Background: Tau hyperphosphorylation is involved in the progression of Alzheimer's disease (AD). In the present study, we aimed to evaluate the role of linc00507 with respect to modulating Tau phosphorylation in ab AD animal and an Aβ42-SH-SY5Y cell model. Methods: Aβ precursor protein (APP)/PS transgenic mice and Aβ42-SH-SY5Y cell model were used to investigate the role of linc00507 in AD. A quantitative real-time polymerase chain reaction evaluated the RNA expression of linc00507, miR-181c-5p and microtubule-associated protein tau (MAPT)/tau-tubulin kinase-1 (TTBK1). The interactions between the genes were investigated through changes in one gene expression by regulating another gene in cells and, in addition, correlation assays were performed in mice. Western blot assays examined the protein expression of MAPT/TTBK1, phosphorylation of tau and signaling proteins P25/P35/GSK3β in response to the regulation of linc00507, miR-181c-5p and MAPT/TTBK1 in cells and also in mice. Results: linc00507 was significantly elevated in hippocampus, and cerebral cortex of APP/PS transgenic mice and AD-like SH-SY5Y cells. It could bind miR-181c-5p and thereby regulate the expression of microtubule-associated protein Tau (MAPT) and tau-tubulin kinase-1 (TTBK1) as a competitive endogenous RNA (ceRNA). MAPT (encoding the tau protein) and TTBK1 (encoding a tau kinase) were identified as direct target genes of miR-181c-5p. Furthermore, linc00507 mediated tau protein hyperphosphorylation by the activation of the P25/P35/GSK3β signaling pathway through regulating MAPT/TTBK1 by sponging miR-181c-5p. Conclusions: The findings of the present highlight the regulatory role of linc00507 in tau phosphorylation miR-181c-5p as ceRNA of MAPT/TTBK1 in vitro and in vivo, providing a basis for novel diagnostic and treatment strategies for AD.

Stroke is the leading cause of severe disability worldwide, with up to 15 million of people suffer stroke every year. Survivors of stroke can recover their physical strength, provided they undergo proper rehabilitation. However, most of the rehabilitation centres provide only basic tools as they can rarely afford the expensive and advanced rehabilitation devices. Besides that, training with therapists is limited to few hours per week due to the large number of patients and the stroke patients are generally sent home once they are mobile, although their upper limbs functions are not recovered. Stroke patients need to continue training after stroke to avoid muscle contraction, but due to large number of patients, they are not able to train frequently in the hospital. Therefore, the goal of this project is to develop a low-cost, simple yet compact rehabilitation robot for stroke patient to train both upper and lower limbs reaching movement. Compact Rehabilitation Robot (CR2) is expected to help the stroke patients training reaching movement in an enhanced virtual reality environment with haptic feedback and to provide the stroke patients with a faster track towards recovery.

Background Increased serum Lp‐PLA2 levels have been reported in patients who experienced an ischemic stroke; however, the relationship between Lp‐PLA2 and H‐type hypertension in patients with ischemic stroke remains unclear. Methods In the present study, we investigated the correlation between serum Lp‐PLA2 and H‐type hypertension in patients with ischemic stroke. A total of 135 patients who experienced acute ischemic stroke were enrolled in Tianjin Huanhu Hospital during October 2015 to May 2016. The demographic characteristics of the patients were collected, and biochemical parameters were detected. Results Among the 135 patients, 111 patients had essential hypertension, including 41 patients with H‐type hypertension and 70 with non‐H‐type hypertension. There were higher proportions of males and patients with diabetes mellitus in the H‐type hypertension group compared with the non‐H‐type hypertension group (P < .05). Lp‐PLA2, glucose, and LDL‐C levels were higher in the H‐type hypertension group than in the non‐H‐type hypertension group (P < .05). Multivariate logistic regression showed that Lp‐PLA2 levels >208.46 mg/L were independently associated with H‐type hypertension in patients with ischemic stroke (OR: 2.560, 95% CI: 1.085‐6.040, P = .032). The area under the ROC curve of Lp‐PAL2 levels in the H‐type hypertension group was 0.665 (95% CI: 0.561‐0.768, P = .004). Conclusion Synergetic effects of H‐type hypertension and Lp‐PLA2 levels were noted in the pathogenesis of ischemic stroke.

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