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Despite extensive research on neurological disorders, unanswered questions remain regarding the molecular mechanisms underpinning the course of these diseases, and the search continues for effective biomarkers for early diagnosis, prognosis, or therapeutic intervention. These questions are especially acute in the study of spinal cord injury (SCI) and neurodegenerative diseases. It is believed that the changes in gene expression associated with processes triggered by neurological disorders are the result of post-transcriptional gene regulation. microRNAs (miRNAs) are key regulators of post-transcriptional gene expression and, as such, are often looked to in the search for effective biomarkers. We propose that cerebrospinal fluid (CSF) is potentially a source of biomarkers since it is in direct contact with the central nervous system and therefore may contain biomarkers indicating neurodegeneration or damage to the brain and spinal cord. However, since the abundance of miRNAs in CSF is low, their isolation and detection is technically difficult. In this review, we evaluate the findings of recent studies of CSF miRNAs as biomarkers of spinal cord injury (SCI) and neurodegenerative diseases. We also summarize the current knowledge concerning the methods of studying miRNA in CSF, including RNA isolation and normalization of the data, highlighting the caveats of these approaches and possible solutions.

The results of axonal regeneration in peripheral nerves and of the modulating effect of estrogens on the posttraumatic plasticity of motor neurons through the classical and alternative genomic mechanisms involving the activation of estrogen receptors ERalpha and ERbeta and increased transcription of specific neuroprotective control genes. New mechanisms of the neuroprotective effect of estrogens related to the cross interaction of estrogens with intracellular signaling cascades of many other biologically active compounds, in particular, vascular endothelial growth factor and endothelin, are proposed.

The authors studied the ability for anaphylactic contraction in vitro of musculus plantaris, diaphragmatic muscle and musculus soleus of guinea pig. The muscles of double sensitized pigs were denervated and 4 weeks after the nerve cut the muscles' specimens were studied for anaphylactic contraction. The addition of the resolving dose of the specific antigen to incubation medium resulted in anaphylactic contraction of the diaphragmatic muscle and musculus soleus. Musculus plantaris did not respond. Mechanisms of anaphylactic contraction of the skeletal muscle are discussed.