Extra virgin olive oil intake delays the development of amyotrophic lateral sclerosis associated with reduced reticulum stress and autophagy in muscle of SOD1G93A mice

Oliván, Sara; Martínez‐Beamonte, Roberto; Calvo, Ana C.; Surra, Joaquín C.; Manzano, Raquel; Arnal, Carmen; Osta, Rosario; Osada, Jesús

doi:10.1016/j.jnutbio.2014.04.005

Cited by 38 publications

(29 citation statements)

References 38 publications

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“…In contrast, stimulation of the b-oxidation of fatty acids by L-carnitine ameliorated motor function and extended survival (57). Highly energetic diets, mainly in the form of elevated lipid content, also prolonged life expectancy, and improved muscle function and motor neuron survival (35, 76,86).…”

Section: Muscles Are a Primary Site For Therapeutic Interventionmentioning

confidence: 99%

The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis

et al. 2016

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Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset disease primarily characterized by upper and lower motor neuron degeneration, muscle wasting and paralysis. It is increasingly accepted that the pathological process leading to ALS is the result of multiple disease mechanisms that operate within motor neurons and other cell types both inside and outside the central nervous system. The implication of skeletal muscle has been the subject of a number of studies conducted on patients and related animal models. In this review, we describe the features of ALS muscle pathology and discuss on the contribution of muscle to the pathological process. We also give an overview of the therapeutic strategies proposed to alleviate muscle pathology or to deliver curative agents to motor neurons. ALS muscle mainly suffers from oxidative stress, mitochondrial dysfunction and bioenergetic disturbances. However, the way by which the disease affects different types of myofibers depends on their contractile and metabolic features. Although the implication of muscle in nourishing the degenerative process is still debated, there is compelling evidence suggesting that it may play a critical role. Detailed understanding of the muscle pathology in ALS could, therefore, lead to the identification of new therapeutic targets.

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Section: Muscles Are a Primary Site For Therapeutic Interventionmentioning

confidence: 99%

The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis

et al. 2016

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“…Besides, MS can enhance glucose‐regulated protein 78 kDa (grp78) expression, which is known to be a member of the heat shock protein (hsp) 70 family localized to the ER. [17b] Grp78 is reported to increase MRF expression . Ras homolog family member A (RhoA), which is known to enhance the expression MRFs, is also upregulated by MS …”

Section: Resultsmentioning

confidence: 99%

Thermosensitive, Stretchable, and Piezoelectric Substrate for Generation of Myogenic Cell Sheet Fragments from Human Mesenchymal Stem Cells for Skeletal Muscle Regeneration

Yoon

Misra

et al. 2017

Adv Funct Materials

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In a native muscle microenvironment, electrical and mechanical stimuli exist in the form of action potentials and muscle contraction. Here, a cell culture system is developed that can mimic the in vivo microenvironment and provide these stimuli to cultured cells, and it is tested whether the stimulation can promote myogenic differentiation of human umbilical cord blood mesenchymal stem cells (hUCBMSCs). A thermosensitive, stretchable, and piezoelectric substrate (TSPS) is fabricated by polydimethylsiloxane spin-coating of aligned ZnO nanorods and subsequent poly(N-isopropylacrylamide) grafting on the polydimethylsiloxane surface. Pulsatile mechanoelectrical cues are provided to hUCBMSCs cultured on the TSPS by subjecting the TSPS to cyclic stretching and bending, resulting in significant promotion of myogenic differentiation of hUCBMSCs as well as intracellular signaling related to the differentiation. After differentiation ex vivo, the cells are detached from the TSPS in the form of cell sheet fragments. Injection of the cell sheet fragments of differentiated cells into injured mouse skeletal muscle shows improved cell retention and muscle regeneration as compared to injection of either undifferentiated cells or differentiated dissociated cells. This system may serve as a tool for research on the electrical and mechanical regulation of stem cells and may be used to potentiate stem cell therapies.

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“…In SOD1 G93A mice, a high-fat diet (21% fat, 0.15% cholesterol) increased weight, survival and spinal cord motoneuron numbers while a calorie-restricted diet (60% of average ad libitum food intake) had the opposite effect compared to animals fed on a regular rodent chow (Zhao et al, 2015). Variable extents of improvement on lifespan and/or neuromuscular phenotype have also been reported in SOD1 G93A and SOD1 G86R mice on specific dietary regimens such as the Deanna protocol (Ari et al, 2014), a ketogenic diet (Zhao et al, 2006), extra virgin olive oil (Oliván et al, 2014), vitamin D3 (Gianforcaro and Hamadeh, 2012), a high calorie diet (Dupuis et al, 2004) and vitamin E (Gurney et al, 1996). Finally, similar to SMA studies, a combinatorial approach of dietary (21% fat and 0.15% cholesterol Calorie Energy supplemented Diet) and drug (M30) interventions has a synergistic benefit on survival and motor function (Golko-Perez et al, 2016).…”

Section: Please Place Figure Herementioning

confidence: 99%

Pathogenic commonalities between spinal muscular atrophy and amyotrophic lateral sclerosis: Converging roads to therapeutic development

Bowerman

Murray

Scamps

et al. 2018

European Journal of Medical Genetics

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Spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS) are the two most common motoneuron disorders, which share typical pathological hallmarks while remaining genetically distinct. Indeed, SMA is caused by deletions or mutations in the survival motor neuron 1 (SMN1) gene whilst ALS, albeit being mostly sporadic, can also be caused by mutations within genes, including superoxide dismutase 1 (SOD1), Fused in Sarcoma (FUS), TAR DNA-binding protein 43 (TDP-43) and chromosome 9 open reading frame 72 (C9ORF72). However, it has come to light that these two diseases may be more interlinked than previously thought. Indeed, it has recently been found that FUS directly interacts with an Smn-containing complex, mutant SOD1 perturbs Smn localization, Smn depletion aggravates disease progression of ALS mice, overexpression of SMN in ALS mice significantly improves their phenotype and lifespan, and duplications of SMN1 have been linked to sporadic ALS. Beyond genetic interactions, accumulating evidence further suggests that both diseases share common pathological identities such as intrinsic muscle defects, neuroinflammation, immune organ dysfunction, metabolic perturbations, defects in neuron excitability and selective motoneuron vulnerability. Identifying common molecular effectors that mediate shared pathologies in SMA and ALS would allow for the development of therapeutic strategies and targeted gene therapies that could potentially alleviate symptoms and be equally beneficial in both disorders. In the present review, we will examine our current knowledge of pathogenic commonalities between SMA and ALS, and discuss how furthering this understanding can lead to the establishment of novel therapeutic approaches with wide-reaching impact on multiple motoneuron diseases.

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Extra virgin olive oil intake delays the development of amyotrophic lateral sclerosis associated with reduced reticulum stress and autophagy in muscle of SOD1G93A mice

Cited by 38 publications

References 38 publications

The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis

The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis

Thermosensitive, Stretchable, and Piezoelectric Substrate for Generation of Myogenic Cell Sheet Fragments from Human Mesenchymal Stem Cells for Skeletal Muscle Regeneration

Pathogenic commonalities between spinal muscular atrophy and amyotrophic lateral sclerosis: Converging roads to therapeutic development

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