Researchers Database

Tsuji Ai

FacultyFaculty Division of Human Life and Environmental Sciences Research Group of Food Science and Nutrition
PositionAssistant Professor
Last Updated :2022/10/06


Profile and Settings

  • Name (Japanese)

  • Name (Kana)



  • Doctor of Philosophy

Research Areas

  • Humanities & social sciences, Home economics, lifestyle science

Research Experience

  • Apr. 2019, 9999, 神戸学院大学 非常勤講師
  • Apr. 2018, 9999, 奈良女子大学 生活環境学部 食物栄養学科・助教
  • Apr. 2019, Mar. 2020, 神戸常磐大学 非常勤講師
  • Apr. 2017, Mar. 2018, 辻製菓専門学校 非常勤講師
  • Oct. 2016, Mar. 2018, 神戸学院大学 栄養学部 食品機能学部門・博士研究員
  • Apr. 2016, Sep. 2016, 神戸大学 科学技術イノベーション研究科・学術研究員


  • Apr. 2013, Mar. 2016, 滋賀県立大学大学院, 人間文化学研究科, 生活文化学専攻
  • Apr. 2011, Mar. 2013, 滋賀県立大学大学院, 人間文化学研究科, 生活文化学専攻
  • Apr. 2007, Mar. 2011, 滋賀県立大学, 人間文化学部, 生活文化学科 食生活コース

Teaching Experience

  • 食品学各論, Kobe Gakuin University, 99 Apr. 2021
  • 病態生理・生化学実験, Nara Women's University, 99 Apr. 2018
  • 基礎栄養学実験, Nara Women's University, 99 Apr. 2018
  • 食品学総論実験, Kobe Gakuin University, 20 Apr. 2019
  • 栄養代謝学, Kobe Tokiwa University, 20 Apr. 2019
  • 食品衛生学, 20 Apr. 2017

Association Memberships

  • 日本栄養・食糧学会
  • 日本栄養改善学会
  • The Japan Society for Bioscience, Biotechnology and Agrychemistry
  • 日本フードファクター学会


Published Papers

  • Refereed, Biomedical reports, Spandidos Publications, Role of tumor suppressor molecules in genomic perturbations and damaged DNA repair involved in the pathogenesis of cancer and neurodegeneration (Review)., Satoru Matsuda; Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi, Genomic perturbations due to inaccurate DNA replication, including inappropriate chromosomal segregation often underlie the development of cancer and neurodegenerative diseases. The incidence of these two diseases increases with age and exhibits an inverse association. Therefore, elderly subjects with cancer exhibit a reduced risk of a neurodegenerative disease, and vice versa. Both of these diseases are associated with aging and share several risk factors. Cells have multiple mechanisms to repair DNA damage and inaccurate replication. Previous studies have demonstrated that tumor suppressor proteins serve a critical role in the DNA damage response, which may result in genomic instability and thus induction of cellular apoptosis. Tumor suppressor genes, such as phosphatase and tensin homologue deleted on chromosome 10 (PTEN), breast cancer susceptibility gene 1 (BRCA1) and TP53 reduce genomic susceptibility to cancer by repairing the damaged DNA. In addition, these genes work cooperatively to ensure the inhibition of the development of several types of cancer. PTEN, BRCA1 and TP53 have been recognized as the most frequently deleted and/or mutated genes in various types of human cancer. Recently, tumor suppressor genes have also been shown to be involved in the development of neurodegenerative diseases. The present review summarizes the recent findings of the functions of these tumor suppressors that are associated with genomic stability, and are involved in carcinogenic and neurodegenerative cell signaling. A summary is presented regarding the interactions of these tumor suppressors with their partners which results in transduction of downstream signals. The implications of these functions for cancer and neurodegenerative disease-associated biology are also highlighted., Sep. 2020, 13, 3, 10, 10, Scientific journal, True
  • Refereed, Biomedical reports, Special bioactive compounds and functional foods may exhibit neuroprotective effects in patients with dementia (Review)., Mutsumi Murakami; Yuka Ikeda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Dementia is a failure of cognitive ability characterized by severe neurodegeneration in select neural systems, and Alzheimer's disease (AD) is the most common type of neurodegenerative disease. Although numerous studies have provided insights into the pathogenesis of AD, the underlying signaling and molecular pathways mediating the progressive decline of cognitive function remain poorly understood. Recent progress in molecular biology has provided an improved understanding of the importance of molecular pathogenesis of AD, and has proposed an association between DNA repair mechanisms and AD. In particular, the fundamental roles of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and breast cancer gene 1 (BRCA1) tumor suppressors have been shown to regulate the pathogenesis of neurodegeneration. Consequently, onset of neurodegenerative diseases may be deferred with the use of dietary neuroprotective agents which alter the signaling mediated by the aforementioned tumor suppressors. In a healthy neuron, homeostasis of key intracellular molecules is of great importance, and preventing neuronal apoptosis is one of the primary goals of treatments designed for dementia-associated diseases. In the present review, progress into the understanding of dietary regulation for preventing or limiting development of dementia is discussed with a focus on the modulatory roles of PTEN and BRCA1 signaling., Aug. 2020, 13, 2, 1, 1, Scientific journal, True
  • Refereed, Biomedical reports, Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling., Yuka Ikeda; Mutsumi Murakami; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration., Jun. 2020, 12, 6, 295, 302, Scientific journal, True
  • Refereed, J Clin Nutr Metab, Effects of Biotin Deficiency on the Urinary Excretion of B-Group Vitamins in Mice, Ai Tsuji; Katsumi Shibata, Mar. 2019, 3, 1
  • Refereed, Diseases (Basel, Switzerland), Roles of PI3K/AKT/GSK3 Pathway Involved in Psychiatric Illnesses., Satoru Matsuda; Yuka Ikeda; Mutsumi Murakami; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi, Psychiatric illnesses may be qualified to the cellular impairments of the function for survival or death in neurons, which may consequently appear as abnormalities in the neuroplasticity. The molecular mechanism has not been well understood, however, it seems that PI3K, AKT, GSK3, and their downstream molecules have crucial roles in the pathogenesis. Through transducing cell surviving signal, the PI3K/AKT/GSK3 pathway may organize an intracellular central network for the action of the synaptic neuroplasticity. In addition, the pathways may also regulate cell proliferation, cell migration, and apoptosis. Several lines of evidence have supported a role for this signaling network underlying the development and treatment for psychiatric illnesses. Indeed, the discovery of molecular biochemical phenotypes would represent a breakthrough in the research for effective treatment. In this review, we summarize advances on the involvement of the PI3K/AKT/GSK3 pathways in cell signaling of neuronal cells. This study may provide novel insights on the mechanism of mental disorder involved in psychiatric illnesses and would open future opportunity for contributions suggesting new targets for diagnostic and/or therapeutic procedures., 13 Feb. 2019, 7, 1, Scientific journal, True
  • Refereed, Neural regeneration research, By using either endogenous or transplanted stem cells, which could you prefer for neural regeneration?, Satoru Matsuda; Yukie Nakagawa; Kumi Amano; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi, Oct. 2018, 13, 10, 1731, 1732, Scientific journal, True
  • Refereed, Molecules (Basel, Switzerland), Binding of Catechins to Staphylococcal Enterotoxin A., Yuko Shimamura; Mio Utsumi; Chikako Hirai; Shogo Nakano; Sohei Ito; Ai Tsuji; Takeshi Ishii; Takahiro Hosoya; Toshiyuki Kan; Norio Ohashi; Shuichi Masuda, Staphylococcal enterotoxin A (SEA) is a toxin protein, and is the most common cause of staphylococcal food poisoning. Polyphenols, such as catechins, are known to interact with proteins. In this study, we investigated the binding of catechins to SEA using SPR (Biacore), Fourier transform infrared spectroscopy (FT-IR), isothermal titration calorimetry (ITC), and protein-ligand docking. We found that (−)-epigallocatechin gallate (EGCG) could strongly bind to SEA. According to thermodynamic parameters, a negative ΔG indicated that the interaction between EGCG and SEA was spontaneous, and the electrostatic force accompanied by hydrophobic binding forces may play a major role in the binding. Data from Western blot analysis and docking simulation suggest that the hydroxyl group at position 3 of the galloyl group in the catechin structure was responsible for binding affinity with the Y91 of the A-6 region of SEA active sites. Our results provide further understanding of the binding interactions between catechins and SEA, and the inhibition of toxin activities by catechins., 09 May 2018, 23, 5, Scientific journal, True
  • Refereed, Diseases, MDPI AG, Implications of PI3K/AKT/PTEN Signaling on Superoxide Dismutases Expression and in the Pathogenesis of Alzheimer’s Disease, Satoru Matsuda; Yukie Nakagawa; Ai Tsuji; Yasuko Kitagishi; Atsuko Nakanishi; Toshiyuki Murai, Alzheimer’s disease is a neurodegenerative sickness, where the speed of personal disease progression differs prominently due to genetic and environmental factors such as life style. Alzheimer’s disease is described by the construction of neuronal plaques and neurofibrillary tangles composed of phosphorylated tau protein. Mitochondrial dysfunction may be a noticeable feature of Alzheimer’s disease and increased production of reactive oxygen species has long been described. Superoxide dismutases (SODs) protect from excess reactive oxygen species to form less reactive hydrogen peroxide. It is suggested that SODs can play a protective role in neurodegeneration. In addition, PI3K/AKT pathway has been shown to play a critical role on the neuroprotection and inhibiting apoptosis via the enhancing expression of the SODs. This pathway appears to be crucial in Alzheimer’s disease because it is related to the tau protein hyper-phosphorylation. Dietary supplementation of several ordinary compounds may provide a novel therapeutic approach to brain disorders by modulating the function of the PI3K/AKT pathway. Understanding these systems may offer a better efficacy of new therapeutic approaches. In this review, we summarize recent progresses on the involvement of the SODs and PI3K/AKT pathway in neuroprotective signaling against Alzheimer’s disease., 20 Apr. 2018, 6, 2, 28, 28, Scientific journal, True
  • Refereed, Nutrition and metabolic insights, Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes., Ai Tsuji; Toshinobu Nakamura; Katsumi Shibata, We investigated the effects of vitamin B1 deficiency on the meiosis maturation of oocytes. Female Crl:CD1 (ICR) mice were fed a 20% casein diet (control group) or a vitamin B1-free diet (test group). The vitamin B1 concentration in ovary was approximately 30% lower in the test group than in the control group. Oocyte meiosis was not affected by vitamin B1 deficiency when the deficiency was not accompanied by body weight loss. On the contrary, frequency of abnormal oocyte was increased by vitamin B1 deficiency when deficiency was accompanied by body weight loss (referred to as severe vitamin B1 deficiency; frequency of abnormal oocyte, 13.8% vs 43.7%, P = .0071). The frequency of abnormal oocytes was decreased by refeeding of a vitamin B1-containing diet (13.9% vs 22.9%, P = .503). These results suggest that severe vitamin B1 deficiency inhibited meiotic maturation of oocytes but did not damage immature oocytes., 2017, 10, 1178638817693824, 1178638817693824, Scientific journal, True
  • Not Refereed, PloS one, High-dose thiamine prevents brain lesions and prolongs survival of Slc19a3-deficient mice., Kaoru Suzuki; Kenichiro Yamada; Yayoi Fukuhara; Ai Tsuji; Katsumi Shibata; Nobuaki Wakamatsu, SLC19A3 deficiency, also called thiamine metabolism dysfunction syndrome-2 (THMD2; OMIM 607483), is an autosomal recessive neurodegenerative disorder caused by mutations in SLC19A3, the gene encoding thiamine transporter 2. To investigate the molecular mechanisms of neurodegeneration in SLC19A3 deficiency and whether administration of high-dose thiamine prevents neurodegeneration, we generated homozygous Slc19a3 E314Q knock-in (KI) mice harboring the mutation corresponding to the human SLC19A3 E320Q, which is associated with the severe form of THMD2. Homozygous KI mice and previously reported homozygous Slc19a3 knock-out (KO) mice fed a thiamine-restricted diet (thiamine: 0.60 mg/100 g food) died within 30 and 12 days, respectively, with dramatically decreased thiamine concentration in the blood and brain, acute neurodegeneration, and astrogliosis in the submedial nucleus of the thalamus and ventral anterior-lateral complex of the thalamus. These findings may bear some features of thiamine-deficient mice generated by pyrithiamine injection and a thiamine-deficient diet, suggesting that the primary cause of THMD2 could be thiamine pyrophosphate (TPP) deficiency. Next, we analyzed the therapeutic effects of high-dose thiamine treatment. When the diet was reverted to a conventional diet (thiamine: 1.71 mg/100 g food) after thiamine restriction, all homozygous KO mice died. In contrast, when the diet was changed to a high-thiamine diet (thiamine: 8.50 mg/100 g food) after thiamine restriction, more than half of homozygous KO mice survived, without progression of brain lesions. Unexpectedly, when the high-thiamine diet of recovered mice was reverted to a conventional diet, some homozygous KO mice died. These results showed that acute neurodegeneration caused by thiamine deficiency is preventable in most parts, and prompt high-dose thiamine administration is critical for the treatment of THMD2. However, reduction of thiamine should be performed carefully to prevent recurrence after recovery of the disease., 2017, 12, 6, e0180279, Scientific journal, True
  • Refereed, Journal of nutritional science and vitaminology, Folic Acid Deficiency Does Not Adversely Affect Oocyte Meiosis in Mice., Ai Tsuji; Rina Noguchi; Toshinobu Nakamura; Katsumi Shibata, Spindle defect and chromosome misalignment occuring in oocyte meiosis induce nondisjunction. Nondisjunction causes Down syndrome, also known as trisomy 21. Folic acid (FA) is an essential nutrient composition for fetal growth and development. It has been reported that FA nutritional status is associated with the risk of Down syndrome. However, to our knowledge, little is known about the effect of FA deficiency on abnormal oocytes (spindle defects, chromosome misalignments and immature oocyte) in vivo. In the present study, we investigate the effects of FA deficiency on oocyte meiosis in female mice. In order to induce FA deficiency in mice, female Crl:CD1 mice were fed a FA-free diet for 58 d. The diet also contained an antibiotic which has functions on limiting FA formation by intestinal microorganisms. The level of FA deficiency was determined by measuring the concentration of FA in the liver, hemocyte, uterus, ovary, and urine. FA concentrations in these samples from the FA-deficient group were 50-90% lower. Despite this, the frequency of abnormal oocytes was no different between the FA-deficient and control groups (20.0% vs 14.6%). According to the past research, FA transporter was strongly expressed in oocytes. Hence, it is possible that FA-free diets may not affect the concentration of oocyte FA in mice. To sum up these data, our study concluded that FA deficiency did not adversely affect oocyte meiosis., 2016, 62, 6, 375, 379, Scientific journal, False
  • Refereed, Bioscience, biotechnology, and biochemistry, Biotin-deficient diet induces chromosome misalignment and spindle defects in mouse oocytes., Ai Tsuji; Toshinobu Nakamura; Katsumi Shibata, Increased abnormal oocytes due to meiotic chromosome misalignment and spindle defects lead to elevated rates of infertility, miscarriage, and trisomic conceptions. Here, we investigated the effect of biotin deficiency on oocyte quality. Three-week-old female ICR mice were fed a biotin-deficient or control diet (0, 0.004 g biotin/kg diet) for 21 days. On day 22, these mouse oocytes were analyzed by immunofluorescence. Due to biotin, undernutrition increased the frequency of abnormal oocytes (the biotin deficient vs. control: 40 vs. 16%). Next, the remaining mice in the biotin-deficient group were fed a control or biotin-deficient diet from day 22 to 42. Although biotin nutritional status in the recovery group was restored, the frequency of abnormal oocytes in the recovery group was still higher than that in the control group (48 vs. 18%). Our results indicate that steady, sufficient biotin intake is required for the production of high-quality oocytes in mice., 2015, 79, 2, 292, 9, Scientific journal, True
  • Refereed, Journal of nutritional science and vitaminology, Effects of Fatty Liver Induced by Excess Orotic Acid on B-Group Vitamin Concentrations of Liver, Blood, and Urine in Rats., Katsumi Shibata; Nobuya Morita; Tomoyo Kawamura; Ai Tsuji; Tsutomu Fukuwatari, Fatty liver is caused when rats are given orotic acid of the pyrimidine base in large quantities. The lack of B-group vitamins suppresses the biosynthesis of fatty acids. We investigated how orotic acid-induced fatty liver affects the concentrations of liver, blood, and urine B-group vitamins in rats. The vitamin B6 and B12 concentrations of liver, blood, and urine were not affected by orotic acid-induced fatty liver. Vitamin B2 was measured only in the urine, but was unchanged. The liver, blood, and urine concentrations of niacin and its metabolites fell dramatically. Niacin and its metabolites in the liver, blood, and urine were affected as expected. Although the concentrations of vitamin B1, pantothenic acid, folate, and biotin in liver and blood were decreased by orotic acid-induced fatty liver, these urinary excretion amounts showed a specific pattern toward increase. Generally, as for the typical urinary excretion of B-group vitamins, these are excreted when the body is saturated. However, the ability to sustain vitamin B1, pantothenic acid, folate, and biotin decreased in fatty liver, which is hypothesized as a specific phenomenon. This metabolic response might occur to prevent an abnormally increased biosynthesis of fatty acids by orotic acid., 2015, 61, 5, 355, 61, Scientific journal, False
  • Refereed, International Journal of Tryptophan Research, SAGE Publications, L-Tryptophan Metabolism in Pregnant Mice Fed a High L-Tryptophan Diet and the Effect on Maternal, Placental, and Fetal Growth, Ai Tsuji; Chifumi Nakata; Mitsue Sano; Tsutomu Fukuwatari; Katsumi Shibata, Excess L-tryptophan (L-Trp) in the diet decreases fetal body weight. However, the relationship between L-Trp concentration and its effects on maternal, placental, and fetal growth are not well-understood. We investigated the effects of excess L-Trp intake on maternal, placental, and fetal growth. Female mice were fed a 20% casein diet (control diet) or control diet plus 2% or 5% L-Trp during gestation. Pup weights did not differ between the control (L-Trp intake: 0.04 g/kg body weight (BW)/day) and 2% L-Trp groups (L-Trp intake: 3.3 g/kg BW/day), but were significantly lower in the 5% L-Trp group (L-Trp intake: 7.0 g/kg BW/day) than in the control and 2% L-Trp groups. These results show that less than 3.3 g/kg BW/day L-Trp intake in pregnant mice during gestation does not affect fetal growth or L-Trp homeostasis in the placenta or fetus., Jan. 2013, 6, IJTR.S12715, IJTR.S12715, Scientific journal, True
  • Refereed, Journal of Advances in Medicine and Medical Research, Save Children from Mortal Shock of COVID-19, Satoru Matsuda; Yuka Ikeda; Mutsumi Murakami; Ai Tsuji, 2020, 32, 8, 23, 25, Scientific journal
  • Refereed, Journal of Psychiatry and Behavioral Health Forecast, Gut in Mind!, Behavioral Health Forecast, 2020, 3, 1, 1, 2, Scientific journal
  • Refereed, Clinical Obstetrics, Gynecology and Reproductive Medicine, COVID-19, an infertility risk?, Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Satoru Matsuda, 2020, 6, 1, Scientific journal
  • International journal of preventive medicine, Prevention in Daily Life against Progression of COVID-19., Mutsumi Murakami; Yuka Ikeda; Ai Tsuji; Satoru Matsuda, 2020, 11, 99, 99, Scientific journal, True
  • Refereed, Reproductive medicine and biology, d-Leucine protects oocytes from chronic psychological stress in mice., Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda, Purpose: Psychological stress could negatively influence female reproductive ability. d-Leucine (d-Leu) is a d-type amino acid found in foods and mammalian tissues. We have examined the protective effects of d-Leu on oocyte abnormality induced by psychological stress. Methods: Female mice (6-week-old) were divided into three groups: control, restraint stress (RS), and RS/d-Leu. The RS and RS/d-Leu mice were holed for 3 hours daily during 14 days. RS/d-Leu mice were fed 0.3% d-Leu diet. The oocyte maturation failure was analyzed by shapes of spindles and chromosomes. In addition, levels of heme-oxygenase-1 (HO-1) and superoxide dismutase (SOD) expression in the ovaries were also examined. Whether d-Leu reduces the generation of reactive oxygen species (ROS) in cultured cells, K562 cells were treated with d-Leu, and then ROS in K562 were analyzed. Results: Oocyte maturation failure was increased in RS mice. d-Leu reduced abnormal oocytes to control level. The expression levels of HO-1 and SOD2 increased in RS/d-Leu mice compared to those of RS mice. ROS levels were decreased in K562 cells with d-Leu in a dose-dependent manner. Conclusions: We concluded that d-Leu protects oocytes from psychological stress through the induction of HO-1 and SOD2 expression then by reducing oxidative stress., Oct. 2021, 20, 4, 477, 484, Scientific journal, False
  • Refereed, Nutr. Re. Pract, Reduction of oocyte lipid droplets and meiotic failure due to biotin deficiency was not rescued by restoring the biotin nutritional status, Ai Tsuji; Yuka Ikeda; Mutsumi Murakami; Yasuko Kitagishi; Satoru Matsuda, Sep. 2021, 15, e71
  • Diseases (Basel, Switzerland), D-Amino Acids as a Biomarker in Schizophrenia., Kurumi Taniguchi; Haruka Sawamura; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, D-amino acids may play key roles for specific physiological functions in different organs including the brain. Importantly, D-amino acids have been detected in several neurological disorders such as schizophrenia, amyotrophic lateral sclerosis, and age-related disorders, reflecting the disease conditions. Relationships between D-amino acids and neurophysiology may involve the significant contribution of D-Serine or D-Aspartate to the synaptic function, including neurotransmission and synaptic plasticity. Gut-microbiota could play important roles in the brain-function, since bacteria in the gut provide a significant contribution to the host pool of D-amino acids. In addition, the alteration of the composition of the gut microbiota might lead to schizophrenia. Furthermore, D-amino acids are known as a physiologically active substance, constituting useful biomarkers of several brain disorders including schizophrenia. In this review, we wish to provide an outline of the roles of D-amino acids in brain health and neuropsychiatric disorders with a focus on schizophrenia, which may shed light on some of the superior diagnoses and/or treatments of schizophrenia., 31 Jan. 2022, 10, 1, Scientific journal, True
  • World journal of biological chemistry, Neuroprotection by dipeptidyl-peptidase-4 inhibitors and glucagon-like peptide-1 analogs via the modulation of AKT-signaling pathway in Alzheimer's disease., Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Alzheimer's disease (AD) is the most common reason for progressive dementia in the elderly. It has been shown that disorders of the mammalian/mechanistic target of rapamycin (mTOR) signaling pathways are related to the AD. On the other hand, diabetes mellitus (DM) is a risk factor for the cognitive dysfunction. The pathogenesis of the neuronal impairment caused by diabetic hyperglycemia is intricate, which contains neuro-inflammation and/or neurodegeneration and dementia. Glucagon-like peptide-1 (GLP1) is interesting as a possible link between metabolism and brain impairment. Modulation of GLP1 activity can influence amyloid-beta peptide aggregation via the phosphoinositide-3 kinase/AKT/mTOR signaling pathway in AD. The GLP1 receptor agonists have been shown to have favorable actions on the brain such as the improvement of neurological deficit. They might also exert a beneficial effect with refining learning and memory on the cognitive impairment induced by diabetes. Recent experimental and clinical evidence indicates that dipeptidyl-peptidase-4 (DPP4) inhibitors, being currently used for DM therapy, may also be effective for AD treatment. The DPP-4 inhibitors have demonstrated neuroprotection and cognitive improvements in animal models. Although further studies for mTOR, GLP1, and DPP4 signaling pathways in humans would be intensively required, they seem to be a promising approach for innovative AD-treatments. We would like to review the characteristics of AD pathogenesis, the key roles of mTOR in AD and the preventive and/ or therapeutic suggestions of directing the mTOR signaling pathway., 27 Nov. 2021, 12, 6, 104, 113, Scientific journal, True
  • Refereed, Exploration of Medicine, Open Exploration Publishing, Reactive oxygen species may influence on the crossroads of stemness, senescence, and carcinogenesis in a cell via the roles of APRO family proteins, Yuka Ikeda; Kurumi Taniguchi; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Excessive reactive oxygen species (ROS) may cause oxidative stress which is involved in aging and in the pathogenesis of various human diseases. Whereas unregulated levels of the ROS may be harmful, regulated basal level of ROS are even necessary to support cellular functions as a second messenger for homeostasis under physiological conditions. Therefore, redox medicine could develop as a new therapeutic concept for human health-benefits. Here, we introduce the involvement of ROS on the crossroads of stemness, senescence, and carcinogenesis in a stem cell and cancer cell biology. Amazingly, the anti-proliferative (APRO) family anti-proliferative proteins characterized by immediate early growth responsive genes may also be involved in the crossroads machinery. The biological functions of APRO proteins (APROs) seem to be quite intricate, however, which might be a key modulator of microRNAs (miRNAs). Given the crucial roles of ROS and APROs for pathophysiological functions, upcoming novel therapeutics should include vigilant modulation of the redox state. Next generation of medicine including regenerative medicine and/or cancer therapy will likely comprise strategies for altering the redox environment with the APROs via the modulation of miRNAs as well as with the regulation of ROS of cells in a sustainable manner., 31 Oct. 2021, Scientific journal
  • Refereed, Oxygen, MDPI AG, Comprehension of the Relationship between Autophagy and Reactive Oxygen Species for Superior Cancer Therapy with Histone Deacetylase Inhibitors, Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Kurumi Taniguchi; Yasuko Kitagishi; Satoru Matsuda, Epigenetics contains various mechanisms by which cells employ to regulate the transcription of many DNAs. Histone acetylation is an obvious example of the epigenetic mechanism regulating the expression of several genes by changing chromatin accessibility. Histone deacetylases (HDACs) are a class of enzymes that play a critical role in the epigenetic regulation by deacetylation of histone proteins. Inhibitors of the histone deacetylase could result in hyperacetylation of histones, which eventually induce various cellular consequences such as generation of reactive oxygen species (ROS), activation of apoptotic pathways, and initiating autophagy. In particular, excessive levels of ROS have been proposed to contribute to the pathophysiology of various diseases including cancer. Cancers are, as it were, a class of redox diseases. Low levels of ROS are beneficial for cells, however, cancer cells generally have high levels of ROS, which makes them more susceptible than normal cells to the further increases of ROS levels. Cancer cells exhibit metabolic alterations for managing to sustain these oxidative stresses. There is a growing interest in the use of HDAC inhibitors as promising cancer therapeutics with potentiating the activity of established therapeutic applications. Therefore, it should be important to understand the underlying relationship between the regulation of HDACs, ROS production, and cancer cell biology., 25 Jul. 2021, 1, 1, 22, 31, Scientific journal
  • Refereed, AIMS Bioengineering, American Institute of Mathematical Sciences (AIMS), Implications of Gut-Brain axis in the pathogenesis of Psychiatric disorders, Kurumi Taniguchi; Yuka Ikeda; Nozomi Nagase; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda,

    <abstract> <p>Psychiatric disorders may extremely impair the quality of life with patients and are important reasons of social disability. Several data have shown that psychiatric disorders are associated with an altered composition of gut microbiota. Dietary intake could determine the microbiota, which contribute to produce various metabolites of fermentation such as short chain fatty acids. Some of the metabolites could result in epigenetic alterations leading to the disease susceptibility. Epigenetic dysfunction is in fact implicated in various psychiatric and neurologic disorders. For example, it has been shown that neuroepigenetic dysregulation occurs in psychiatric disorders including schizophrenia. Several studies have demonstrated that the intestinal microbiome may influence the function of central nervous system. Furthermore, it has been proved that the alterations in the gut microbiota-composition might affect in the bidirectional communication between gut and brain. Similarly, evidences demonstrating the association between psychiatric disorders and the gut microbiota have come from preclinical studies. It is clear that an intricate symbiotic relationship might exist between host and microbe, although the practical significance of the gut microbiota has not yet to be determined. In this review, we have summarized the function of gut microbiota in main psychiatric disorders with respect to the mental health. In addition, we would like to discuss the potential mechanisms of the disorders for the practical diagnosis and future treatment by using bioengineering of microbiota and their metabolites.</p> </abstract>, 2021, 8, 4, 243, 256, Scientific journal

  • Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences, COVID-19 cellular pathogenesis in brief., Yuka Ikeda; Ai Tsuji; Mutsumi Murakami; Satoru Matsuda, 2021, 26, 129, 129, Scientific journal, True
  • Academia Letters,, COVID-19 and Glaucoma, Satoru Matsuda; Nozomi Nagase; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi, 16 Jul. 2021, Scientific journal
  • World Journal of Diabetes, Baishideng Publishing Group Inc., Efficacy of probiotics on the modulation of gut microbiota in the treatment of diabetic nephropathy, Nozomi Nagase; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, 15 Mar. 2022, 13, 3, 150, 160, Scientific journal
  • Recent Progress in Nutrition, LIDSEN Publishing Inc, Gut Microbiota Potentiates the Effect of Immune Checkpoint Therapy against Cancers, Haruka Sawamura; Kurumi Taniguchi; Yuka Ikeda; Ai Tsuji; Yasuko Kitagishi; Satoru Matsuda, Immune checkpoints have been aggressively investigated for anti-cancer immunotherapy. The power of microbiota on the outcome of this immunotherapy has attracted much attention. For example, intestinal microorganisms play a key role in the effectiveness of programmed cell death 1 (PD1) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) blockade. Additionally, short-chain fatty acids produced in the gut may modulate anti-CTLA4 and anti-PD1 stimulated immune responses and their anti-tumor efficacy. Enhancing the anti-tumor effects of CTLA4 blockade depends on specific Bacteroides sp. of the gut microbiota, suggesting novel approaches to improve such immunotherapies. However, the molecular mechanism of the immune-potentiation remains largely unknown. Changes in the microbiota are influenced by dietary and environmental factors. Here, we have suggested the molecular mechanism of action regarding the interplay between gut microbiota and the anti-cancer immune system with APRO family proteins, which might contribute to innovative cancer therapy in the future., 16 Nov. 2021, 2, 1, 1, 1, Scientific journal


  • Not Refereed, FASEB JOURNAL, FEDERATION AMER SOC EXP BIOL, Novel mechanism responsible for regulation of branched-chain alpha-ketoacid dehydrogenase kinase, Yoshiharu Shimomura; Yusuke Kondo; Rina Ito; Ai Tsuji; Katsumi Shibata; Yasuyuki Kitaura, Apr. 2016, 30, Summary international conference
  • 日本農芸化学会大会講演要旨集(Web), ビタミン欠乏が卵母細胞の質におよぼす影響, 辻愛; 中村肇伸; 柴田克己, 2017, 2017
  • 日本栄養・食糧学会大会講演要旨集, 低葉酸栄養状態では卵子の質は劣化しない, 辻愛; 野口里奈; 中村肇伸; 柴田克己, 2016, 70th
  • 日本栄養・食糧学会近畿支部大会および公開シンポジウム講演抄録集, Vitamin B1栄養が卵子の質におよぼす影響, 辻愛; 中村肇伸; 柴田克己, 2015, 54th
  • ビタミン, マウスにおけるビオチン欠乏は卵子の染色体および紡錘体形成異常を増加させる, 柴田克己; 辻愛; 中村肇伸, 2015, 89, 8


  • 辻 愛; 樺澤 理紗子; 池田 祐香; 中川 友希江; 村上 睦美; 北岸 靖子; 松田 覚, 第93回日本生化学会, ビオチン欠乏および再摂取が卵子中脂肪滴、卵巣中脂質代謝におよぼす影響, Poster presentation, Sep. 2020
  • 池田 祐香; 村上 睦美; 北岸 靖子; 辻 愛; 松田 覚, 第93回日本生化学会, 慢性的心因性ストレスの生体への影響とその保護に働く食品成分, Poster presentation, Sep. 2020
  • 第92回日本生化学会(横浜), ビオチン欠乏による減数分裂異常とその要因の解明, 19 Sep. 2019
  • 、第92回日本生化学会(横浜), 脂質代謝に関与する食成分が卵子の健康に及ぼす影響, Poster presentation, 19 Sep. 2019
  • 第92回日本生化学会(横浜), 非アルコール性脂肪性肝疾患(NAFLD)におけるD-Trp摂取の影響, Poster presentation, 18 Sep. 2019
  • Tsuji Ai; Ai Tsuji; Katsumi Shiabta, 第57回日本栄養・食糧学会 近畿支部大会, ビオチン欠乏食が尿中水溶性ビタミン排泄量に及ぼす影響, Oral presentation, Dec. 2018, 畿央大学(奈良)
  • Tsuji Ai, 第91回日本生化学会大会, オウバク成分は非アルコール性脂肪肝疾患(NAFLD)改善に関与するか?, Poster presentation, Sep. 2018, 京都, False
  • Tsuji Ai, 第91回日本生化学会大会, 脂肪性肝障害に対する少量アセトアルデヒド摂取の影響, Poster presentation, Sep. 2018, False
  • Tsuji Ai, 日本農芸化学会2018年度大会, 渋味を呈するポリフェノールの分子特性解析, Oral presentation, 2018
  • Tsuji Ai, 第 22回日本フードファクター学会学術集会, ウーロンホモビスフラバン類の消化管タンパク質に対する強力な修飾作用, Oral presentation, 2017
  • Tsuji Ai, 日本農芸化学会2017年度大会, ビタミン欠乏が卵母細胞の質におよぼす影響, Oral presentation, 2017
  • Tsuji Ai, 日本農芸化学会2017年度大会, フラボノイドの分子会合に寄与する構造特性, Oral presentation, 2017
  • Tsuji Ai, 第496回日本農芸化学会 近畿支部大会, 日本ヨモギエタノール抽出物が糖尿病モデルマウスにおよぼす影響, 2016
  • Tsuji Ai, 第70回日本栄養・食糧学会大会, 低葉酸栄養状態では卵子の質は劣化しない, 2016
  • Tsuji Ai, ISTRY 2015, L-Tryptophan metabolism in pregnant mice fed a high L-tryptophan diet and the effect on maternal, placental, and fetal growth., 2015, True
  • Tsuji Ai, 第13回 日本栄養改善学会近畿支部学術総会, マウスにおけるビオチン欠乏は卵子の質を劣化させる, 2014
  • 池田祐香; 岡本恵実; 宮原朋佳; 中川友希江; 村上睦美; 辻愛; 北岸靖子; 松田 覚, 第74回日本栄養・食糧学会, ストレス保護に関与する食品成分の検討, Others, 2020, 2020, rm:research_project_id
  • 辻愛; 樺澤理紗子; 池田祐香; 中川友希江; 村上睦美; 北岸靖子; 松田覚, 第74回日本栄養・食糧学会, Lipid droplets in oocyte were decreased by biotin-deficiency., Others, 2020, 2020, rm:research_project_id
  • 池田祐香; 長瀬のぞみ; 北岸靖子; 辻愛,松田覚, 第93回日本生化学会大会, 潰瘍性大腸炎モデルマウスの作製と食品成分の関与, Poster presentation, Nov. 2021
  • 長瀬のぞみ,池田祐香,辻愛,北岸靖子,松田覚, 第93回日本生化学会大会, 慢性的ストレス環境がもたらすマウスへの影響と行動テストによる検出, Poster presentation, Nov. 2021
  • 辻愛、柴田桜、長瀬のぞみ、池田祐香、北岸靖子、 松田覚, 第75回日本栄養・食糧学会大会, 心理的ストレス環境下におけるD-アスパラギン酸の卵子およびホルモンに対する影響, Poster presentation, 2021

Research Projects

  • Grant-in-Aid for Early-Career Scientists, 01 Apr. 2020, 31 Mar. 2024, 20K19638, Nutritional prevention and treatment to protect oocytes from psychogenic stress, 辻 愛, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists, Nara Women's University, 4160000, 3200000, 960000, rm:presentations
  • Grant-in-Aid for Research Activity start-up, 24 Aug. 2018, 31 Mar. 2020, 19K21511, Analysis of the factors of mouse oocyte aging by biotin deficiency, 辻 愛, Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity start-up, Nara Women's University, 2990000, 2300000, 690000, 卵子の質の劣化は、減数分裂異常を引き起こし、流産、染色体異常、不妊症の原因となる。卵子の質が劣化する要因には活性酸素、ミトコンドリア機能の低下、代謝異常やそれに付随するエネルギー不足など、様々な要因があるとされている。先行研究により水溶性ビタミンであるビオチン不足によって、卵子の質が低下することを明らかにしたが、上記に述べた要因が関与しているのかは不明であった。そこで、ビオチン不足・欠乏によって起きる減数分裂異常の要因が何かを明らかにすることを目的とした。ビオチンは補酵素として脂肪酸合成にも関与するため、不足によって卵子中の脂肪酸蓄積量は低下すると予想した。脂肪酸は減数分裂時のエネルギー源として利用されることから、脂肪酸蓄積量の低下によってエネルギー不足となる。これが要因となって減数分裂異常が引き起こされたと仮説を立てた。また、仮説以外の要因を検討するために、活性酸素およびミトコンドリア機能を調べた。ビオチン不足あるいは欠乏モデルマウスを作製し、卵子の脂肪酸量をNile Redを用いて解析した。また、卵子の活性酸素、ミトコンドリア活性を測定した。その結果、ビオチン不足によって卵子中の脂肪酸蓄積量が低下し、ミトコンドリア機能も低下することが分かった。次に、不足モデルマウスにビオチンを与えた。脱毛症状の消失などから栄養状態は回復したと考えられるが、脂肪酸蓄積量およびミトコンドリア機能は対照群と同等レベルにまで回復しないことが分かった。よって、ビオチン不足・欠乏による減数分裂異常には、脂肪酸合成量の低下およびミトコンドリア機能の低下によるエネルギー不足が要因の一つであることが示唆された。, rm:published_papers;rm:presentations
  • 若手研究助成金, Apr. 2019, Mar. 2020, Principal investigator, 食成分が卵子の質におよぼす影響, 日本栄養・食糧学会
  • 栄養状態の統合的理解, 0, 0, 0, Competitive research funding
  • 卵子の質と栄養素の関係に関する研究, 0, 0, 0, Competitive research funding

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