Diet

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Petr75
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Re: Diet

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2021 Aug 21
Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
The association between dietary total antioxidant capacity and NMO-IgG seropositivity in patients with neuromyelitis optica spectrum disorder
https://pubmed.ncbi.nlm.nih.gov/34461362/

Abstract

Objectives: There is growing evidence highlighting the role of environmental risk factors of NMO-IgG seropositivity in patients with neuromyelitis optica spectrum disorder (NMOSD). The present study investigated the possible association between dietary total antioxidant capacity (TAC) and NMO-IgG seropositivity in NMOSD patients.

Methods: Fifty-six patients with a definite diagnosis of NMOSD were included in the study. Data on patients' age, gender, height, weight, cigarette smoking status, and alcohol consumption were collected and recorded. Body mass index (BMI) was also calculated. In addition, dietary habits of patients were evaluated using an adjusted semi-quantitative food frequency questionnaire (FFQ) that consists of 168 food items. Dietary TAC was calculated using the oxygen radical absorption capacity (ORAC) method. Enzyme-linked immunosorbent assay (ELISA) method was used to determine the NMO-IgG serum status. The association between dietary TAC and odds of NMO-IgG seropositivity was measured using the logistic regression analysis.

Results: The mean of dietary TAC was 8362.8 (μmolTE/1000 kcal) in seronegative patients and 6609.9 (μmolTE/1000 kcal) in seropositive patients and had a significant difference between the mentioned groups of patients (P: 0.02). An inverse association was found between dietary TAC and odds of NMO-IgG seropositivity in all three regression models. The higher dietary intake of antioxidant resulted in significant findings as follows: 92% (95% CI: 0.01-0.53), 97% (95% CI: 0.00-0.34), and 97% (95% CI: 0.00-0.32) lower odds of NMO-IgG seropositivity in the fourth quartiles of the first, the second, and the third regression model, respectively. Moreover, the inverse association between fruit intake and odds of NMO-IgG seropositivity was significant in the third quartile (OR:0.10; 95%CI: 0.01-0.97).

Conclusion: The present study indicated a significant inverse association between dietary TAC and NMO-IgG seropositivity of NMOSD patients. As no definite treatment can be offered for NMOSD and nutrition is a modifiable factor in this regard, specification of dietary factors affecting the risk of NMOSD is of great value.
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Petr75
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Re: Diet

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2021 Sep 7
Department of Physical Medicine and Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, USA
Critical Role of Astrocyte NAD + Glycohydrolase in Myelin Injury and Regeneration
https://pubmed.ncbi.nlm.nih.gov/34493542/


Abstract

Western-style diets cause disruptions in myelinating cells and astrocytes within the mouse central nervous system (CNS). CD38 shows increased expression in the cuprizone and experimental autoimmune encephalomyelitis models of demyelination; in addition, CD38 is the main nicotinamide adenine dinucleotide (NAD+)-depleting enzyme in the CNS. Altered NAD+ metabolism is linked to both high fat consumption and multiple sclerosis (MS). Here, we identify increased CD38 expression in the male mouse spinal cord following chronic high fat consumption, after focal toxin (lysolecithin[LL])-mediated demyelinating injury and in reactive astrocytes within active MS lesions. We demonstrate that CD38-catalytically inactive mice are substantially protected from high fat-induced NAD+ depletion, oligodendrocyte loss, oxidative damage, and astrogliosis. A CD38 inhibitor, 78c, increased NAD+ and attenuated neuroinflammatory changes induced by saturated fat applied to astrocyte cultures. Conditioned media from saturated fat-exposed astrocytes applied to oligodendrocyte cultures impaired myelin protein production, suggesting astrocyte-driven indirect mechanisms of oligodendrogliopathy. In cerebellar organotypic slice cultures subject to LL demyelination, saturated fat impaired signs of remyelination effects that were mitigated by concomitant 78c treatment. Significantly, oral 78c increased counts of oligodendrocytes and remyelinated axons after focal LL-induced spinal cord demyelination. Using a Ribotag approach, we identified a unique in vivo brain astrocyte translatome profile induced by 78c-mediated CD38 inhibition in mice, including decreased expression of pro-inflammatory astrocyte markers and increased growth factors. Our findings suggest high fat diet impairs oligodendrocyte survival and differentiation through astrocyte-linked mechanisms mediated by the NAD+ase CD38 and highlight CD38 inhibitors as potential therapeutic candidates to improve myelin regeneration.SIGNIFICANCE STATEMENTMyelin disturbances and oligodendrocyte loss can leave axons vulnerable leading to permanent neurologic deficits. The results of this study suggest that metabolic disturbances, triggered by consumption of a diet high in fat, promote oligodendrogliopathy and impair myelin regeneration through astrocyte-linked indirect NAD+-dependent mechanisms. We demonstrate that restoring nicotinamide adenine dinucleotide (NAD+) levels via genetic inactivation of CD38 can overcome these effects. Moreover, we show that therapeutic inactivation of CD38 can enhance myelin regeneration. Together, these findings point to a new metabolic targeting strategy positioned to improve disease course in multiple sclerosis and other conditions in which the integrity of myelin is a key concern.
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Petr75
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Re: Diet

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2021 Sep 10
Department of Clinical Biochemistry, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
Carbohydrate and lipid metabolism in multiple sclerosis: Clinical implications for etiology, pathogenesis, diagnosis, prognosis, and therapy
https://pubmed.ncbi.nlm.nih.gov/34517010/

Abstract

Multiple sclerosis (MS) is a complicated autoimmune disease characterized by inflammatory and demyelinating events in the central nervous system. The exact etiology and pathogenesis of MS have not been elucidated. However, a set of metabolic changes and their effects on immune cells and neural functions have been explained. This review highlights the contribution of carbohydrates and lipids metabolism to the etiology and pathogenesis of MS. Then, we have proposed a hypothetical relationship between such metabolic changes and the immune system in patients with MS. Finally, the potential clinical implications of these metabolic changes in diagnosis, prognosis, and discovering therapeutic targets have been discussed. It is concluded that research on the pathophysiological alterations of carbohydrate and lipid metabolism may be a potential strategy for paving the way toward MS treatment.
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Petr75
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Re: Diet

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2021 Nov
Department of Food Science and Engineering, Ningbo University, China
Department of Food Science, Rutgers, the State University of New Jersey, USA
Polysaccharides confer benefits in immune regulation and multiple sclerosis by interacting with gut microbiota
https://pubmed.ncbi.nlm.nih.gov/34600677/

Abstract

Pharmacological and clinical studies have consistently demonstrated that polysaccharides exhibit great potential on immune regulation. Polysaccharides can interact directly or indirectly with the immune system, triggering cell-cell communication and molecular recognition, leading to immunostimulatory responses. Gut microbiota is adept at foraging polysaccharides as energy sources and confers benefits in the context of immunity and chronic autoimmune disease, such as multiple sclerosis. A compelling set of interconnectedness between the gut microbiota, natural polysaccharides, and immune regulation has emerged. In this review, we highlighted the available avenues supporting the existence of these interactions, with a focus on cytokines-mediated and SCFAs-mediated pathways. Additionally, the neuroimmune mechanisms for gut microbiota communication with the brain in multiple sclerosis are also discussed, which will lay the ground for ameliorate multiple sclerosis via polysaccharide intervention.
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Petr75
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Re: Diet

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Petr75 wrote: Fri Dec 18, 2020 12:48 am 2020 Nov 27
Department of Anatomical Sciences, Faculty of Medicine, AJA University of Medical Sciences, Tehran, Iran
Coenzyme Q10 enhances remyelination and regulate inflammation effects of cuprizone in corpus callosum of chronic model of multiple sclerosis
https://pubmed.ncbi.nlm.nih.gov/33245472/

Abstract

Multiple Sclerosis (MS) is .....
2021 Dec 30
Institute of Physiology Czech Academy of Sciences, Prague, Czech Republic
Coenzyme Q10 effects in neurological diseases

https://pubmed.ncbi.nlm.nih.gov/35199552/


Abstract

Coenzyme Q10 (CoQ10), a lipophilic substituted benzoquinone, is present in animal and plant cells. It is endogenously synthetized in every cell and involved in a variety of cellular processes. CoQ10 is an obligatory component of the respiratory chain in inner mitochondrial membrane. In addition, the presence of CoQ10 in all cellular membranes and in blood. It is the only endogenous lipid antioxidant. Moreover, it is an essential factor for uncoupling protein and controls the permeability transition pore in mitochondria. It also participates in extramitochondrial electron transport and controls membrane physicochemical properties. CoQ10 effects on gene expression might affect the overall metabolism. Primary changes in the energetic and antioxidant functions can explain its remedial effects. CoQ10 supplementation is safe and well-tolerated, even at high doses. CoQ10 does not cause any serious adverse effects in humans or experimental animals. New preparations of CoQ10 that are less hydrophobic and structural derivatives, like idebenone and MitoQ, are being developed to increase absorption and tissue distribution. The review aims to summarize clinical and experimental effects of CoQ10 supplementations in some neurological diseases such as migraine, Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, Friedreich’s ataxia or multiple sclerosis. Cardiovascular hypertension was included because of its central mechanisms controlling blood pressure in the brainstem rostral ventrolateral medulla and hypothalamic paraventricular nucleus. In conclusion, it seems reasonable to recommend CoQ10 as adjunct to conventional therapy in some cases. However, sometimes CoQ10 supplementations are more efficient in animal models of diseases than in human patients (e.g. Parkinson’s disease) or rather vague (e.g. Friedreich’s ataxia or amyotrophic lateral sclerosis).

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