A scientist, Jiankui He of Southern University of Science and Technology of China, recently claimed at the Second International Summit on Human Genome Editing in Hong Kong on 29 November that he has created the world's first genetically altered babies using CRISPR. This announcement sparked controversy and criticism. The newly developed CRISPR/Cas9 technique has been applied to genetic modification of many kinds of animals. However, the technique is still in its infancy and many questions remain to be answered before it can be used for clinical purposes, especially for reproductive purposes.

With the increasingly serious aging of the global population, dementia has already become a severe clinical challenge on a global scale. Dementia caused by Alzheimer's disease (AD) is the most common form of dementia observed in the elderly, but its pathogenetic mechanism has still not been fully elucidated. Furthermore, no effective treatment strategy has been developed to date, despite considerable efforts. This can be mainly attributed to the paucity of animal models of AD that are sufficiently similar to humans. Among the presently established animal models, non-human primates share the closest relationship with humans, and their neural anatomy and neurobiology share highly similar characteristics with those of humans. Thus, there is no doubt that these play an irreplaceable role in AD research. Considering this, the present literature on non-human primate models of AD was reviewed to provide a theoretical basis for future research.

Long noncoding RNAs (lncRNAs) are RNA molecules comprising more than 200 nucleotides, which are not translated into proteins. Many studies have shown that lncRNAs are involved in regulating a variety of biological processes, including immune, cancer, stress, development and differentiation at the transcriptional, epigenetic or post-transcriptional levels. Here, we review the role of lncRNAs in the process of neurodevelopment, neural differentiation, synaptic function, and pathogenesis of Parkinson's disease (PD). These pathomechanisms include protein misfolding and aggregation, disordered protein degradation, mitochondrial dysfunction, oxidative stress, autophagy, apoptosis, and neuroinflammation. This information will provide the basis of lncRNA-based disease diagnosis and drug treatment for PD.