Sarcopenia is an age-related condition that is characterized by progressive and generalized loss of muscle mass and function. Exercise treatment has been the most commonly used intervention among elderly populations. We performed a systematic review and meta-analysis to evaluate the available literature related to the effects of exercise interventions/programs on muscle mass, muscle strength and physical performance in older adults with sarcopenia. We searched PubMed, EMBASE, MEDLINE and the Web of Science for randomized controlled trials and controlled clinical trials exploring exercise in older adults with sarcopenia published through July 2019 without any language restrictions. Pooled analyses were conducted using Review Manager 5.3, with standardized mean differences (SMDs) and fixed-effect models. A total of 3898 titles and abstracts were initially identified, and 22 studies (1041 individuals, 80.75% females, mean age ranged from 60.51 to 85.90 years) were included in the meta-analysis. The exercise programs in the studies consisted of 30 to 80 min of training, with 1 to 5 training sessions weekly for 6 to 36 weeks. Muscle strength (grip strength [SMD 0.57, 95 % CI 0.42 to 0.73, P <0.00001] and timed five chair stands [SMD-0.56, 95 % CI-0.85 to-0.28, P < 0.0001]) and physical performance (gait speed [SMD 0.44, 95 % CI 0.26 to 0.61, P < 0.00001] and the timed up and go test [SMD-0.97, 95 % CI-1.22 to-0.72, P < 0.00001]) showed significant improvement following exercise treatment, while no differences in muscle mass (ASM [SMD 0.15, 95 % CI-0.05 to 0.36, P = 0.15] and ASM/height 2 [SMD 0.21, 95 % CI-0.05 to 0.48, P = 0.12]) were detected. Exercise programs showed overall significant positive effects on muscle strength and physical performance but not on muscle mass in sarcopenic older adults.

Repetitive transcranial magnetic stimulation (rTMS) has been proposed as an experimental approach for the treatment of disorders of consciousness (DOC). To date, there has been little research into the use of rTMS in DOC and the therapeutic effects have been variously documented. This study aimed to examine the effects of 20 Hz rTMS on the electroencephalography (EEG) reactivity and clinical response in patients with DOC and to explore the neuromodulatory effects of high-frequency rTMS. In this randomized, sham-controlled, crossover study, real or sham 20 Hz rTMS was applied to the left primary motor cortex (M1) of patients with DOC for 5 consecutive days. Evaluations were blindly performed at the baseline (T0), immediately after the end of the 5 days of treatment (T1) and 1 week after the treatment (T2) using the JFK coma recovery scale-revised (CRS-R) and resting-state EEG. Only one patient, with a history of 2 months of traumatic brain injury, showed long-lasting (T1, T2) behavioral and neurophysiological modifications after the real rTMS stimulation. The 5 remaining patients presented brain reactivity localized at several electrodes, and the EEG modification was not significant. rTMS stimulation may improve awareness and arousal of DOC. Additionally, EEG represents a potential biomarker for the therapeutic efficacy of rTMS. This trial is registered with (NCT03385278).

The vegetative state (VS) and minimally conscious state (MCS) are two major types of chronic disorders of consciousness (DoC). The assessment of these two consciousness states generally relies on the Coma Recovery Scale-Revised (CRS-R) score, but a high misdiagnosis rate limits the generalized use of this score. To identify metabolites in human plasma that can accurately distinguish VS from MCS patients, comprehensive plasma metabolic profiles were obtained with targeted metabolomics analysis and untargeted and targeted lipidomics analysis. Univariate and multivariate analyses were used to assess the significance of differences. Compared with healthy controls (HCs), the DoC groups, Emerged from Minimally Conscious State (EMCS) group and Alzheimer's disease (AD) group had significantly different metabolic profiles. Purine metabolism pathway differed the most between the DoC (MCS and VS) and HC groups. In this pathway, adenosine, ADP, and AMP, which are the derived products of ATP degradation, were decreased in the MCS and VS groups compared to healthy controls. More importantly, we identified certain lipids for which the levels were enriched in the VS or MCS groups. Specifically, phosphatidylcholine, (38:5)-H (PC(38:5)-H), and arachidonic acid (AA) differed substantially between the VS and MCS groups and may be used to distinguish these two groups of patients. Together, our findings suggest that metabolic profiling is significantly altered in patients with chronic DoC.

Alzheimer's disease (AD) is a leading cause of dementia. However, the mechanisms responsible for development of AD, especially for the sporadic variant, are still not clear. In our previous study, we discovered that a small noncoding RNA (miR‐188‐3p) targeting β‐site amyloid precursor protein cleaving enzyme (BACE)‐l, a key enzyme responsible for Aβ formation, plays an important role in the development of neuropathology in AD. In the present study, we identified that miR‐338‐5p, a new miRNA that also targets BACE1, contributes to AD neuropathology. We observed that expression of miR‐338‐5p was significantly down‐regulated in the hippocampus of patients with AD and 5XFAD transgenic (TG) mice, an animal model of AD. Overexpression of miR‐338‐5p in the hippocampus of TG mice reduced BACE1 expression, Aβ formation, and neuroinflammation. Overexpression of miR‐338‐5p functionally prevented impairments in long‐term synaptic plasticity, learning ability, and memory retention in TG mice. In addition, we provide evidence that down‐regulated expression of miR‐338‐5p in AD is regulated through the NF‐κB signaling pathway. Our results suggest that down‐regulated expression of miR‐338‐5p plays an important role in the development of AD.—Qian, Q., Zhang, J., He, F.‐P., Bao, W.‐X., Zheng, T.‐T., Zhou, D.‐M., Pan, H.‐Y., Zhang, H., Zhang, X.‐Q., He, X., Sun, B.‐G., Luo, B.‐Y., Chen, C., Peng, G.‐P. Down‐regulated expression of microRNA‐338‐5p contributes to neuropathology in Alzheimer's disease. FASEB J. 33,4404–4417 (2019). http://www.fasebj.org

This study discussed potential mechanisms of complement cascade underlying chronic stage in severe TBI.