Donepezil, an anti-Alzheimer's disease drug, promotes differentiation and regeneration in injured skeletal muscle through the elevation of the expression of myogenic regulatory factors

2021 ◽  
Vol 911 ◽  
pp. 174528
Author(s):  
Hiroshi Todaka ◽  
Mikihiko Arikawa ◽  
Tatsuya Noguchi ◽  
Atsushi Ichikawa ◽  
Takayuki Sato
Keyword(s):  
Alzheimer’S Disease ◽  
Skeletal Muscle ◽  
Alzheimer's Disease ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors

scholarly journals Forgot to Exercise? Exercise Derived Circulating Myokines in Alzheimer's Disease: A Perspective

2021 ◽  
Vol 12 ◽  
Author(s):  
Rajesh Gupta ◽  
Rizwan Khan ◽  
Constanza J. Cortes
Keyword(s):  
Alzheimer’S Disease ◽  
Skeletal Muscle ◽  
Alzheimer's Disease ◽  
Expression Profiles ◽  
Metabolic Stress ◽  
Bioactive Molecules ◽  
Neuroprotective Effects ◽  
Metabolic Remodeling ◽  
Therapeutic Tools ◽  
Ad Prevention

Regular exercise plays an essential role in maintaining healthy neurocognitive function and central nervous system (CNS) immuno-metabolism in the aging CNS. Physical activity decreases the risk of developing Alzheimer's Disease (AD), is associated with better AD prognosis, and positively affects cognitive function in AD patients. Skeletal muscle is an important secretory organ, communicating proteotoxic and metabolic stress to distant tissues, including the CNS, through the secretion of bioactive molecules collectively known as myokines. Skeletal muscle undergoes significant physical and metabolic remodeling during exercise, including alterations in myokine expression profiles. This suggests that changes in myokine and myometabolite secretion may underlie the well-documented benefits of exercise in AD. However, to date, very few studies have focused on specific alterations in skeletal muscle-originating secreted factors and their potential neuroprotective effects in AD. In this review, we discuss exercise therapy for AD prevention and intervention, and propose the use of circulating myokines as novel therapeutic tools for modifying AD progression.

Relationship between skeletal muscle mass and swallowing function in patients with Alzheimer's disease

2016 ◽  
Vol 17 (3) ◽  
pp. 402-409 ◽  
Author(s):  
Daisuke Takagi ◽  
Hirohiko Hirano ◽  
Yutaka Watanabe ◽  
Ayako Edahiro ◽  
Yuki Ohara ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Skeletal Muscle ◽  
Alzheimer's Disease ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Swallowing Function

Myogenic regulatory factors transactivate the Tceal7 gene and modulate muscle differentiation

2010 ◽  
Vol 428 (2) ◽  
pp. 213-221 ◽  
Author(s):  
Xiaozhong Shi ◽  
Daniel J. Garry
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Cellular Proliferation ◽  
Elongation Factor ◽  
Muscle Differentiation ◽  
Myogenic Regulatory Factors ◽  
Mobility Shift ◽  
Regulatory Factors ◽  
E Box

Recurrent injuries eventually exhaust the capacity of skeletal muscle to fully restore or regenerate its cellular architecture. Therefore a comprehensive understanding of the muscle regeneration programme is needed to provide a platform for new therapies for devastating diseases such as Duchenne muscular dystrophy. To begin to decipher the molecular programme that directs muscle regeneration, we undertook an unbiased strategy using microarray analysis of cardiotoxin-injured skeletal muscle at defined time periods in the adult mouse. Using this strategy, we identified Tceal7 [transcription elongation factor A (SII)-like 7], which was dynamically regulated during muscle regeneration. Our studies revealed that Tceal7 was restricted to the skeletal muscle lineage during embryogenesis. Using transgenic technologies and transcriptional assays, we defined an upstream 0.7 kb fragment of the Tceal7 gene that directed the LacZ reporter to the developing skeletal muscle lineage. Analysis of the Tceal7 promoter revealed evolutionarily conserved E-box motifs within the 0.7 kb upstream fragment that were essential for promoter activity, as mutation of the E-box motifs resulted in the loss of reporter expression in the somites of transgenic embryos. Furthermore, we demonstrated that MRFs (myogenic regulatory factors) were Tceal7 upstream transactivators using transcriptional assays, EMSAs (electrophoretic mobility-shift assays), and ChIP (chromatin immunoprecipitation) assays. Overexpression of Tceal7 in C2C12 myoblasts decreased cellular proliferation and enhanced differentiation. Further studies revealed that p27 expression was up-regulated following Tceal7 overexpression. These studies support the hypothesis that MRFs transactivate Tceal7 gene expression and promote muscle differentiation during muscle development and regeneration.

Exercise training alters DNA methylation patterns in genes related to muscle growth and differentiation in mice

2015 ◽  
Vol 308 (10) ◽  
pp. E912-E920 ◽  
Author(s):  
Timo Kanzleiter ◽  
Markus Jähnert ◽  
Gunnar Schulze ◽  
Joachim Selbig ◽  
Nicole Hallahan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Dna Methylation ◽  
Exercise Training ◽  
Metabolic Regulation ◽  
Muscle Growth ◽  
Epigenetic Mechanism ◽  
Myogenic Regulatory Factors ◽  
Regulatory Factors ◽  
A Genome

The adaptive response of skeletal muscle to exercise training is tightly controlled and therefore requires transcriptional regulation. DNA methylation is an epigenetic mechanism known to modulate gene expression, but its contribution to exercise-induced adaptations in skeletal muscle is not well studied. Here, we describe a genome-wide analysis of DNA methylation in muscle of trained mice ( n = 3). Compared with sedentary controls, 2,762 genes exhibited differentially methylated CpGs ( P < 0.05, meth diff >5%, coverage >10) in their putative promoter regions. Alignment with gene expression data ( n = 6) revealed 200 genes with a negative correlation between methylation and expression changes in response to exercise training. The majority of these genes were related to muscle growth and differentiation, and a minor fraction involved in metabolic regulation. Among the candidates were genes that regulate the expression of myogenic regulatory factors ( Plexin A2) as well as genes that participate in muscle hypertrophy ( Igfbp4) and motor neuron innervation ( Dok7). Interestingly, a transcription factor binding site enrichment study discovered significantly enriched occurrence of CpG methylation in the binding sites of the myogenic regulatory factors MyoD and myogenin. These findings suggest that DNA methylation is involved in the regulation of muscle adaptation to regular exercise training.

Evaluation Of Skeletal Muscle Oxidative Metabolism In Alzheimer’S Disease

2015 ◽  
Vol 47 ◽  
pp. 633
Author(s):  
SIMONE PORCELLI ◽  
Giuseppe Bellistri ◽  
Matthew Ramaglia ◽  
Letizia Rasica ◽  
Federica Veronesi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Skeletal Muscle ◽  
Alzheimer's Disease ◽  
Oxidative Metabolism
Sign in / Sign up

Export Citation Format

Share Document