Dyslipidemia is a protective factor in amyotrophic lateral sclerosis

Goldstein, Mark R.; Mascitelli, Luca; Pezzetta, Francesca

doi:10.1212/01.wnl.0000285080.70324.27

Cited by 480 publications

(429 citation statements)

References 26 publications

Supporting

Mentioning

384

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, with the limitation period between 25-35% of total energy intake, and nutritional recommendations dont involve replacing dairy products by skimmed and whole decrease in consumption of food of animal origin. Dupuis et al 46 observed that dyslipidemia plays a protective factor for disease progression over 12 months in the survival of such patients. Suggested treatments to control dyslipidemia may meddle in ALS progression.…”

Section: Important Clinical Characteristicsmentioning

confidence: 99%

Nutritional care in motor neurone disease/ amyotrophic lateral sclerosis

Salvioni

Stanich

Almeida

et al. 2014

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

Patients with amyotrophic lateral sclerosis (ALS) often present changes in nutritional status. Based on weight loss and on difficulty in nutritional management, this study aims to review the different possibilities and to present guidelines concerning nutritional treatment to such patients. Diet characteristics, types of treatment and nutritional therapy indicating administration routes and discussing the details of the disease are described herein. Nutritional therapy has been a substantial therapeutic resource for ALS development.

show abstract

Section: Important Clinical Characteristicsmentioning

confidence: 99%

Nutritional care in motor neurone disease/ amyotrophic lateral sclerosis

Salvioni

Stanich

Almeida

et al. 2014

Arq. Neuro-Psiquiatr.

View full text Add to dashboard Cite

show abstract

“…Furthermore, SOD1 G93A and SOD1 G86R mice show a decrease in body weight and fat mass during disease progression, reduced levels of circulating triglycerides, and evidence of increased lipolysis (Dodge et al 2013, Kim et al 2011a, Fergani et al 2007, Dupuis et al 2004. ALS patients also exhibit higher resting levels of energy expenditure, weight loss, a hypermetabolic phenotype and increased lipolysis (Kasarskis et al 1996, Desport et al 2005, Dupuis et al 2008, Bouteloup et al 2009, Funalot et al 2009, Dodge et al 2013. Hence, there is growing evidence for decreased glucose utilisation and metabolic re-programming in…”

Section: Introductionmentioning

confidence: 99%

“Preconditioning” with latrepirdine, an adenosine 5′-monophosphate-activated protein kinase activator, delays amyotrophic lateral sclerosis progression in SOD1G93A mice

Coughlan

Mitchem

Hogg

et al. 2015

Neurobiology of Aging

View full text Add to dashboard Cite

“…Lipid metabolism was described as deeply involved in ALS pathophysiology [52,53]. In particular, several studies reported hyperlipidemia in patients with ALS [53][54][55][56][57], with a potential link with patient survival [53].…”

Section: Moderate Effect On Metabolismmentioning

confidence: 99%

Combined Metabolomics and Transcriptomics Approaches to Assess the IL-6 Blockade as a Therapeutic of ALS: Deleterious Alteration of Lipid Metabolism

et al. 2016

View full text Add to dashboard Cite

In amyotrophic lateral sclerosis (ALS), motor neuron degeneration occurs simultaneously with systemic metabolic impairment and neuroinflammation. Playing an important role in the regulation of both phenomena, interleukin (IL)-6, a major cytokine of the inflammatory response has been proposed as a target for management of ALS. Although a pilot clinical trial provided promising results in humans, another recent preclinical study showed that knocking out the IL-6 gene in mice carrying ALS did not improve clinical outcome. In this study, we aimed to determine the relevance of the IL-6 pathway blockade in a mouse model of ALS by using a pharmacological antagonist of IL-6, a murine surrogate of tocilizumab, namely MR16-1. We analyzed the immunological and metabolic effects of IL-6 blockade by cytokine measurement, blood cell immunophenotyping, targeted metabolomics, and transcriptomics. A deleterious clinical effect of MR16-1 was revealed, with a speeding up of weight loss (p = 0.0041) and decreasing body weight (p < 0.05). A significant increase in regulatory T-cell count (p = 0.0268) and a decrease in C-X-C ligand-1 concentrations in plasma (p = 0.0479) were observed. Metabolomic and transcriptomic analyses revealed that MR16-1 mainly affected branchedchain amino acid, lipid, arginine, and proline metabolism. IL-6 blockade negatively affected body weight, despite a moderated anti-inflammatory effect. Metabolic effects of IL-6 were mild compared with metabolic disturbances observed in ALS, but a modification of lipid metabolism by

show abstract

Dyslipidemia is a protective factor in amyotrophic lateral sclerosis

Cited by 480 publications

References 26 publications

Nutritional care in motor neurone disease/ amyotrophic lateral sclerosis

Nutritional care in motor neurone disease/ amyotrophic lateral sclerosis

“Preconditioning” with latrepirdine, an adenosine 5′-monophosphate-activated protein kinase activator, delays amyotrophic lateral sclerosis progression in SOD1G93A mice

Combined Metabolomics and Transcriptomics Approaches to Assess the IL-6 Blockade as a Therapeutic of ALS: Deleterious Alteration of Lipid Metabolism

Contact Info

Product

Resources

About