Original contributionMonitoring glutamate levels in the posterior cingulate cortex of thyroid dysfunction patients with TE-averaged PRESS at 3 T
Introduction
Patients with hyperthyroidism or hypothyroidism may have neuropsychiatric disorders such as a lack of concentration, poor memory, depression, anxiety, and mania. These symptoms indicate that the thyroid hormones may be related to mood. However, the underlying process of this dysfunction is not well understood, but has been studied extensively in recent years [1], [2]. In vivo magnetic resonance spectroscopy (1H MRS) is a particularly powerful technique capable of assessing biochemical contents and pathways in normal and pathological tissue. This enables embedded insights into the thyroid–brain relationship.
Glutamate (Glu) is an abundant excitatory neurotransmitter in the mammalian nervous system [3]. The dynamic glutamate–glutamine (Glu-Gln) cycle plays a key role in the regulation of neurotransmission, while the regulation of pre-/post-synaptic ionic and metabotropic glutamate receptors has been implicated in the pathophysiology of mood disorders [4].
Thus, the accurate and noninvasive measurements of brain Glu concentrations may be a valuable tool for the diagnosis and monitoring of these pathologic conditions. Here, we used TE-averaged PRESS that fully separates the signal of the Glu C4 protons (2.35 ppm) from the overlap with Glutamine (Gln) and N-acetylaspartate (NAA). The detection of Glu is very important to test whether neurophysiological symptoms of thyroid abnormalities are associated with Glu dysregulation rather than with the combination of glutamate and glutamine (Glx) or Gln levels.
Previous researchers have studied abnormalities in the patients' brain with hyper- or hypo-thyroidism. They have all focused on regional perfusion and blood flow in the posterior cingulate cortex (PCC) [5], [6], [7]. No one has yet looked at metabolite levels using MRS on patients with these two thyroid conditions.
The aim of this study is to investigate that whether the levels of Glu, Cho, and NAA change in the PCC of the patients with thyroid diseases and whether these metabolic abnormalities are related to the level of thyroid hormones.
Section snippets
Participants
We initially recruited 42 patients, but 6 of them were excluded due to neurological disease (n = 1) and refusals (n = 5). Finally, 36 newly diagnosed and untreated patients were recruited with thyroid dysfunction including 18 (5 men and 13 women) hyperthyroid patients and 18 (5 men and 13 women) hypothyroid patients. The diagnosis of these diseases was based on the clinical features including hyper-/hypo-metabolism, goiter and/or ophthalmopathy, and examinations including abnormality of serum
Characteristics of the patients and controls
Table 1 lists the age, gender; and serum thyroid hormone levels of patients and controls. The serum thyroid hormone levels are significantly different between the groups (P < 0.05).
The MRS spectrum obtained from the posterior cingulate cortex in patients and control
The MRS spectrum of patients and controls is shown in the Fig. 2. Glutamate was measured as a single peak at 2.35 ppm.
The metabolite concentrations of the three groups and the correlation between serum thyroid hormone levels and metabolite concentrations.
The metabolite concentrations of the three groups and correlation analysis of serum thyroid hormone levels and metabolites are listed in Table 2.
The metabolites levels in patients groups (hypothyroid and
Discussion
Glutamate is a classical neurotransmitter, and glutamatergic projections participate in virtually all circuits in the adult central nervous system. The major finding in this study was that Glu significantly changed (hyperthyroidism decreased and hypothyroidism increased) and correlated with T3 (triodthyronine) relative to controls within the PCC. Cellular and circuit-level effects of glutamate dysregulation may be the abnormalities in glutamate transport that lead to maldistribution of
Conclusions
Signal intensity of glutamate shows significant differences in the posterior cingulate cortex in patients with thyroid dysfunction. This change indicated a potential role of glutamate in the brain dysfunction in thyroid hormone disorders.
Acknowledgments
We thank Dr. Changyi Song from the Department of Nuclear Medicine and Wang Junhong from the Endocrine Department for patient referral. We thank LetPub (www.letpub.com) for its linguistic assistance during the preparation of this manuscript.
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