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Glutamine is a type of non-essential xognitive acid functoin is naturally produced Glutamine and cognitive function Glutamime human body. It is Glutamine and cognitive function mostly in the skeletal anx and circulates through the Certified Humane Animal Welfare to perform cognitivee activities.
Glutamines supply fuel to the brain, Glutaminw lining, muscles,and most importantly, to the white cognltive cells.
Glutamine is an essential component to maintain a healthy cogniitive and mind. Funciton given is a qnd of Glutamine benefits Homemade versions of favorite snacks. There are cogbitive uses of Glutamine that we will discuss in the next sections.
Several research and clinical studies have revealed that functioj can cure sexual dysfunction. By providing energy Glutamune the brain, it functiion alertness and works as a Energy boost supplements stimulant.
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Glutamine uses expand to the athletics domain as it is a common ingredient in the formulation of sports drinks, protein shakes, and nutritional energy bars due to its energy-boosting property.
As we explored multiple uses of glutamine in the medical and sports field, we should also discuss the precautions regarding the consumption of glutamine. Uncontrolled and self-prescribed consumption of glutamine supplement should be strictly avoided.
Glutamine is naturally produced in our bodies and the essential amino acids can be easily found in dairy products, fish, meat, and nuts. So, if you maintain a balanced diet with a sufficient intake of amino acids and nutrients from daily consumption of foods, there is no need to take supplements.
However, glutamine supplements are prescribed in critical care where the patient is bedridden and unable to extract sufficient nutrients from food. Also, athletes are often recommended glutamine supplements to prevent injuries and weaknesses during rigorous training sessions.
Glutamines are best to consume by mixing them with protein shakes. People with chronic kidney and liver ailments are not recommended to use these supplements. Also, lactating mothers and pregnant women should avoid glutamine completely. Unsupervised consumption of Glutamine supplements may cause serious ill effects.
To avoid any undesired consequences, one must consult a medical expert. Taking into consideration all the benefits that glutamines offer, it is advised to seek expert advice over self-prescription. Consult with a medical practitioner or a nutritionist to examine your medical history, lifestyle, and purpose to determine if glutamine is beneficial to your health.
He can also recommend the best dosage and composition for optimum gains. Thanks for subscribing! This email has been registered! Skip to content. Genetic Life. Close Sidebar. Recent Post Is Grass-Fed Whey Protein Right For You?
Creatine: Essential Factors to Consider Before Taking 29 December Add to wishlist Add to wishlist. Bio Whey UMF Whey Protein Powder. Regular price From Rs. Regular price Rs. Choose Options. Mass Attack Superior Mass Gainer. GENETIC NUTRITION MASS ATTACK: Mass Attack is the ultimate weight gain and muscle-building formula.
With over calories per serving and 28g of protein to support muscle recovery, Mass Attack is a Hi-Calorie, Hi-Protein formula that makes the ideal post-workout and between-meals shake for Glutamine and Mental Performance: Enhancing Focus and Cognitive Function by SEO DIGITAL 01 Sep Glutamine — what it means?
Glutamine — Benefits Glutamine is an essential component to maintain a healthy body and mind. Below given is a list of Glutamine benefits briefly: Glutamine helps in the cell division of white blood cells. It has healing properties and in the absence of enough glutamine in our body, wound healing takes longer.
Glutamine plays a vital role in fighting infections and boosts immunity. Most hospitals opt for glutamine to cure infectious diseases.
It can cure peptic ulcers, mouth ulcers, muscle strains, joint pains, and side effects from chemotherapy in cancer patients. Athletes trust L Glutamine supplements to prevent the effects of strenuous physical training sessions. It improves performance and makes post-workout recovery faster.
It also has bodybuilding properties for increased muscle mass and strength. Some reports have proven glutamine usage to be effective in anti-aging treatment. It is also a safe alternative to steroids in stimulating testosterone levels when applied in an injectable form.
Other Glutamine uses — treating mental disorders Several research and clinical studies have revealed that glutamine can cure sexual dysfunction. Dosage and Recommendations As we explored multiple uses of glutamine in the medical and sports field, we should also discuss the precautions regarding the consumption of glutamine.
When you should avoid glutamines Glutamines are best to consume by mixing them with protein shakes. Concluding Remarks Taking into consideration all the benefits that glutamines offer, it is advised to seek expert advice over self-prescription.
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: Glutamine and cognitive function| The Health Benefits of Glutamine | There are more uses of Glutamine that we will discuss in the next sections. Several research and clinical studies have revealed that glutamine can cure sexual dysfunction. By providing energy to the brain, it increases alertness and works as a brain stimulant. People suffering from neural disorders and cognitive disabilities are prescribed glutamine supplements as it helps treat these conditions. GABA, a neurotransmitter made from Glutamine helps treat several mental disorders by making the brain more alert and responsive to external stimuli. It helps reduce anxiety and induce calmness among the patients. Glutamine uses expand to the athletics domain as it is a common ingredient in the formulation of sports drinks, protein shakes, and nutritional energy bars due to its energy-boosting property. As we explored multiple uses of glutamine in the medical and sports field, we should also discuss the precautions regarding the consumption of glutamine. Uncontrolled and self-prescribed consumption of glutamine supplement should be strictly avoided. Glutamine is naturally produced in our bodies and the essential amino acids can be easily found in dairy products, fish, meat, and nuts. So, if you maintain a balanced diet with a sufficient intake of amino acids and nutrients from daily consumption of foods, there is no need to take supplements. However, glutamine supplements are prescribed in critical care where the patient is bedridden and unable to extract sufficient nutrients from food. Also, athletes are often recommended glutamine supplements to prevent injuries and weaknesses during rigorous training sessions. Glutamines are best to consume by mixing them with protein shakes. People with chronic kidney and liver ailments are not recommended to use these supplements. Also, lactating mothers and pregnant women should avoid glutamine completely. Unsupervised consumption of Glutamine supplements may cause serious ill effects. To avoid any undesired consequences, one must consult a medical expert. Taking into consideration all the benefits that glutamines offer, it is advised to seek expert advice over self-prescription. Consult with a medical practitioner or a nutritionist to examine your medical history, lifestyle, and purpose to determine if glutamine is beneficial to your health. He can also recommend the best dosage and composition for optimum gains. Thanks for subscribing! This email has been registered! Skip to content. Genetic Life. Close Sidebar. Recent Post Is Grass-Fed Whey Protein Right For You? Creatine: Essential Factors to Consider Before Taking 29 December Add to wishlist Add to wishlist. Bio Whey UMF Whey Protein Powder. Regular price From Rs. Regular price Rs. Choose Options. Mass Attack Superior Mass Gainer. GENETIC NUTRITION MASS ATTACK: Mass Attack is the ultimate weight gain and muscle-building formula. With over calories per serving and 28g of protein to support muscle recovery, Mass Attack is a Hi-Calorie, Hi-Protein formula that makes the ideal post-workout and between-meals shake for Glutamine and Mental Performance: Enhancing Focus and Cognitive Function by SEO DIGITAL 01 Sep Glutamine — what it means? Glutamine — Benefits Glutamine is an essential component to maintain a healthy body and mind. Below given is a list of Glutamine benefits briefly: Glutamine helps in the cell division of white blood cells. It has healing properties and in the absence of enough glutamine in our body, wound healing takes longer. Glutamine plays a vital role in fighting infections and boosts immunity. Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer's disease. Neurochem Int. Dong XX, Wang Y, Qin ZH. Molecular mechanisms of excitotoxicity and their relevance to pathogenesis of neurodegenerative diseases. Acta Pharmacol Sin. Paula-Lima AC, Brito-Moreira J, Ferreira ST. Deregulation of excitatory neurotransmission underlying synapse failure in Alzheimer's disease. J Neurochem. Wang R, Reddy PH. Role of glutamate and NMDA receptors in Alzheimer's disease. J Alzheimers Dis. Lipton SA. The molecular basis of memantine action in Alzheimer's disease and other neurologic disorders: low-affinity, uncompetitive antagonism. Curr Alzheimer Res. McKeage K. Memantine: a review of its use in moderate to severe Alzheimer's disease. CNS Drugs — Berman RM, Cappiello A, Anand A, Oren DA, Heninger GR, Charney DS, et al. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry —4. Zarate CA Jr, Singh JB, Carlson PJ, Brutsche NE, Ameli R, Luckenbaugh DA, et al. A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Arch Gen Psychiatry — Bak LK, Schousboe A, Waagepetersen HS. Walton HS, Dodd PR. Glutamate-glutamine cycling in Alzheimer's disease. Pomara N, Singh R, Deptula D, Chou JC, Schwartz MB, LeWitt PA. Glutamate and other CSF amino acids in Alzheimer's disease. Am J Psychiatry —4. Jimenez-Jimenez FJ, Molina JA, Gomez P, Vargas C, de Bustos F, Benito-Leon J, et al. Neurotransmitter amino acids in cerebrospinal fluid of patients with Alzheimer's disease. J Neural Transm. CrossRef Full Text Google Scholar. Kaiser E, Schoenknecht P, Kassner S, Hildebrandt W, Kinscherf R, Schroeder J. Cerebrospinal fluid concentrations of functionally important amino acids and metabolic compounds in patients with mild cognitive impairment and Alzheimer's disease. Neurodegener Dis. Tohgi H, Abe T, Takahashi S, Kimura M. A selective reduction of excitatory amino acids in cerebrospinal fluid of patients with Alzheimer type dementia compared with vascular dementia of the Binswanger type. Neurosci Lett. Martinez M, Frank A, Diez-Tejedor E, Hernanz A. Amino acid concentrations in cerebrospinal fluid and serum in Alzheimer's disease and vascular dementia. J Neural Transm Park Dis Dement Sect. Smith CC, Bowen DM, Francis PT, Snowden JS, Neary D. Putative amino acid transmitters in lumbar cerebrospinal fluid of patients with histologically verified Alzheimer's dementia. J Neurol Neurosurg Psychiatry — Degrell I, Hellsing K, Nagy E, Niklasson F. Amino acid concentrations in cerebrospinal fluid in presenile and senile dementia of Alzheimer type and multi-infarct dementia. Arch Gerontol Geriatr. D'Aniello A, Fisher G, Migliaccio N, Cammisa G, D'Aniello E, Spinelli P. Amino acids and transaminases activity in ventricular CSF and in brain of normal and Alzheimer patients. Procter AW, Palmer AM, Francis PT, Lowe SL, Neary D, Murphy E, et al. Evidence of glutamatergic denervation and possible abnormal metabolism in Alzheimer's disease. Levine J, Panchalingam K, Rapoport A, Gershon S, McClure RJ, Pettegrew JW. Increased cerebrospinal fluid glutamine levels in depressed patients. Biol Psychiatry — Frye MA, Tsai GE, Huggins T, Coyle JT, Post RM. Low cerebrospinal fluid glutamate and glycine in refractory affective disorder. Garakani A, Martinez JM, Yehuda R, Gorman JM. Cerebrospinal fluid levels of glutamate and corticotropin releasing hormone in major depression before and after treatment. J Affect Disord. Hashimoto K, Bruno D, Nierenberg J, Marmar CR, Zetterberg H, Blennow K, et al. Abnormality in glutamine-glutamate cycle in the cerebrospinal fluid of cognitively intact elderly individuals with major depressive disorder: a 3-year follow-up study. Transl Psychiatry 6:e Hulstaert F, Blennow K, Ivanoiu A, Schoonderwaldt HC, Riemenschneider M, De Deyn PP, et al. Improved discrimination of AD patients using beta-amyloid and tau levels in CSF. Tabaraud F, Leman JP, Milor AM, Roussie JM, Barriere G, Tartary M, et al. Alzheimer CSF biomarkers in routine clinical setting. Acta Neurol Scand. Reis T, Brandao CO, Freire Coutinho ES, Engelhardt E, Laks J. Cerebrospinal fluid biomarkers in Alzheimer's disease and geriatric depression: preliminary findings from Brazil. CNS Neurosci Ther. Morris JC. The Clinical Dementia Rating CDR : current version and scoring rules. Neurology —4. Folstein MF, Folstein SE, McHugh PR. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorder , 4th ed. Washington, DC: American Psychiatric Association Hamilton M. A rating scale for depression. Moreno DH, Moreno RA, Calil HM. A Brazilian experience of treatment-resistant depression. In Clin Psychopharmacol. Maier W, Philipp M. Comparative analysis of observer depression scales. Acta Psychiatr Scand. Mental Behavioral and Developmental Disorders. In International Statistical Classification of Diseases. Geneva: WHO Hashimoto A, Nishikawa T, Oka T, Takahashi K, Hayashi T. Determination of free amino acid enantiomers in rat brain and serum by high-performance liquid chromatography after derivatization with N-tert-butyloxycarbonyl-L-cysteine and o-phthaldialdehyde. J Chromatogr. Calcia MA, Madeira C, Alheira FV, Silva TC, Tannos FM, Vargas-Lopes C, et al. Plasma levels of D-serine in Brazilian individuals with schizophrenia. Schizophr Res. Madeira C, Lourenco MV, Vargas-Lopes C, Suemoto CK, Brandão CO, Reis T, et al. D-serine levels in Alzheimer's disease: implications for novel biomarker development. Transl Psychiatry 5:e Hashimoto K, Malchow B, Falkai P, Schmitt A. Glutamate modulators as potential therapeutic drugs in schizophrenia and affective disorders. Eur Arch Psychiatry Clin Neurosci. Kochhann R, Varela JS, Lisboa CS de M, Chaves MLF. The Mini Mental State Examination: Review of cutoff points adjusted for schooling in a large Southern Brazilian sample. Dement Neuropsychol. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Jack CR Jr, Albert MS, Knopman DS, McKhann GM, Sperling RA, Carrillo MC, et al. Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Alzheimers Dement. McKhann GM, Knopman DS, Chertkow H, Hyman BT, Jack CR, Jr. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease. Hurley LL, Tizabi Y. Neuroinflammation, neurodegeneration, and depression. Neurotox Res. Leonard BE. The concept of depression as a dysfunction of the immune system. Curr Immunol Rev. Hermida AP, McDonald WM, Steenland K, Levey A. The association between late-life depression, mild cognitive impairment and dementia: is inflammation the missing link? Expert Rev Neurother. Miller AH, Maletic V, Raison CL. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Niciu MJ, Ionescu DF, Richards EM, Zarate CA. Glutamate and its receptors in the pathophysiology and treatment of major depressive disorder. Miller AH, Raison CL. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nat Rev Immunol. Heser K, Tebarth F, Wiese B, Eisele M, Bickel H, Kohler M, et al. Age of major depression onset, depressive symptoms, and risk for subsequent dementia: results of the German Study on Ageing, Cognition, and Dementia in Primary Care Patients AgeCoDe. Riedel G, Platt B, Micheau J. Glutamate receptor function in learning and memory. Behav Brain Res. Machado-Vieira R, Salvadore G, Ibrahim LA, Diaz-Granados N, Zarate CA Jr. Targeting glutamatergic signaling for the development of novel therapeutics for mood disorders. Curr Pharm Des. Selkoe DJ. Alzheimer's disease. Cold Spring Harb Perspect Biol. Google Scholar. Ferreira ST, Lourenco MV, Oliveira MM, De Felice FG. Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's disease. Front Cell Neurosci. Brito-Moreira J, Paula-Lima AC, Bomfim TR, Oliveira FB, Sepulveda FJ, De Mello FG, et al. Abeta oligomers induce glutamate release from hippocampal neurons. Figueiredo CP, Clarke JR, Ledo JH, Ribeiro FC, Costa CV, Melo HM, et al. Memantine rescues transient cognitive impairment caused by high-molecular-weight aβ oligomers but not the persistent impairment induced by low-molecular-weight oligomers. Lourenco MV, Clarke JR, Frozza RL, Bomfim TR, Forny-Germano L, Batista AF, et al. TNF-α mediates PKR-dependent memory impairment and brain IRS-1 inhibition induced by Alzheimer's β-amyloid oligomers in mice and monkeys. Cell Metab. Keywords: Alzheimer's disease, depression, glutamate, glutamine, cerebrospinal fluid, innotest amyloid tau index. Citation: Madeira C, Vargas-Lopes C, Brandão CO, Reis T, Laks J, Panizzutti R and Ferreira ST Elevated Glutamate and Glutamine Levels in the Cerebrospinal Fluid of Patients With Probable Alzheimer's Disease and Depression. Psychiatry Received: 19 June ; Accepted: 17 October ; Published: 06 November Copyright © Madeira, Vargas-Lopes, Brandão, Reis, Laks, Panizzutti and Ferreira. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. br Sergio T. Ferreira, ferreira bioqmed. Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. Top bar navigation. About us About us. Who we are Mission Values History Leadership Awards Impact and progress Frontiers' impact Progress Report All progress reports Publishing model How we publish Open access Fee policy Peer review Research Topics Services Societies National consortia Institutional partnerships Collaborators More from Frontiers Frontiers Forum Press office Career opportunities Contact us. Sections Sections. About journal About journal. Article types Author guidelines Editor guidelines Publishing fees Submission checklist Contact editorial office. ORIGINAL RESEARCH article Front. Psychiatry , 06 November This article is part of the Research Topic Glutamate-Related Biomarkers for Neuropsychiatric Disorders View all 13 articles. Elevated Glutamate and Glutamine Levels in the Cerebrospinal Fluid of Patients With Probable Alzheimer's Disease and Depression. Introduction Epidemiological and clinical studies suggest an association between Alzheimer's disease AD and depression 1 , 2 , the latter being a risk factor for development of AD and other forms of dementia 3 — 5. Table 1. Characteristics of study subjects. a PubMed Abstract CrossRef Full Text Google Scholar. x PubMed Abstract CrossRef Full Text Google Scholar. Keywords: Alzheimer's disease, depression, glutamate, glutamine, cerebrospinal fluid, innotest amyloid tau index Citation: Madeira C, Vargas-Lopes C, Brandão CO, Reis T, Laks J, Panizzutti R and Ferreira ST Elevated Glutamate and Glutamine Levels in the Cerebrospinal Fluid of Patients With Probable Alzheimer's Disease and Depression. Edited by: Hsien-Yuan Lane , China Medical University, Taiwan. |
| Customer Section | CAS PubMed Google Scholar Kan MJ, et funcyion. Glutamine and cognitive function Res. Whether the qnd glutamine metabolism contributes to oxidative stress and therefore to the disease cogntiive Glutamine and cognitive function be directly supported by the present data Golf and Tennis Tips is the focus of future investigations. Strikingly, higher mitochondrial oxygen respiratory capacity in the NAc in male rodents is positively related to the capacity to win a social competition [ 5960 ]. Furthermore, we uncover dysregulation of the metabolic enzymes phosphate-activated glutaminase PAG and glutamate dehydrogenase human isoform 2 GDH2crucial regulators in brain glutamate-glutamine homeostasis, in FTD3 pathogenesis. Agostini F, Giolo G. |
| Background | Download references. Funxtion DIV9—11, neurons Probiotics for IBS Hormone-balancing detox diets with cognitivd medium with different concentrations of Glutamax. Unsupervised consumption of Glutamine fknction may cause Glutamine and cognitive function ill effects. We show that exquisitely sensitive glutamate-glutamine homeostasis is profoundly affected, implicating the functional involvement of PAG, GDH and GS in FTD3 pathology. Inducible presynaptic glutamine transport supports glutamatergic transmission at the calyx of Held synapse. PloS ONE ;4:e L-Glutamine and Hunger Pangs. |
| Glutamine Information | Mount Sinai - New York | Sign In Create Glutamine and cognitive function Account. Funftion J. Sequeira A, Glutamnie F, Ernst C, Vawter MP, Bunney WE, Lebel V, et al. Waagepetersen HS, Sonnewald U, Schousboe A. Excitotoxicity: bridge to various triggers in neurodegenerative disorders. |
Glutamine and cognitive function -
Our computational model-based analysis approach, which has been successful in elucidating internal behavioral variables of reward-based learning such as learning rates [ 42 ], exploration—explotation balance [ 30 ], discounting [ 43 ], episodic memory [ 29 ], effort [ 14 ], mood [ 44 ], social [ 45 ], and economic preferences [ 46 , 47 ] , allowed us here to provide key insights into the specific components of motivated performance that relate to accumbal metabolites.
We found that the Gln-to-Glu ratio is positively linked to stamina necessary to maintain performance over longer periods, whereas the competition context leads to substantially improved initial performance accompanied by a faster loss in stamina, and which was particularly pronounced in individuals with low resting Gln-to-Glu levels.
Importantly, our data suggests that Gln rather than Glu or GABA is the main contributor to the reported association between accumbal Gln-to-Glu ratio and endurance stamina ε end.
In addition, the nucleus accumbens receives GABAergic and glutamatergic projections from multiple brain regions [ 48 , 49 ]. Therefore, Glu and GABA concentrations measured in the NAc through 1 H-MRS represent pools of both accumbal and afferent neurons. Due to the more local nature of glial cells, Gln levels in our data primarily represent production by accumbal glial cells including astrocytes and oligodendrocytes [ 50 , 51 ].
Therefore, our findings point towards a key contribution of accumbal glial-derived Gln, and particularly the Gln-to-Glu ratio, on effortful endurance in motivated behavior. It is important to note that, in addition to its role in neurotransmitter production, Gln is also involved in mitochondrial oxidative phosphorylation and, consequently, cellular energy production [ 20 , 52 ].
Accordingly, high Gln concentrations might allow for enhanced GABA and Glu concentrations to be achieved via just-in-time synthesis during task performance [ 55 ], accommodating the behavioral requirements to succeed. Indeed, our results suggest that performance is not maintained via already present GABA or Glu pools, because neither resting-state GABA nor Glu predicted endurance performance.
In addition, high Gln concentrations may contribute to fuel mitochondrial function under enhanced NAc engagement during motivated and effortful behaviors, which are recognized accumbal putative actions [ 10 , 13 , 56 , 57 ].
In support of this hypothesis, work in rodents has shown that the capacity to remain on task for longer and to overcome greater effort costs is related to the magnitude of NAc oxygen responses to delivered rewards [ 58 ]. Oxygen consumption reflects mitochondrial respiration, a critical mitochondrial function and partial proxy for energy production in the form of ATP.
Strikingly, higher mitochondrial oxygen respiratory capacity in the NAc in male rodents is positively related to the capacity to win a social competition [ 59 , 60 ]. Therefore, our results relating accumbal Gln-to-Glu ratio to the capacity to exert motivated effort provide novel metabolic insights to this body of data.
One of the mechanisms whereby Gln-to-Glu ratio may contribute to differences in endurance and sprint stamina is the capacity of individuals with a high Gln-to-Glu ratio to overcome fatigue. Fatigue induced by prolonged active task engagement can have a negative impact on endurance performance.
In sports, for example, the psychobiological model of endurance performance states that effort perception plays a crucial role in explaining how fatigue reduces the willingness to perform [ 62 ] and negatively affects performance [ 61 ].
Recent accounts of human motivated performance emphasize the perception of effort as a crucial factor underlying motor endurance performance [ 63 ]. The inverse relationship that we found between Gln-to-Glu levels and effort perception may provide support for this account, especially in light of our decomposition of motivated performance into an early component that is boosted in low Gln-to-Glu individuals under competition as a sign of excessive effort and the stamina component, which is, subsequently, reduced in the same individuals.
Although, to the best of our knowledge, no previous study assessed NAc metabolism in the context of fatigue, substantial influence relates fatigue with reduced Gln in blood [ 64 ] and potentially also with alterations in Gln metabolism in the brain [ 65 ].
Oral glutamine supplementation has been reported to reduce subjective fatigue and ratings of perceived exertion during demanding tasks [ 66 , 67 ] and to increase striatal Gln levels [ 68 ]. At the neurobiological level, several mechanisms may account for the observed differences in Gln and Gln-to-Glu ratio, including differences in Gln production, metabolite catabolism and the availability of cellular transporters for Gln and Glu.
The nucleus accumbens has been implicated in anhedonia, reduced motivation, and decreased energy typically found in individuals with depression [ 69 ] and substantial data indicate alterations in these metabolic pathways and depression.
For example, reduced cortical density of glutamine synthetase-expressing astrocytes has been found in post mortem brains of major depression patients [ 50 ] and genetic variation in the gene coding for this enzyme associated with depression [ 70 ].
In addition, reduced levels in NAc Gln were reported in a rat model of stress-induced depression [ 44 ]. We also found that performance in our task was enhanced by social competition, in alignment with a reported facilitative role of competition in task performance [ 25 , 26 , 27 , 28 ].
Our computational model revealed that the facilitating effect of competition on the overall performance was mostly due to improvement in initial performance expressed through lower values of effort cost baseline b , which persisted despite lower values of sprint stamina ε spr , which manifested itself in poorer performance in later task sessions.
Furthermore, we found a significant interaction between competition context and Gln-to-Glu ratios in determining initial performance: the initial performance boost triggered by social competition was only observed for participants with a low Gln-to-Glu ratio.
Participants characterized by a high Gln-to-Glu ratio seemed to have superior task engagement from the onset of the task, which was not significantly boosted by competition.
This observation suggests a link between high accumbal Gln-to-Glu and self-motivated performance in effortful incentivized challenges. Finally, the associations between metabolites and performance were not observed in the occipital lobe, in agreement with reports indicating a lack of correspondence in Gln or Gln-to-Glu levels across different brain regions [ 71 ].
However, a note of caution should be added, as due to technical limitations, metabolites in the occipital lobe were acquired on a different day in a subsample of the participants. This implies that the power to detect a significant behavior—metabolite association in the occipital lobe was lower, and it would be important in future studies to verify the specificity of the reported associations for the NAc.
In this study, only males were included as our prediction for a link between accumbal metabolism and motivated performance was inspired in background studies involving male rodents [ 59 , 72 , 73 ].
Therefore, future studies are warranted to test whether our findings are generalized to the general population. Finally, although our approach allowed us to reveal important components of motivated performance, in the future it will be important to disentangle further aspects such as effort-related decision-making and vigor of response.
In conclusion, our results provide the first solid evidence for the role of accumbal metabolites—particularly the Gln-to-Glu ratio—in different components of effortful performance.
We envision that this approach and findings can help developing metabolism-targeting strategies to ameliorate deficits in motivated effort engagement. This work was supported by grants from the Swiss National Science Foundation CR20I; NCCR Synapsy grant number 51NF and intramural funding from the EPFL.
The authors declare no competing interests. Open Access funding provided by EPFL Lausanne. The data that support the findings of this study are available from the corresponding authors upon request.
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We have now extended these AD-related studies to a second neurodegenerative disease, ataxia-telangiectasia A-T.
The AD model we tested was the R1. These animals are a faithful genetic mimic of early-onset APP-driven dominantly inherited forms of human familial AD. Ataxia-telangiectasia is a recessive genetic condition of childhood neurodegenerative disease caused by mutations in the ATM gene.
It is a true multi-systemic disease, but the neurological symptoms are the most prevalent and the most debilitating. On the surface, AD and A-T seem like very differences diseases, but our research shows that glutamine has a positive impact on the phenotype of both.
This may be mediated through ATM, as we have recently discovered that AD patients often exhibit ATM deficiency, as seen through HDAC4 nuclear translocation in hippocampal neurons [ 35 ]. Our finding on the powerful neuroprotective effects of glutamine in mouse models in both AD and A-T suggests that its benefits are not disease specific, and may be extrapolated to other neurodegenerative disorders — even beyond AD and A-T.
Indeed, Rozas et al. Our discovery that glutamine and ATM interact to influence blood glucose, body weight and the phosphorylation of mTOR emphasizes that, beyond the DNA damage response, ATM has deep connections with the fundamental pathways of cellular metabolism.
This largely cytoplasmic function of ATM is increasingly recognized [ 30 , 37 — 39 ] and applies to energy metabolism in mitochondria as well. Indeed, A-T patients have an unusual form of diabetes [ 21 ], and present with irregularities in their glucose utilization [ 40 ].
A recent study also revealed that adult asymptomatic relatives of A-T patients who would be expected to carry a single mutated allele of ATM have decreased glucose metabolism in cerebellar vermis and hippocampus [ 22 ].
Additionally, we note that loss of retinoblastoma pRB results in reduced glucose utilization and enhanced susceptibility to oxidative stress.
Glutamine rescues these effects by providing an alternative to glucose oxidation and enhancing glutathione production [ 41 ]. The suggestion is that the effects of glutamine on ATM-deficient neurons that we report may share similarities with RB-deficient cells.
The findings by Rozas et. TSC2 is a potent mTOR suppressor and it is noteworthy that ATM activates TSC2 to repress mTOR complex1 in response to oxidative stress [ 30 ]. It is likely that part of this pathway passes through an ATM node, but the finding of Rozas suggest that passage through a TSC2 node is also possible.
Glutamine is not itself a neurotransmitter but it serves as an immediate precursor for glutamate and is only two steps removed from GABA.
It has been shown that presynaptic glutamine transport is involved in the maintenance of excitatory synaptic currents [ 42 ], and glutamine supplementation rescues the rapid synaptic GABA depletion induced by astrogliosis, thus restoring inhibitory synaptic currents in mouse CA1 neurons [ 25 ]. Given that ATM is involved in neuronal vesicle trafficking [ 16 ] and its concentrations are sensitive to the availability of glutamine Fig.
Several additional features of the LTP experiments deserve mention. First, because our measurements were made in isolated brain slices over a period of several hours, it would appear that the effects of glutamine are long-term in nature rather than reflecting short-term, moment-to-moment, changes in transmitters.
The recording medium, in which the slices were bathed during our measurements, contained only balanced salt solution and no added glutamine.
Therefore, the LTP differences must represent chronic changes that remain stable even after the extracellular environment of the synapse is changed. Second, RT-PCR results revealed a partial rescue of BDNF mRNA common exon and almost total restoration of exon 4 expression after glutamine supplementation 8 mM in KU-treated neurons Fig.
The expression data summarized in Fig. Examination of the pathways involved suggests that while glutamine conversion to glutamate is likely upregulated in A-T, the pathways leading beyond glutamate are reduced at least in brain. This would be predicted to deplete local glutamine stores, possibly at the expense of side pathways leading to asparagine and glucosamine Fig.
This decrease in side pathway products could have a multitude of negative effects. For example, decreased asparagine would be expected to be destructive. ASNS-deficiency leads to progressive cerebral atrophy and intellectual disability [ 43 ] and can cause severe neurological impairment without involvement of peripheral tissues.
Because of the poor transport of asparagine across the blood—brain barrier, the brain depends on local synthesis, suggesting that even a small block in its synthesis could have huge effects on brain function [ 44 ]. Glutamine is also an important precursor for de novo synthesis of arginine in humans [ 45 ].
Decreased GFPT expression predicts a lower glucosamine production in A-T brains. Glucosamine exerts a neuroprotective effect via suppression of inflammation through its ability to inhibit NFkB activation [ 47 ]; therefore, lower glucosamine would forecast higher NFkB activity in A-T brains.
Other changes predicted from the expression array data enhance the picture further. For example, α-ketoglutarate is a major metabolite that feeds directly into TCA cycle and its reduction would result in lower cellular energy.
Reduced GAD can lead to reduced GABA synthesis and decreased GABAergic transmission. Lastly, since GSS catalyzes the final step of glutathione production and its expression was significantly reduced in A-T, a situation of lower glutathione production with concomitant reduction in anti-oxidant defenses would be predicted.
Glutamine is known to support fast growing cells in culture and in tumor grafts [ 48 ]. Significantly lower plasma glutamine level has also been reported in breast cancer patients and in male gastrointestinal cancer patients [ 51 ].
Both human and animal studies suggest that glutamine can be given to breast cancer patients without stimulating tumor growth or metastasis.
Whatever the ultimate explanation, it would appear in the right clinical circumstances it is possible to take advantage of the ability of glutamine to improve brain function yet not hasten death due to cancer. We have shown previously that glutamine is neuroprotective in vitro and in mouse models of AD.
We have now extended these AD-related studies to A-T. Unlike AD, A-T is entirely a genetic disease, yet the epigenetic landscape of the chromatin is part of the realization of the phenotype. To the extent that the disease symptoms result in part from these epigenetic changes, it is reasonable to predict that environmental factors can alter the timing and perhaps the extent of various disease events.
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JPEN J Parenter Enteral Nutr. Download references. The authors thank Dr. Ping Xie for her help with plotting survival cure and statistics, Ms Li Deng and Dr.
Jay Tischfield for their support with real-time PCR. This work is supported by grants from the BrightFocus Foundation A, from NIH 1R01NS and from the Hong Kong Research Grants Council HKSAR GRF JC and KH designed the study. YC, JC, LL carried out the blood glutamine, glucose, body weight and life span studies and involved in the data analysis.
JC, YC, HC and YZ did the neuronal culture experiments RT-PCR, western blot and immunostaining and participated in data analysis. GV and MP carried out LTP recording experiments and data analysis. JL and RH performed the expression studies and data analysis. JC drafted the manuscript.
JC, KH, HC, RH and MP participated in the revision of the manuscript. All authors read and approved the manuscript. All animal procedures were approved by the Rutgers University Institutional Animal Care and Use Committee protocol 06— Department of Cell Biology and Neuroscience, Rutgers University, Allison Road, Piscataway, NJ, , USA.
Jianmin Chen, Yanping Chen, Graham Vail, Lauren Louie, Jiali Li, Ronald P. Hart, Mark R. Division of Life Science, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China. You can also search for this author in PubMed Google Scholar. Correspondence to Jianmin Chen. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.
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Search all BMC articles Search. Download PDF. Research article Open access Published: 18 August The impact of glutamine supplementation on the symptoms of ataxia-telangiectasia: a preclinical assessment Jianmin Chen ORCID: orcid.
Hart 1 , Mark R. Background Glutamine Gln or Q is the most abundant free amino acid in the human blood stream. Methods A-T mouse models For our A-T model, we chose the Atm tm1Awb mutant allele [ 13 ] and the Atm tm1Bal mutant allele [ 14 ] from The Jackson Laboratories.
Blood glucose and glutamine measurements About 0. Western blots and immunocytochemistry For western blot analysis, cultured neurons were lysed in RIPA buffer Thermo Scientific containing proteinase and phosphatase inhibitors Roche Diagnostics. RT PCR and real-time PCR Total RNA was purified using TRIzol reagent Life Technologies following the standard protocol.
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