HAB rats correlate with anxiety-like behaviours

Neuropeptide Y, calcitonin gene-related peptide, and neurokinin A in brain regions of HAB rats correlate with anxiety-like behaviours

Assessment of the relationship between thyroid function and panic disorder: A mendelian randomization study

4-Ethylphenol—fluxes, metabolism and excretion of a gut microbiome derived neuromodulator implicated in autism

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