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Fulltext Development and validation of the 22-item Tarumi's Modern-Type Depression Trait Scale: Avoidance of Social Roles, Complaint, and Low Self-Esteem (TACS-22)

Kato TA, Katsuki R, Kubo H, Shimokawa N, Sato-Kasai M, Hayakawa K, et al.

Psychiatry Clin Neurosci, 2019 Aug;73(8):448-457.
PMID: 30900331 DOI: 10.1111/pcn.12842

AIM: Understanding premorbid personality is important, especially when considering treatment selection. Historically, the premorbid personality of patients with major depression in Japan was described as Shuchaku-kishitsu [similar to Typus melancholicus], as proposed by Shimoda in the 1930s. Since around 2000, there have been increased reports in Japan of young adults with depression who have had premorbid personality differing from the traditional type. In 2005, Tarumi termed this novel condition 'dysthymic-type depression,' and more recently the condition has been called Shin-gata/Gendai-gata Utsu-byo [modern-type depression (MTD)]. We recently developed a semi-structured diagnostic interview to evaluate MTD. Development of a tool that enables understanding of premorbid personality in a short time, especially at the early stage of treatment, is desirable. The object of this study was to develop a self-report scale to evaluate the traits of MTD, and to assess the scale's psychometric properties, diagnostic accuracy, and biological validity.
METHODS: A sample of 340 participants from clinical and community settings completed measures. Psychometric properties were assessed with factor analysis. Diagnostic accuracy of the MTD traits was compared against a semi-structured interview.
RESULTS: The questionnaire contained 22 items across three subscales, thus we termed it the 22-item Tarumi's Modern-Type Depression Trait Scale: Avoidance of Social Roles, Complaint, and Low Self-Esteem (TACS-22). Internal consistency, test-retest reliability, and convergent validity were all satisfactory. Among patients with major depression, the area under the curve was 0.757 (sensitivity of 63.1% and specificity of 82.9%) and the score was positively correlated with plasma tryptophan.
CONCLUSION: The TACS-22 possessed adequate psychometric properties and diagnostic accuracy in an initial sample of Japanese adults. Additional research on its ability to support clinical assessment of MTD is warranted.

Matched MeSH terms: Tryptophan/blood
Fulltext Effect of quantity and quality of pre-exercise carbohydrate meals on central fatigue

Khong TK, Selvanayagam VS, Hamzah SH, Yusof A

J Appl Physiol (1985), 2018 10 01;125(4):1021-1029.
PMID: 29975601 DOI: 10.1152/japplphysiol.00221.2018

Both the quantity and quality of pre-exercise carbohydrate (CHO) meals have been shown to improve endurance performance. However, their role in attenuating central fatigue (CF) is inconclusive. The use of neurophysiological techniques, such as voluntary activation (VA) and the central activation ratio (CAR), alongside maximum voluntary contraction (MVC) and sustained MVC (sMVC) can provide information on CF. Hence, the objective of this study was to investigate the effects of isocaloric pre-exercise meals: 1) a high versus low quantity of CHO and 2) a high quantity of CHO with a high versus low glycemic index (GI) on MVC, VA, and CAR following a 90-min run. The high and low quantity of CHO was 1.5 and 0.8 g/kg body wt, respectively, and high and low GI was ~75 and ~40, respectively. Blood insulin, serotonin, tryptophan, and gaseous exchange were also measured. High CHO preserved sMVC, VA, CAR, and serotonin postrunning with greater CHO oxidation and insulin response, whereas in low CHO, greater reductions in sMVC, VA, and CAR were accompanied by higher serotonin and fat oxidation with lower insulin response. These observations indicate central involvements. Meanwhile, high GI CHO better preserved force (sMVC), CAR, and tryptophan with greater CHO oxidation and insulin response compared with low GI. The findings of this study suggest that pre-exercise meals with varying quantity and quality of CHO can have an effect on CF, where greater CHO oxidation and insulin response found in both high CHO and high GI lead to attenuation of CF. NEW & NOTEWORTHY This paper examined the effects of carbohydrate interventions (high and low: quantity and quality wise) on central activity during prolonged exercise using mainly neurophysiological techniques along with gaseous exchange and blood insulin, serotonin, and tryptophan data.

Matched MeSH terms: Tryptophan/blood
Fulltext Activation of the kynurenine pathway and increased production of the excitotoxin quinolinic acid following traumatic brain injury in humans

Yan EB, Frugier T, Lim CK, Heng B, Sundaram G, Tan M, et al.

J Neuroinflammation, 2015 May 30;12:110.
PMID: 26025142 DOI: 10.1186/s12974-015-0328-2

During inflammation, the kynurenine pathway (KP) metabolises the essential amino acid tryptophan (TRP) potentially contributing to excitotoxicity via the release of quinolinic acid (QUIN) and 3-hydroxykynurenine (3HK). Despite the importance of excitotoxicity in the development of secondary brain damage, investigations on the KP in TBI are scarce. In this study, we comprehensively characterised changes in KP activation by measuring numerous metabolites in cerebrospinal fluid (CSF) from TBI patients and assessing the expression of key KP enzymes in brain tissue from TBI victims. Acute QUIN levels were further correlated with outcome scores to explore its prognostic value in TBI recovery.
METHODS: Twenty-eight patients with severe TBI (GCS ≤ 8, three patients had initial GCS = 9-10, but rapidly deteriorated to ≤8) were recruited. CSF was collected from admission to day 5 post-injury. TRP, kynurenine (KYN), kynurenic acid (KYNA), QUIN, anthranilic acid (AA) and 3-hydroxyanthranilic acid (3HAA) were measured in CSF. The Glasgow Outcome Scale Extended (GOSE) score was assessed at 6 months post-TBI. Post-mortem brains were obtained from the Australian Neurotrauma Tissue and Fluid Bank and used in qPCR for quantitating expression of KP enzymes (indoleamine 2,3-dioxygenase-1 (IDO1), kynurenase (KYNase), kynurenine amino transferase-II (KAT-II), kynurenine 3-monooxygenase (KMO), 3-hydroxyanthranilic acid oxygenase (3HAO) and quinolinic acid phosphoribosyl transferase (QPRTase) and IDO1 immunohistochemistry.
RESULTS: In CSF, KYN, KYNA and QUIN were elevated whereas TRP, AA and 3HAA remained unchanged. The ratios of QUIN:KYN, QUIN:KYNA, KYNA:KYN and 3HAA:AA revealed that QUIN levels were significantly higher than KYN and KYNA, supporting increased neurotoxicity. Amplified IDO1 and KYNase mRNA expression was demonstrated on post-mortem brains, and enhanced IDO1 protein coincided with overt tissue damage. QUIN levels in CSF were significantly higher in patients with unfavourable outcome and inversely correlated with GOSE scores.
CONCLUSION: TBI induced a striking activation of the KP pathway with sustained increase of QUIN. The exceeding production of QUIN together with increased IDO1 activation and mRNA expression in brain-injured areas suggests that TBI selectively induces a robust stimulation of the neurotoxic branch of the KP pathway. QUIN's detrimental roles are supported by its association to adverse outcome potentially becoming an early prognostic factor post-TBI.

Matched MeSH terms: Tryptophan/blood

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