Journal of Cachexia, Sarcopenia and Muscle最新文献

We are writing in response to the article ‘Bidirectional Transitions of Sarcopenia States in Older Adults: The Longitudinal Evidence from CHARLS’ [1]. This study significantly advances our understanding of the complex relationships between the probability and intensity of transition from non-sarcopenia to possible sarcopenia, sarcopenia and death in older adults. It also highlights the critical role that early screening and intervention can play in preventing the progression of sarcopenia. We commend the authors for their valuable contributions and offer several suggestions for further consideration.

First, this study primarily focuses on the elderly population in China, lacking direct comparisons with other countries or regions. As a result, the findings may not be generalizable to older adults in different cultural contexts or healthcare systems, highlighting a clear regional limitation. Second, although the study utilized a multivariate Markov model (MSM) to analyse transition probabilities in subgroups such as age, body mass index (BMI) and physical function impairment, further subgroup analyses are recommended. These could include examining sex differences, mental health status, lifestyle factors, comorbid chronic conditions and socioeconomic status to better understand their impact on sarcopenia transitions in older adults [2-4]. Such analyses would enable the development of more targeted and personalized intervention strategies. Third, although the study analysed transitions over different years, the follow-up period was relatively short, averaging 3.29 years. Given that sarcopenia is a chronic and progressive condition, longer follow-up periods could yield more comprehensive data and more robust analytical results.

As healthcare professionals, we recognize a significant opportunity to contribute to this field. Although the study did not specifically address early intervention strategies, we can effectively slow the progression of sarcopenia and improve the physical function and quality of life in older adults through early interventions such as regular screening and monitoring, personalized exercise programmes, nutritional support, lifestyle modifications, management of comorbidities and providing psychological support and social engagement.

In conclusion, we greatly appreciate the valuable insights this article provides on sarcopenia outcomes. Building on this research, we can develop more targeted intervention strategies for managing sarcopenia in older adults.

Sir, we read Du's study [1] with great interest. In this study, they aimed to investigate the predictive capacity of lymphocyte subpopulations, sarcopenia and myosteatosis for clinical outcomes in patients who underwent gastric cancer surgery. Additionally, the prognostic significance of CD3+/CD4+ cells in conjunction with myosteatosis was explored. Based on their statistical analysis, they found that CD3+/CD4+ cells, CD4+/CD8+ ratio and CD19+ cells are indicative of clinical prognosis in gastric cancer surgery patients. Sarcopenia and myosteatosis are also associated with the patient's prognosis. Despite promising results, in this letter, we raise some statistical concerns about the results of this study.

Firstly, we noted that there were 38 variables in Table 2 or Table 3 for univariate and multivariate analysis for progression-free survival or overall survival. Thus, according to the basic statistical rule demands that 1 covariate per 10 outcomes for the prediction analysis [2-5], analysing 38 covariates demands at least 380 death gastric cancer patients in Du's study. In contrast, there were only a total of 190 gastric cancer patients, let alone fewer death patients (approximately <100 death patients) in this study. Thus, these logistic regression analysis models were too overfitted, the statistical result may not be accurate, and it needs another larger cohort to validate their risk factors's results.

Secondly, the author could reduce the number of covariates by making the comparison between the dead and survival groups, screening the reduced covariates and using these reduced variables to do the logistic regression analysis. It can get more reliable results.

Thirdly, did these gastric cancer patients receive chemotherapy in this study, while this chemotherapy could severely influence the results of haematological parameters? As staff worked in the clinical laboratory, we know that the haematological parameters were severely influenced by chemotherapy drugs. The same patient may have different results on the same day. Thus, the author should discuss the chemotherapy drug's effect on these covariates, such as the influence on the lymphocyte subsets and other haematological parameters. Without considering this influence, these gastric cancers may have different baselines, resulting in inaccurate risk factors results.

Finally, we show great respect for Du's outstanding study despite these comments.

Background: While the gradually aggravated motor and non-motor disorders of Parkinson's disease (PD) lead to progressive disability and frequent falling, skeletal muscle impairment may contribute to this condition. The leucine-rich repeat kinase2 (LRRK2) is a common disease-causing gene in PD. Little is known about its role in skeletal muscle impairment and its underlying mechanisms.

Methods: To investigate whether the mutation in LRRK2 causes skeletal muscle impairment, we used 3-month-old (3mo) and 14-month-old (14mo) LRRK2^G2019S transgenic (TG) mice as a model of PD, compared with the age-matched littermate wild-type (WT) controls. We measured the muscle mass and strength, ultrastructure, inflammatory infiltration, mitochondrial morphology and dynamics dysfunction through behavioural analysis, electromyography (EMG), immunostaining, transmission electron microscopy (TEM) and other molecular biology techniques.

Results: The 3mo-TG mice display mild skeletal muscle impairment with spontaneous potentials in EMG (increased by 130%, p < 0.05), myofibre necrosis (p < 0.05) and myosin heavy chain-II changes (reduced by 19%, p < 0.01). The inflammatory cells and macrophage infiltration are significantly increased (CD8a⁺ and CD68⁺ cells up 1060% and 579%, respectively, both p < 0.0001) compared with the WT mice. All of the above pathogenic processes are aggravated by aging. The 14mo-TG mice EMG examinations show a reduced duration (by 31%, p < 0.01) and increased polyphasic waves of motor unit action potentials (by 28%, p < 0.05). The 14mo-TG mice present motor behavioural deficits (p < 0.05), muscle strength and mass reduction by 37% and 8% (p < 0.05 and p < 0.01, respectively). A remarkable increase in inflammatory infiltration is accompanied by pro-inflammatory cytokines in the skeletal muscles. TEM analysis shows muscle fibre regeneration with the reduced length of sarcomeres (by 6%;p < 0.05). The muscle regeneration is activated as Pax7⁺ cells increased by 106% (p < 0.0001), andmyoblast determination protein elevated by 71% (p < 0.01). We also document the morphological changes and dynamics dysfunction of mitochondria with the increase of mitofusin1 by 43% (p < 0.05) and voltage-dependent anion channel 1 by 115% (p < 0.001) in the skeletal muscles of 14mo-TG mice.

Conclusions: Taken together, these findings may provide new insights into the clinical and pathogenic involvement of LRRK2^G2019 mutation in muscles, suggesting that the diseases may affect not only midbrain dopaminergic neurons, but also other tissues, and it may help overall clinical management of this devastating disease.