Triggering receptor expressed in myeloid cells (TREM)2 is a genetic high‐risk factor for sporadic Alzheimer's disease (AD) and is considered a potential target for AD diagnosis and therapy, although its role in the different stages of AD remains controversial. We generated an embryonic deletion of Trem2 (whole body deletion) and induced hippocampa1‐ and cortical‐specific knockdown of microglial Trem2 at different stages of the AD process in amyloid precursor protein/Psen1 mice by adeno‐associated virus (AAV) infection. AAV infection induced microglial Trem2 overexpression in the hippocampus of wild‐type (WT) and thymus cell antigen 1–enhanced green fluorescent protein mice. Mice were subjected to ethological and pathologic tests. Whole body genetic deletion of Trem2 exerted different electrophysiological outcomes between different AD pathologic stages, which results from a complex integration of synaptic loss and amyloid aggregation. Interestingly, knockdown of Trem2 at the early‐middle stage of AD (2–6 mo) prevents synaptic loss through directly inhibiting microglial phagocytosis, whereas knockdown of Trem2 at the middle‐late stage of AD (6–10 mo) accelerates synaptic dysfunction because of more severe amyloid deposition caused by the depression of microglial phagocytosis. Additionally, hippocampal overexpression of Trem2 in WT mice results in significant synaptic impairment. Here, with transgenic technology and electrophysiological assay, we revealed that TREM2 up‐regulation promotes microglial phagocytosis equally against synapse and amyloid plaques and eventually results in different outcomes. During the early‐middle pathologic stage, TREM2 enhancing microglial phagocytosis mainly causes synaptic loss. However, TREM2 up‐regulating microglial phagocytosis gradually supports a positive role when amyloid deposition occupies the leading position at the middle‐late pathologic stage. In this study, we highlighted that TREM2 triggers synaptic loss during AD pathology development.—Sheng, L., Chen, M., Cai, K., Song, Y., Yu, D., Zhang, H., Xu, G. Microglial Trem2 induces synaptic impairment at early stage and prevents amyloidosis at late stage in APP/PS1 mice. FASEB J. 33,10425‐10442 (2019). www.fasebj.org

Brain-computer interfaces (BCIs) represent a groundbreaking approach to enabling direct communication for individuals with severe motor impairments, circumventing traditional neural and muscular pathways. Among the diverse array of BCI technologies, electroencephalogram (EEG)-based systems are particularly favored due to their non-invasive nature, user-friendly operation, and cost-effectiveness. Recent advancements have facilitated the development of adaptive bidirectional closed-loop BCIs, which dynamically adjust to users’ brain activity, thereby enhancing responsiveness and efficacy in neurorehabilitation. These systems support real-time modulation and continuous feedback, fostering personalized therapeutic interventions that align with users’ neural and behavioral responses. By incorporating machine learning algorithms, these BCIs optimize user interaction and promote recovery outcomes through mechanisms of activity-dependent neuroplasticity. This paper reviews the current landscape of EEG-based adaptive bidirectional closed-loop BCIs, examining their applications in the recovery of motor and sensory functions, as well as the challenges encountered in practical implementation. The findings underscore the potential of these technologies to significantly enhance patients’ quality of life and social interaction, while also identifying critical areas for future research aimed at improving system adaptability and performance. As advancements in artificial intelligence continue, the evolution of sophisticated BCI systems holds promise for transforming neurorehabilitation and expanding applications across various domains.

Background: The effects of whole body vibration (WBV) on chronic stroke (CS) patients have been investigated by some previous studies. However, controversy still exists. Objective: The objective of this meta-analysis was to review existing studies that assess the effects of WBV training on CS patients. Methods: We searched Medline, Web of Science, EMBASE, and the Cochrane Library for papers published between January 2000 and January 2014.The meta-analyses were performed using Review Manage Version 5.2.Weighted mean difference (WMD) or standard mean difference (SMD) and its 95% confidence intervals (CI) were used as summary statistics. Funnel plot was used to assess the publication bias. Results: Seven studies with 298 CS patients (159 patients underwent WBV training in experimental group and 139 patients underwent nothing or the same exercise without vibration or with a “placebo” vibrating platform in control group) were included. No significant difference was found in muscle strength (isometric knee extension strength: SMD = − 0.15, 95% CI, − 0.43 to 0.13, P = 0.30; isometric knee flexion strength: WMD = − 0.05, 95% CI, − 0.13 to 0.03, P = 0.22), balance (berg balance scale, WMD = − 0.23, 95% CI, − 1.54 to 1.09; P = 0.74) and gait performance (6-min walk test, WMD = − 50.40, 95% CI, − 118.14 to 17.34; P = 0.14) between groups. No indication of publication bias was found in the funnel plot. Conclusions: WBV training had no beneficial effects in muscle strength, balance and gait performance of CS patients.

Effects of Repetitive Transcranial Magnetic Stimulation (rTMS) and Treadmill Training on Recovery of Motor Function in a Rat Model of Partial Spinal Cord Injury - Article abstract #931601