Shared molecular signatures between coronavirus infection and neurodegenerative diseases provide targets for broad-spectrum drug development.

Growing evidences have suggested the association between coronavirus infection and neurodegenerative diseases. However, the molecular mechanism behind the association is complex and remains to be clarified. This study integrated human genes involved in infections of three coronaviruses including SARS-CoV-2, SARS-CoV and MERS-CoV from multi-omics data, and investigated the shared genes and molecular functions between coronavirus infection and two neurodegenerative diseases, namely Alzheimer's Disease (AD) and Parkinson's Disease (PD). Seven genes including HSP90AA1, ALDH2, CAV1, COMT, MTOR, IGF2R and HSPA1A, and several inflammation and stress response-related molecular functions such as MAPK signaling pathway, NF-kappa B signaling pathway, responses to oxidative or chemical stress were common to both coronavirus infection and neurodegenerative diseases. These genes were further found to interact with more than 20 other viruses. Finally, drugs targeting these genes were identified. The study would not only help clarify the molecular mechanism behind the association between coronavirus infection and neurodegenerative diseases, but also provide novel targets for the development of broad-spectrum drugs against both coronaviruses and neurodegenerative diseases.

Virome analysis provides new insights into the association between viruses and Parkinson's disease.

Parkinson's disease (PD) is a kind of neurodegenerative disease that causes a huge burden to society. Previous studies have suggested the association between PD and multiple viruses. However, there is still a lack of a virome study about PD. This study systematically identified viruses from the public RNA-sequencing data of more than 700 samples from both PD patients and the control group (most were healthy people). Only nine viruses such as human betaherpesvirus 5 and Merkel cell polyomavirus have been detected in several human brain tissues of the central nervous system, the appendix, and blood of PD patients, and all of these viruses were also detected in the control group. Most viruses were observed to have low abundance in no more than three tissues. No statistically significant differences were observed between the virus abundance in the PD patients and the control group for all viruses. The positive rates of most viruses in PD patients were higher or similar to that in the control group, although those were less than 5% for most viruses. Overall, this is the first study to systematically investigate the virome in PD patients, and provides new insights into the association between viruses and PD.

Fragile X syndrome and fragile X-associated disorders.

Fragile X syndrome (FXS) is caused by a full mutation on the FMR1 gene and a subsequent lack of FMRP, the protein product of FMR1. FMRP plays a key role in regulating the translation of many proteins involved in maintaining neuronal synaptic connections; its deficiency may result in a range of intellectual disabilities, social deficits, psychiatric problems, and dysmorphic physical features. A range of clinical involvement is also associated with the FMR1 premutation, including fragile X-associated tremor ataxia syndrome, fragile X-associated primary ovarian insufficiency, psychiatric problems, hypertension, migraines, and autoimmune problems. Over the past few years, there have been a number of advances in our knowledge of FXS and fragile X-associated disorders, and each of these advances offers significant clinical implications. Among these developments are a better understanding of the clinical impact of the phenomenon known as mosaicism, the revelation that various types of mutations can cause FXS, and improvements in treatment for FXS.

[Bridging rat sciatic nerve defects with the composite nerve-muscle autografts wrapped with human amnion matrix membrane].

OBJECTIVE: To explore the possibility of bridging the sciatic nerve defects with the composite nerve-muscle (NM) autografts wrapped with human amnion matrix membrane (HAMM) in rats. METHODS: Fifty-four Wistar rats were divided randomly into 3 groups (n = 18), and about 10 mm of right sciatic nerve defects were bridged with the composite NM autografts, the nerve autografts and the denatured skeletal muscle autografts respectively (Group A, B, and C), and all grafts were wrapped with HAMM. After the operation, the regenerated nerves were assessed by Fast blue retrograde tracing, neurofilament (NF) immnohistochemical staining, regenerated axons counting, measuring the diameter and myelin thickness of the regenerated axons, and quantifying the wet weight of tibialis anterior muscle. RESULTS: In Group A and B, there were more fluorescent-labeled cells in dorsal root ganglion and spinal cord than in Group C. The regenerated NFs were sparse and disordered in Group C, but dense and regular in Group A and B. Group A and Group B showed results superior to Group C as to other histologic and morphologic characters (P < 0.05), whereas there was no significant difference between Group A and B (P > 0.05). CONCLUSION: The composite NM autografts wrapped with HAMM in this study can well bridge and repair sciatic nerve defects in rats.