Modern advances in spinal cord regeneration: hydrogel combined with neural stem cells.

Severe spinal cord injuries (SCI) lead to loss of functional activity of the body below the injury site, affect a person's ability to self-care and have a direct impact on performance. Due to the structural features and functional role of the spinal cord in the body, the consequences of SCI cannot be completely overcome at the expense of endogenous regenerative potential and, developing over time, lead to severe complications years after injury. Thus, the primary task of this type of injury treatment is to create artificial conditions for the regenerative growth of damaged nerve fibers through the area of the SCI.

Neuronal differentiation and inhibition of glial differentiation of murine neural stem cells by pHPMA hydrogel for the repair of injured spinal cord.

Currently, several therapeutic methods of treating the effects of spinal cord injury (SCI) are being considered. On the one hand, transplantation of stem cells (SCs), in particular, neural stem/progenitor cells (NSPCs), is promising, as these cells have the potential to differentiate into nervous tissue cells, able to enhance endogenous regeneration and prevent the development of inflammatory processes. On the other hand, it is quite promising to replace the damaged nervous tissue with synthetic matrices, in particular hydrogels, which can create artificial conditions for the regenerative growth of injured nerve fibers through the spinal cord injury area, i.

Heterogeneous pHPMA hydrogel promotes neuronal differentiation of bone marrow derived stromal cellsand.

Synthetic hydrogels composed of polymer pore frames are commonly used in medicine, from pharmacologically targeted drug delivery to the creation of bioengineering constructions used in implantation surgery. Among various possible materials, the most common are poly-[N(2-hydroxypropyl)methacrylamide] (pHPMA) derivatives. One of the pHPMA derivatives is biocompatible hydrogel, NeuroGel.

Perturbed Ca-dependent signaling of DYT2 hippocalcin mutant as mechanism of autosomal recessive dystonia.

A recent report of autosomal-recessive primary isolated dystonia (DYT2 dystonia) identified mutations in HPCA, a gene encoding a neuronal calcium sensor protein, hippocalcin (HPCA), as the cause of this disease. However, how mutant HPCA leads to neuronal dysfunction remains unknown. Using a multidisciplinary approach, we demonstrated the failure of dystonic N75K HPCA mutant to decode short bursts of action potentials and theta rhythms in hippocampal neurons by its Ca-dependent translocation to the plasma membrane.