Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease.

[This retracts the article DOI: 10.3892/etm.2015.2531.].

Synergistic effect of moxibustion and rehabilitation training in functional recovery of post-stroke spastic hemiplegia.

OBJECTIVE: To evaluate the therapeutic benefit of combining moxibustion and rehabilitation training for functional recovery in post-stroke spastic hemiplegic patients. METHODS: We randomly divided 84 cases subjecting to inclusion criteria into moxibustion plus rehabilitation training group (MRT group, n=44) and rehabilitation training group (RT group, n=40). Evaluation of therapeutic effect was observed before treatment, 2 weeks during treatment and 6 months after treatment. Spasticity was evaluated using modified Ashworth scale (MAS) and Clinical Spasticity Index (CSI), recovery of motor function was assessed by Brunnstrom recovery stages and Simplified Fugl-Meyer Motor Scale, and performance of activities of daily living (ADL) was measured, and the quality of life was assessed by Patient Reported Outcomes (PRO). RESULTS: Evaluation of upper limbs, hands and lower limbs based on CSI and MAS revealed significant improvements in patients treated with MRT, compared to RT alone, both during and after therapy. CSI and MAS also showed significant improvement in patients at each time point in the MRT group, compared to RT group. Marked improvement in Fugl-Meyer Motor Scale was also observed in MRT group at each time point. Based on Brunnstrom grades of upper limbs, hands and lower limbs, significant differences between the two groups were recorded at all time points during and after therapy. Barthel index (BI) and PRO also confirmed the dramatic differences between the two therapy groups. CONCLUSIONS: Our results demonstrate that combination therapy with moxibustion and rehabilitation training offers greater clinical benefits in relieving spasticity, promoting function recovery of motion, improving the performance of ADL, and increasing quality of life in post-stroke spastic hemiplegic patients, compared to RT alone.

Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease.

In previous years, increasing evidence has indicated that paraptosis and mitochondrial-mediated apoptosis may be associated with Alzheimer's disease (AD). However, the association between paraptosis and mitochondrial-mediated apoptosis, and the pathological processes underlying AD, remain elusive. In the present study, the ß-amyloid precursor protein gene, and the gene mutations PS1M146L and L286V, were transfected to an SH-SY5Y cell line to establish an AD cell model. Subsequently, an MTT assay was used to examine the cell viability of the AD cell model, while a TUNEL assay was employed to observe the number of positively stained apoptotic cells. Cytoplasmic vacuolization was examined using light microscopy and images were photographed. Furthermore, western blot analysis was utilized to detect the expression of golden biomarkers of the mitochondrial pathway, including Bcl-2 and Bax. The paraptosis inhibitor, cycloheximide, was selected to treat the AD model cells in order to observe the association between paraptosis and mitochondrial-mediated apoptosis. The results indicated that the decrease in the cell viability of the AD cells was initiated at 24 h, as compared with the normal cells (P<0.05). TUNEL-positive stained cells were observed at 48 h, which was later compared with the cell death initiation. In addition, examination of cytoplasmic vacuolization using microscopy indicated that there were a small number of paraptosis cells present at 24 h. The expression levels of Bcl-2 was significantly decreased, while Bax was significantly increased at 48 h. Furthermore, cycloheximide treatment was demonstrated to significantly increase Bcl-2 expression, while decreasing Bax expression (P>0.05). In conclusion, the occurrence of paraptosis was demonstrated in the early pathological stages of AD, which may subsequently damage the mitochondria and trigger mitochondrial pathway-mediated apoptosis. Thus, paraptosis may trigger programmed cell death directly, or indirectly through the regulation of Bcl-2 and Bax protein expression.