Mechanisms of carnosine-induced activation of neuronal cells

Yamashita, Shuntaro; Sato, Marc; Mutoh, T.; Kadooka, Keishi; Hasegawa, Takanori; Fujimura, Tadao; Katakura, Yoshinori

doi:10.1080/09168451.2017.1413325

Cited by 28 publications

(20 citation statements)

References 15 publications

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“…Zinc deficiency induces depression, irritability, and mood lability, 60 with zinc supplementation improving these symptoms. l -Carnosine induces glial cells to secrete neurotrophins that activate neuronal cells, 61 and can inhibit monoamine oxidase in the brain, 62 indicating its potential for mood improvement. l -Carnosine also ameliorates amygdaloid-kindled seizures via its histaminergic action, 63 which could be beneficial for inhibiting trauma-related fear memory that occurs in binge eating patients.…”

Section: Discussionmentioning

confidence: 99%

Polaprezinc (Zinc–l-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions

Sakae

Suka

Yanagisawa

2020

J Clin Psychopharmacol

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Background Zinc plays an important role in appetite regulation. l -Carnosine, an endogenous dipeptide, may also regulate eating behavior via its histaminergic and antiglutamatergic properties. Polaprezinc (zinc– l -carnosine complex) is a medication for gastric ulcers. A small case series reported successful treatment of binge eating with add-on polaprezinc. Methods This was an open trial of add-on polaprezinc in patients with binge eating disorder (BED; n = 22) or bulimia nervosa (BN; n = 7) receiving antidepressants. A 4-week baseline period was followed by a 16-week polaprezinc treatment at 150 mg/d (containing 34 mg zinc and 116 mg l -carnosine) in addition to ongoing psychotropic medications. We also assessed their zinc status via a laboratory index and zinc deficiency–related symptoms. Results At the study end, both conditions showed a significant reduction in the 4-week frequency of combined objective and subjective binge eating episodes, the 4-week frequency of days when at least 1 such episode occurred (only in BED), several aspects of eating disorder psychopathology (rated by the Eating Disorder Examination–Questionnaire), and comorbid depressive symptoms (rated by the 16-item Quick Inventory of Depressive Symptomatology [Self-Report]). Serum copper/zinc ratio decreased from 1.4 to 1.1 on average in both conditions. All patients had multiple zinc deficiency–related symptoms at baseline that substantially improved after polaprezinc treatment. Overall, the effectiveness of polaprezinc was greater in BED patients than in BN patients, with minor adverse effects. Conclusions These findings offer preliminary evidence for the effectiveness of polaprezinc in treating BED and BN and suggest the involvement of zinc deficiency in these conditions.

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Section: Discussionmentioning

confidence: 99%

Polaprezinc (Zinc–l-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions

Sakae

Suka

Yanagisawa

2020

J Clin Psychopharmacol

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“…Interestingly, Yamashita et al . () demonstrated that carnosine permeates the BBB and activates glial cells within the brain, causing them to secrete neurotrophins such as BDNF and NGF.…”

Section: Food Protein‐derived Peptides For Preventing Cognitive Declinementioning

confidence: 97%

“…Further evidence suggests that carnosine functions as a molecular chaperone and as an inducer of antioxidant systems in oxidative stress conditions (Bellia et al, 2015). Interestingly, Yamashita et al (2018) demonstrated that carnosine permeates the BBB and activates glial cells within the brain, causing them to secrete neurotrophins such as BDNF and NGF.…”

Section: Healthy Cognitive Function Cognitive Declinementioning

confidence: 99%

Emerging roles of bioactive peptides on brain health promotion

Katayama

Nakamura

2018

Int J of Food Sci Tech

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Summary Cognitive dysfunction is a major debilitating age‐related disorder. Natural dietary bioactive compounds with potential neuroprotective and brain health benefits, including the prevention of cognitive impairment and dementia, have received increasing attention. Because cognitive decline is thought to result from dysfunctional synaptic plasticity, the induction of neuroprotective proteins, including neurotrophic factors, protein chaperones, and antioxidant enzymes, by dietary bioactive compounds may help prevent age‐related cognitive decline. Phytochemicals and bioactive peptides have been demonstrated to have a preventive effect on cognitive decline in different animal models and in human studies. This review focuses on the in vivo effects of bioactive peptides on brain function and the expression of neuroprotective factors.

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“…Moreover, carnosine has anti-oxidative capacity against agents increasing ROS [28]. Another neuroprotective action of carnosine includes its attenuation of neurotoxicity induced by NMDA [29], beta amyloid, and inducible nitric oxide synthase [30] as well as increased trophic factors expression [31] (Figure 1). The effects of carnosine were reversed by inhibiting histidine decarboxylase (HDC) as well as histamine H 1 and H 3 antagonists, which suggests that carnosine’s neuroprotective mechanisms include not only the carnosine-histidine-histamine pathway, but also H 1 and H 3 receptors [29].…”

Section: Proposed Mechanisms Mediating the Role Of Carnosine In Thmentioning

confidence: 99%

The Potential of Carnosine in Brain-Related Disorders: A Comprehensive Review of Current Evidence

Schön

Mousa²,

Berk

et al. 2019

Nutrients

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Neurological, neurodegenerative, and psychiatric disorders represent a serious burden because of their increasing prevalence, risk of disability, and the lack of effective causal/disease-modifying treatments. There is a growing body of evidence indicating potentially favourable effects of carnosine, which is an over-the-counter food supplement, in peripheral tissues. Although most studies to date have focused on the role of carnosine in metabolic and cardiovascular disorders, the physiological presence of this di-peptide and its analogues in the brain together with their ability to cross the blood-brain barrier as well as evidence from in vitro, animal, and human studies suggest carnosine as a promising therapeutic target in brain disorders. In this review, we aim to provide a comprehensive overview of the role of carnosine in neurological, neurodevelopmental, neurodegenerative, and psychiatric disorders, summarizing current evidence from cell, animal, and human cross-sectional, longitudinal studies, and randomized controlled trials.

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Mechanisms of carnosine-induced activation of neuronal cells

Cited by 28 publications

References 15 publications

Polaprezinc (Zinc–l-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions

Polaprezinc (Zinc–l-Carnosine Complex) as an Add-on Therapy for Binge Eating Disorder and Bulimia Nervosa, and the Possible Involvement of Zinc Deficiency in These Conditions

Emerging roles of bioactive peptides on brain health promotion

The Potential of Carnosine in Brain-Related Disorders: A Comprehensive Review of Current Evidence

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