Recently, researchers have been exploring how exosomes can help treat neurodegenerative diseases, such as Alzheimer’s disease (AD), has attracted considerable attention. This study aimed to investigate behavioral, biochemical, histological, and electrophysiological changes following the administration of bone marrow stem cell-derived exosomes (Exo-BMSCs) in AD model rats. Animals were divided into control, Lesion (Lesion, Lesion + saline), and treatment (Lesion + BMSCs, Lesion + Exo-BMSCs) groups. BMSCs were extracted from the bone marrow of newborn rats. Exosomes were extracted from the BMSCs culture medium using a chemical kit. Saline, BMSCs, and Exo-BMSCs were injected bilaterally into the nucleus of Meynert (NBM) one week after electrical lesion. 28 days after injection, behavioral, electrophysiological, and histological changes, as well as ACh and BDNF expression levels in the hippocampus, were evaluated. Electrical lesion of the NBM caused a significant decrease in passive avoidance memory retrieval, a significant decrease in ACh and BDNF levels, changes in EEG wave frequencies in the hippocampus, and histological changes in the NBM, similar to those observed in AD. On the other hand, injection of BMSCs and Exo-BMSCs into the NBM significantly improved passive avoidance memory, an increase in BDNF levels, an increase in power of gamma waves, and improved histological changes compared to the Lesion groups. The increase in power of gamma waves was significant only in the Exo-BMSC-treated group. Injection of BMSCs and Exo-BMSCs into the NBM can significantly improve disease symptoms. This improvement was more pronounced in the Exo-BMSCs-treated group. The concurrent increase in BDNF suggests that this neurotrophin contributes to the observed effects.
Despite growing evidence that motor training modifies action observation networks, the specific brain regions that change longitudinally remain unclear. Here we used functional MRI to track brain activation during an active observation task (drumming videos with one-back detection) across a 21-week drumming training programme in 14 healthy adults. Paired-samples t-tests of six prespecified, hypothesis-driven bilateral ROIs identified nominal Pre-to-Post increases in the IFG pars opercularis [t(13) = −3.302, p = 0.006, d = 0.882], Broca area [p = 0.011, d = 0.790], and supramarginal gyrus [p = 0.033, d = 0.638], and nominal decreases in the hippocampus, angular gyrus, and lingual gyrus (all p < 0.05). After Bonferroni correction across the six prespecified ROIs, only the IFG pars opercularis increase remained significant. Exploratory correlations between neural and behavioural measures were examined separately. The execution task at post-training produced robust activation of sensorimotor regions, representing a post-training snapshot only. These findings motivate future controlled studies examining premotor and auditory cortex activation in clinical populations.
Prolonged walking challenges gait performance in individuals with transtibial amputation (TTA), yet the underlying alterations in muscle activation remain unclear. This study aimed to characterize changes in muscle activation and co-activation strategies following a tolerance-limited prolonged walking task, lasting 10–20 min for TTA and 20 min for controls, in ten males with unilateral TTA and ten able-bodied controls. Participants performed walking trials at baseline and post-task, during which surface electromyography (EMG) signals were recorded from the rectus femoris, biceps femoris, tibialis anterior, and lateral gastrocnemius. Analysis of key metrics revealed divergent neuromuscular responses between groups following the task. Specifically, significant interactions in root mean square revealed that post-task, the TTA intact limb intensified lateral gastrocnemius activation during the second double support phase, while the residual limb increased rectus femoris activity during swing, contrasting with the phase-specific redistribution observed in controls. Regarding peak EMG, the TTA intact limb exhibited higher maximum intensities for the biceps femoris and tibialis anterior during single support. Additionally, integrated EMG was significantly elevated for the rectus femoris and biceps femoris in the TTA residual limb during initial weight acceptance. Finally, the co-contraction index for the rectus femoris-biceps femoris pair increased in the TTA residual limb during swing, whereas controls exhibited pronounced reductions. These findings suggest that following this tolerance-limited task, individuals with TTA adopt distinct muscle activation patterns that appear to prioritize co-activation. While hypothesized to enhance joint stability, this reliance on sustained co-contraction may impose high cumulative activation demands, indicating that rehabilitation might focus on enhancing proximal muscle endurance and mitigating high-demand co-activation strategies.
The left and right hands, beyond being physically identical structures, have a number of functional connections. Their representations are both morphologically similar and highly integrated, in primary somatosensory cortex as well as higher cortical areas. Previous studies have shown that there is a highly consistent pattern of tactile confusions made between fingers of the left and right hand, but none have directly compared the patterns on the two hands. Here, we investigated the similarity of patterns of confusions across the fingers of the left and right hands. We also investigated whether there are individual differences in response patterns that are shared across the two hands. We obtained confusions matrices showing the pattern of tactile mislocalisations on the hairy skin surfaces of the fingers of the left and right hands, and show that these patterns are similar. Using a decoding approach, we show that there are idiosyncratic differences in individual participants’ patterns of confusions that are shared across the fingers of both hands, despite the overall patterns of confusions being highly consistent across participants. These results demonstrate that there is a common high-level representation of the hands that does not distinguish body-side, as has been suggested in previous studies.
High-intensity interval training (HIIT) has emerged as a promising non-pharmacological strategy for neuroprotection, although its molecular effects in Alzheimer's disease (AD) remain unclear. This study investigated the effects of HIIT on gene expression (FNDC5, PPARGC1A, APP), protein expression, cognitive performance, and neuronal apoptosis in a beta-amyloid-induced rat model of AD. Sixty male Wistar rats were divided into four groups: sham sedentary (SS), sham trained (ST), Alzheimer sedentary (AS), and Alzheimer trained (AT). AD-like pathology was induced by intrahippocampal infusion of beta-amyloid (A beta 1-42). Animals underwent an 8-week HIIT protocol. Gene expression was assessed by qPCR using the Delta Ct method, and statistical analyses were performed using two-way ANOVA or mixed-design ANOVA followed by Tukey's post hoc test. HIIT significantly increased PPARGC1A expression (p < 0.05), while FNDC5 gene expression remained unchanged (p > 0.05). However, FNDC5 protein expression was increased in trained groups. APP gene expression was significantly reduced at the transcriptional level (p < 0.05), whereas APP protein abundance differed among experimental conditions without a uniform training-related reduction. HIIT improved physical performance (p < 0.0001) and reduced hippocampal neuronal apoptosis (p < 0.05). In the Morris water maze, improvement was observed only within the Alzheimer-trained group, with no significant differences between groups. HIIT was associated with molecular and cellular adaptations consistent with a neuroprotective response in this beta-amyloid-induced model, including metabolic-pathway modulation, reduced APP transcription, and attenuated neuronal apoptosis. These effects were not accompanied by robust between-group cognitive improvement.
