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1. Proton magnetic resonance spectroscopy assessment of metabolite status of the anterior cingulate cortex in chronic pain patients and healthy controls

Author

Ito T, Tanaka-Mizuno S, Iwashita N, Tooyama I, Shiino A, Miura K, and Fukui S

Subjects
chronic pain, magnetic resonance spectroscopy, glutamic acid, myo-inositol, N–acetylaspartate, creatine, Medicine (General), R5-920
Abstract

Takahiro Ito,1 Sachiko Tanaka-Mizuno,2,3 Narihito Iwashita,4 Ikuo Tooyama,5 Akihiko Shiino,6 Katsuyuki Miura,1,7 Sei Fukui4 1Department of Public Health, Shiga University of Medical Science, 2Department of Medical Statistics, Shiga University of Medical Science, Otsu, Japan; 3The Center for Data Science Education and Research, Shiga University, Hikone, Japan; 4Department of Anesthesiology, Interdisciplinary Pain Management Center, Shiga University of Medical Science Hospital, 5Molecular Neuroscience Research Center, Shiga University of Medical Science, 6Biomedical MR Science Center, Shiga University of Medical Science, 7Center for Epidemiologic Research in Asia, Shiga University of Medical Science, Otsu, Japan Background: Chronic pain is a common cause of reduced quality of life. Recent studies suggest that chronic pain patients have a different brain neurometabolic status to healthy people. Proton magnetic resonance spectroscopy (1H-MRS) can determine the concentrations of metabolites in a specific region of the brain without being invasive. Patients and methods: We recruited 56 chronic pain patients and 60 healthy controls to compare brain metabolic characteristics. The concentrations of glutamic acid (Glu), myo-inositol (Ins), N-acetylaspartate (NAA), Glu + glutamine (Glx), and creatine + phosphocreatine (total creatine [tCr]) in the anterior cingulate cortex of participants were measured using 1H-MRS. We used age- and gender-adjusted general linear models and receiver-operating characteristic analyses for this investigation. Patients were also assessed using the Hospital Anxiety and Depression Scale (HADS) to reveal the existence of any mental health issues. Results: Our analysis indicates that pain patients have statistically significantly higher levels of Glu/tCr (p=0.039) and Glx/tCr (p

Published
2017

10. Identification and localization of a neuron-specific isoform of TAF1 in rat brain: implications for neuropathology of DYT3 dystonia

Author

Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Graybiel, Ann M., Sako, W., Morigaki, R., Kaji, R., Tooyama, I., Okita, S., Kitazato, K., Nagahiro, S., Goto, S., Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, McGovern Institute for Brain Research at MIT, Graybiel, Ann M., Sako, W., Morigaki, R., Kaji, R., Tooyama, I., Okita, S., Kitazato, K., Nagahiro, S., and Goto, S.

Abstract

The neuron-specific isoform of the TAF1 gene (N-TAF1) is thought to be involved in the pathogenesis of DYT3 dystonia, which leads to progressive neurodegeneration in the striatum. To determine the expression pattern of N-TAF1 transcripts, we developed a specific monoclonal antibody against the N-TAF1 protein. Here we show that in the rat brain, N-TAF1 protein appears as a nuclear protein within subsets of neurons in multiple brain regions. Of particular interest is that in the striatum, the nuclei possessing N-TAF1 protein are largely within medium spiny neurons, and they are distributed preferentially, though not exclusively, in the striosome compartment. The compartmental preference and cell type-selective distribution of N-TAF1 protein in the striatum are strikingly similar to the patterns of neuronal loss in the striatum of DYT3 patients. Our findings suggest that the distribution of N-TAF1 protein could represent a key molecular characteristic contributing to the pattern of striatal degeneration in DYT3 dystonia., Japan. Ministry of Education, Culture, Sports, Science and Technology (Grant-in-aid for Scientific Research 20591025), Japan. Ministry of Education, Culture, Sports, Science and Technology (Grant-in-aid for Scientific Research 2139026900), National Institutes of Health (U.S.) (Grant P50 NS38372), National Institutes of Health (U.S.) (Grant R37 HD028341)

Published
2016

45. Expression profiles of cytokines in the brains of Alzheimer's disease (AD) patients compared to the brains of non-demented patients with and without increasing AD pathology.

Author

Morimoto K, Horio J, Satoh H, Sue L, Beach T, Arita S, Tooyama I, Konishi Y, Morimoto, Kaori, Horio, Juri, Satoh, Haruhisa, Sue, Lucia, Beach, Thomas, Arita, Seizaburo, Tooyama, Ikuo, and Konishi, Yoshihiro

Subjects
BRAIN metabolism, ALZHEIMER'S disease, BRAIN, CYTOKINES, DEMENTIA, GENES, RESEARCH funding, RNA, DISEASE progression
Abstract

Neuroinflammation is involved in the pathology of Alzheimer's disease (AD). Our major focus was to clarify whether neuroinflammation plays an important role in AD pathogenesis, particularly prior to the manifestation of overt dementia. We analyzed cytokine expression profiles of the brain, with focus on non-demented patients with increasing AD pathology, referred to as high pathology control (HPC) patients, who provide an intermediate subset between AD and normal control subjects, referred to as low pathology control (LPC) patients. With real-time PCR techniques, we found significant differences in interleukin (IL)-1β, 10, 13, 18, and 33, tumor necrosis factor-α (TNFα) converting enzyme (TACE), and transforming growth factor β1 (TGFβ1) mRNA expression ratios between HPC and AD patients, while no significant differences in the expression ratios of any cytokine tested here were observed between LPC and HPC patients. The cytokine mRNA expression ratios were determined as follows: first, cytokine mRNA levels were normalized to mRNA levels of a housekeeping gene, peptidyl-prolyl isomerase A (PPIA), which showed the most stable expression among ten housekeeping genes tested here; then, the normalized data of cytokine levels in the temporal cortex were divided by those in the cerebellum, which is resistant to AD pathology. Subsequently, the expression ratios of the temporal cortex to cerebellum were compared among LPC, HPC, and AD patient groups. Our results indicate that cytokines are more mobilized and implicated in the later AD stage when a significant cognitive decline occurs and develops than in the developmental course of AD pathology prior to the manifestation of overt dementia. [ABSTRACT FROM AUTHOR]

Published
2011
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47. Variations in the BDNF gene in autopsy-confirmed Alzheimer's disease and dementia with Lewy bodies in Japan.

Author

Akatsu H, Yamagata HD, Kawamata J, Kamino K, Takeda M, Yamamoto T, Miki T, Tooyama I, Shimohama S, and Kosaka K

Abstract

Background/Aim: Brain-derived neurotrophic factor (BDNF) is associated with the hippocampus and the nigrostriatal dopaminergic function. Data showing that its level was reduced in Alzheimer's disease (AD) and Parkinson's disease (PD) suggested that the BDNF function must play an important role in the pathogenetics of these diseases. Indeed, variation in the BDNF gene may confer susceptibility to AD and PD development. Recently, a functional BDNF Val66Met polymorphism has been found to be associated with episodic memory and hippocampal function, with intracellular trafficking, and with activity-dependent secretion of BDNF. To date, there have been several conflicting reports on the correlation between AD or PD and Val66Met or C270T polymorphism in the BDNF promoter region, although no data on this relationship have been published with respect to dementia with Lewy bodies (DLB). In the present study, we investigated a possible association between such BDNF polymorphisms and susceptibility to AD or DLB. Methods:BDNF genotyping was carried out by the polymerase chain reaction-restriction fragment length polymorphism method in autopsy-confirmed human samples. Results and Conclusion: On comparing patients and controls, the distribution of BDNF genotypes and alleles did not differ significantly. Our findings suggest that it is unlikely that these BDNF polymorphisms play a major role in the pathogenesis of AD and DLB in the Japanese population. Copyright (c) 2006 S. Karger AG, Basel. [ABSTRACT FROM AUTHOR]

Published
2006
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