In spite of great advances in modern medicine, there are a few effective strategies for the treatment of neurodegenerative diseases characterised by neuron loss or degeneration. This results from complex pathogenesis of the diseases and the limited drug uptake of the brain due to the presence of blood‐brain barrier. Nanoparticle‐based drug delivery systems are expected to improve the drug utilisation. Polymeric nanoparticles represent promising drug delivery carriers to the brain due to their unique advantages such as good biodegradability and biocompatibility, flexibility in surface modification and nontoxicity. In addition, the delivery of genetic drugs may stop the progression of neurodegenerative diseases at the genetic level and even avoid the irreversible damage in the central nervous system. In this review, an overview of studies on polymer‐based nanoparticles for drug delivery to the central nervous system in typical neurodegenerative diseases, especially Alzheimer's diseases and Parkinson's diseases, is described. Meanwhile, their applications in gene delivery in these disorders are discussed. And the challenges and future perspectives for the development of polymeric nanoparticles as drug delivery carriers in neurodegenerative diseases are concluded.

Neurodegenerative diseases manifest as progressive loss of neuronal structures and their myelin sheaths and lead to substantial morbidity and mortality, especially in the elderly. Despite extensive research, there are few effective treatment options for the diseases. MicroRNAs have been shown to be involved in the developmental processes of the central nervous system. Mounting evidence suggest they play an important role in the development of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. However, there are few reviews regarding the roles of miRNAs in neurodegenerative diseases. This review summarizes the recent developments in the roles of microRNAs in neurodegenerative diseases and presents the application of microRNA-based methods in the early diagnosis of these diseases.

This manuscript adopted the cardiac modeling and simulation method to study the problems of physiological pacing in clinical application. A multiscale rabbit ventricular electrophysiological model was constructed. We simulated His-bundle pacing (HBP) treatment for left bundle branch block (LBBB) and atrioventricular block (AVB), and left bundle branch pacing (LBBP) treatment for LBBB by setting various moments of the stimulus. The synthetic ECGs and detailed electrical activities were analyzed. Our electrophysiological model accurately simulated the normal state, HBP, and LBBP. The synthetic ECG showed that QRS duration was narrowed by 30% after HBP correction for LBBB. For LBBB correction with LBBP, the synthetic ECGs of LBBP starting before 30 ms (if the end of atrial excitation is set as 0 ms) presented right bundle branch block (RBBB), and those of LBBP starting at 30–38 ms were synchronous, while those of LBBP starting after 42 ms possessed LBBB morphologies. The best pacing results were obtained when LBBP started at 34 ms. This manuscript verified the feasibility of the constructed ventricular model, and studied the physiological pacing mechanism. The results showed that HBP realized correction for AVB and high LBBB. The performance of LBBP can be improved by applying the stimulus within a specific period of time (0–8 ms) after atrial excitation.