The regenerative capability of the central nervous system is limited after traumatic spinal cord injury (SCI) due to intrinsic and extrinsic factors that inhibit spinal cord regeneration, resulting in deficient functional recovery. It has been shown that strategies, such as pre-degenerated peripheral nerve (PPN) grafts or the use of bone marrow stromal cells (BMSCs) or exogenous molecules, such as chondroitinase ABC (ChABC) promote axonal growth and remyelination, resulting in an improvement in locomotor function. These treatments have been primarily assessed in acute injury models. The aim of the present study is to evaluate the ability of several single and combined treatments in order to modify the course of chronic complete SCI in rats. A complete cord transection was performed at the T9 level. One month later, animals were divided into five groups: original injury only (control group), and original injury plus spinal cord re-transection to create a gap to accommodate BMSCs, PPN, PPN + BMSCs, and PPN + BMSCs + ChABC. In comparison with control and single-treatment groups (PPN and BMSCs), combined treatment groups (PPN + BMSCs and PPN + BMSCs + ChABC) showed significative axonal regrowth, as revealed by an increase in GAP-43 and MAP-1B expression in axonal fibers, which correlated with an improvement in locomotor function. In conclusion, the combined therapies tested here improve locomotor function by enhancing axonal regeneration in rats with chronic SCI. Further studies are warranted to refine this promising line of research for clinical purposes.
Background Alzheimer’s disease (AD) is a neurodegenerative disorder and the most common cause of dementia in the elderly. AD is characterized by short‐term to long‐term memory loss, confusion, mood changes, and language difficulties. Numerous studies have focused on the dysregulated genes in AD, but the pathogenesis is still unknown. The underlying risk factors remain largely unclear. The discovery of more accurate AD biomarkers will allow early detection and development of new treatments. Recently bioinformatics has become a relevant research tool for biomedicine. In this study, we explored differential expressed genes (DEGs) potentially involved in the pathogenesis of AD. Method Open access databases of RNA microarrays of tissue from brain and peripheral blood of AD patient, were analyzed after background correction and data normalization; Limma package was used for Differential expression Analysis (DEA) throw statistical R programming language. Data were corrected with the Benjamini and Hochberg approach, and the genes with p values equal to or less than 0.05 were considered significant. The direction of change in gene expression was determined by its variation in the “log2‐fold change” between controls and patients. We performed a functional enrichment analysis of GO using goana and topGO‐Limma. Result With the Brain tissue database, we obtained 17 down regulated genes (DR) and 81 up regulated genes (UR). Functional enrichment analysis of DEGs showed UR pathways: behavior, nervous systems process, post synapses, enzyme binding, while DR were: cellular component organization, RNA metabolic process, protein‐containing complex, nucleoside triphosphatase activity and RNA binding. The blood tissue database showed 850 genes DR and 693 genes UR. The functional enrichment analysis of these DEGs showed UR pathways: regulation of transcription by RNA polymerase‐II and RNA processing, while DR were: cell development and synapses. Finally, the intersection of the DEGs in the two databases showed 3 genes shared between the brain and blood. Conclusion Our in‐silico analysis of brain and blood databases identified several UR and DR genes; the detection of these genes could provide new insight into potential therapies for AD. However, more research is needed to validate these potential new biomarkers and correlate them with the clinical data at different AD stages.
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