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Sodium Benzoate, a D-Amino Acid Oxidase Inhibitor, Increased Volumes of Thalamus, Amygdala, and Brainstem in a Drug-Naïve Patient With Major Depression
Chien-Han Lai, M.D., M.Sc.
The Journal of Neuropsychiatry and Clinical Neurosciences 2013;25:E50-E51. doi:10.1176/appi.neuropsych.12030056
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Sources of financial and material support: National Science Council, Taiwan (NSC-97-2314-B-039-006-MY3 and NSC-100-2627-B-039-001), National Health Research Institutes, Taiwan (NHRI-EX-100-9904NI), and Taiwan Department of Health Clinical Trial and Research Center of Excellence (DOH100-TD-B-111-004).

Department of Psychiatry, Buddhist Tzu-Chi General Hospital, Taipei Branch, Taipei, Taiwan Brain Image Research Unit, Buddhist Tzu-Chi General Hospital, Taipei Branch, Taipei, Taiwan

Correspondence: Dr. Lai; e-mail: t122336257@yahoo.com.tw.

Copyright © 2013 American Psychiatric Association

To the Editor: The inhibitor of D-amino acid oxidase (DAAO) can increase D-amino acid (DAA) through the inhibition of DAAO, which might relieve the symptoms of depression and anxiety. The effects of inhibitor of DAAO on subcortical volumes (SCV) are still unknown. Here, we wanted to report that a drug-naïve case with major depressive disorder (MDD) had significant increases of SCV after a 6-week therapy of sodium benzoate (SB), a kind of inhibitor of DAAO.

“Mr. D” is a 20-year-old, first-episode, drug-naïve nonpsychotic MDD patient with symptoms for 1 month (Hamilton Rating Scale for Depression [Ham-D] score: 25). He refused to take any psychotropic medication because of possible side effects. He just accepted non-pharmacological treatment, such as nutritional and food therapy. After negotiation, he agreed to take SB (500 mg/day) and also signed the informed consent after being notified about the characteristics and side effects of SB. His MDD symptoms improved within the initial 2 weeks of treatment (Ham-D score: 12) and he achieved partial remission after a 6-week therapy with SB (Ham-D score: 9), with residual symptoms of sleep disturbance, anergia, and anhedonia. No intolerable side effects were mentioned during SB therapy. He received structural magnetic resonance imaging (MRI) scanning (3T Siemens Version Scanner housed at magnetic resonance Center, National Yang Ming University) at baseline and the 6th week for the evaluation of brain volume changes after SB treatment. The pulse sequence of MRI scanning was three-dimensional fast-spoiled gradient-echo recovery (3D-FSPGR) T1W1 (TR: 25.30 msec; TE: 3.03 msec; slice thickness: 1 mm(no gap);192 slices; matrix: 224 × 256; field of view: 256 mm; number of excitations: 1). Structural MRI was preprocessed with FMRIB's Integrated Registration and Segmentation Tool function (FIRST Version 1.2) of FSL (FMRIB Software Library, Version 4.1.1) to perform subcortical brain segmentation using a shape and appearance model. The subcortical structures include hippocampus, amygdala, nucleus accumbens, thalamus, pallidum, lentiform nucleus, caudate, and putamen. The volumes of bilateral thalami, brainstem, and right amygdala increased after a 6-week therapy with SB (Table 1).

 
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TABLE 1.Subcortical Volume Increase After a 6-Week Therapy With Sodium Benzoate

Subcortical structures are important regions for an etiological model of MDD. Sheline proposed that cortico-striato-limbic-pallidal-thalamic circuit of patients with MDD might suffer from the damage related to glucorticoid neurotoxicity and reduced neurogenesis due to stress.1 DAAs, such as D-serine or D-cycloserine, would induce limited activations of glutamate receptors through glycine receptor partial agonist and might treat symptoms of depression or anxiety.2 Scholpp et al. reported that neurogenesis of thalamus would be modulated by different gene expressions in the glutamatergic system, which might lead to the establishment of discrete neuronal domains in the thalamus.3 Hamani et al. found that neurogenesis occurred after stimulation of thalamus in rats treated with corticosterone, which is a model for MDD.4 In the meta-analysis of volumes of amygdala in MDD, unmedicated patients seem to have lower volumes of amygdala, and medicated patients seems to have increased volumes of amygdala. It suggests that antidepressant might increase neurogenesis by increasing release of brain-derived neurotrophic factor and protecting against glucocorticoid toxicity in the amygdala.5 Volumetric increases of brainstem in this patient might be related to glutamate-related neurotrophic effects,6 which would be associated with potential antidepressant effects of SB. We have reported a similar phenomenon with brainstem growth in the patients with MDD and panic disorder, which might be related to neurotrophic effects of antidepressant.7 Chronic stress will induce depression and excess of excitatory glutamatergic neurotoxicity toward amygdala. In this case, we found increased volumes of right amygdala after treatment with SB, which can prevent excitotoxicity-induced death and enhance neural plasticity through inhibition of astroglia DAO.8 SB also can inhibit DAAO and increase DAA, which will activate the inhibitory glycinergic receptor to control glutamatergic excitotoxicity and enhance synaptic plasticity.9 Also, glutamate can stimulate the division of human progenitor cells and induce neurogenesis of glial cells due to the increase of neurotrophic factor.6

I thank Professor Hsien-Yuan Lane of the Department of Psychiatry, China Medical University Hospital, Taichung, Taiwan, and Professor Guochuan Emil Tsai of the Department of Psychiatry, Harbor-UCLA Medical Center, and the Los Angeles Biomedical Research Institute, Torrance, CA, USA, for their help.

We also acknowledge MR support from National Yang-Ming University, Taiwan, which is in part supported by the MOE plan for the top university. We also thank Miss Ruao-Ching Wang for MRI acquisition help and technical assistance.

Sheline  YI:  3D MRI studies of neuroanatomic changes in unipolar major depression: the role of stress and medical comorbidity.  Biol Psychiatry 2000; 48:791–800
[CrossRef] | [PubMed]
 
Pencea  V;  Bingaman  KD;  Wiegand  SJ  et al:  Infusion of brain-derived neurotrophic factor into the lateral ventricle of the adult rat leads to new neurons in the parenchyma of the striatum, septum, thalamus, and hypothalamus.  J Neurosci 2001; 21:6706–6717
[PubMed]
 
Scholpp  S;  Delogu  A;  Gilthorpe  J  et al:  Her6 regulates the neurogenetic gradient and neuronal identity in the thalamus.  Proc Natl Acad Sci U S A 2009; 106:19895–19900
[PubMed]
 
Hamani  C;  Stone  SS;  Garten  A  et al:  Memory rescue and enhanced neurogenesis following electrical stimulation of the anterior thalamus in rats treated with corticosterone.  Exp Neurol 2011; 232:100–104
[CrossRef] | [PubMed]
 
Hamilton  JP;  Siemer  M;  Gotlib  IH:  Amygdala volume in major depressive disorder: a meta-analysis of magnetic resonance imaging studies.  Mol Psychiatry 2008; 13:993–1000
[CrossRef] | [PubMed]
 
Suzuki  M;  Nelson  AD;  Eickstaedt  JB  et al:  Glutamate enhances proliferation and neurogenesis in human neural progenitor cell cultures derived from the fetal cortex.  Eur J Neurosci 2006; 24:645–653
[CrossRef] | [PubMed]
 
Lai  CH;  Wu  YT:  Duloxetine’s modest short-term influences in subcortical structures of first episode drug-naïve patients with major depressive disorder and panic disorder.  Psychiatry Res 2011; 194:157–162
[CrossRef] | [PubMed]
 
Park  HK;  Shishido  Y;  Ichise-Shishido  S  et al:  Potential role for astroglial D-amino acid oxidase in extracellular D-serine metabolism and cytotoxicity.  J Biochem 2006; 139:295–304
[CrossRef] | [PubMed]
 
Billard  JM;  Rouaud  E:  Deficit of NMDA receptor activation in CA1 hippocampal area of aged rats is rescued by D-cycloserine.  Eur J Neurosci 2007; 25:2260–2268
[CrossRef] | [PubMed]
 
References Container
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TABLE 1.Subcortical Volume Increase After a 6-Week Therapy With Sodium Benzoate
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References

Sheline  YI:  3D MRI studies of neuroanatomic changes in unipolar major depression: the role of stress and medical comorbidity.  Biol Psychiatry 2000; 48:791–800
[CrossRef] | [PubMed]
 
Pencea  V;  Bingaman  KD;  Wiegand  SJ  et al:  Infusion of brain-derived neurotrophic factor into the lateral ventricle of the adult rat leads to new neurons in the parenchyma of the striatum, septum, thalamus, and hypothalamus.  J Neurosci 2001; 21:6706–6717
[PubMed]
 
Scholpp  S;  Delogu  A;  Gilthorpe  J  et al:  Her6 regulates the neurogenetic gradient and neuronal identity in the thalamus.  Proc Natl Acad Sci U S A 2009; 106:19895–19900
[PubMed]
 
Hamani  C;  Stone  SS;  Garten  A  et al:  Memory rescue and enhanced neurogenesis following electrical stimulation of the anterior thalamus in rats treated with corticosterone.  Exp Neurol 2011; 232:100–104
[CrossRef] | [PubMed]
 
Hamilton  JP;  Siemer  M;  Gotlib  IH:  Amygdala volume in major depressive disorder: a meta-analysis of magnetic resonance imaging studies.  Mol Psychiatry 2008; 13:993–1000
[CrossRef] | [PubMed]
 
Suzuki  M;  Nelson  AD;  Eickstaedt  JB  et al:  Glutamate enhances proliferation and neurogenesis in human neural progenitor cell cultures derived from the fetal cortex.  Eur J Neurosci 2006; 24:645–653
[CrossRef] | [PubMed]
 
Lai  CH;  Wu  YT:  Duloxetine’s modest short-term influences in subcortical structures of first episode drug-naïve patients with major depressive disorder and panic disorder.  Psychiatry Res 2011; 194:157–162
[CrossRef] | [PubMed]
 
Park  HK;  Shishido  Y;  Ichise-Shishido  S  et al:  Potential role for astroglial D-amino acid oxidase in extracellular D-serine metabolism and cytotoxicity.  J Biochem 2006; 139:295–304
[CrossRef] | [PubMed]
 
Billard  JM;  Rouaud  E:  Deficit of NMDA receptor activation in CA1 hippocampal area of aged rats is rescued by D-cycloserine.  Eur J Neurosci 2007; 25:2260–2268
[CrossRef] | [PubMed]
 
References Container
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