Immunization with neural-derived peptides as a neuroprotective therapy for spinal cord injury

2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Andrea Paola Ibarra-García ◽  
Antonio Ibarra

Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches are studied in order to neutralize these destructive mechanisms. In line with this, several studies indicate that after injury, neural tissue could be protected by an adaptive immune response directed against self-antigens. Immunization with neural-derived peptides (INDP) reduces secondary degeneration of neurons after spinal cord insult and promotes a significant motor recovery. The combination of antioxidants or other immunomodulatory peptides after SCI can improve the protective effect induced by INDP. INDP in acute SCI is a promising strategy, so further studies should be addressed to be able to formulate the best strategy.

2019 ◽  
Vol 30 (2) ◽  
pp. 268-278 ◽  
Author(s):  
Ahmed A. Toreih ◽  
Asser A. Sallam ◽  
Cherif M. Ibrahim ◽  
Ahmed I. Maaty ◽  
Mohsen M. Hassan

OBJECTIVESpinal cord injury (SCI) has been investigated in various animal studies. One promising therapeutic approach involves the transfer of peripheral nerves originating above the level of injury into those originating below the level of injury. The purpose of the present study was to evaluate the feasibility of nerve transfers for reinnervation of lower limbs in patients suffering SCI to restore some hip and knee functions, enabling them to independently stand or even step forward with assistive devices and thus improve their quality of life.METHODSThe feasibility of transferring intercostal to gluteal nerves and the ilioinguinal and iliohypogastric nerves to femoral nerves was assessed in 5 cadavers. Then, lumbar cord hemitransection was performed below L1 in 20 dogs, followed by transfer of the 10th, 11th, and 12th intercostal and subcostal nerves to gluteal nerves and the ilioinguinal and iliohypogastric nerves to the femoral nerve in only 10 dogs (NT group). At 6 months, clinical and electrophysiological evaluations of the recipient nerves and their motor targets were performed.RESULTSThe donor nerves had sufficient length to reach the recipient nerves in a tension-free manner. At 6 months postoperatively, the mean conduction velocity of gluteal and femoral nerves, respectively, increased to 96.1% and 92.8% of the velocity in controls, and there was significant motor recovery of the quadriceps femoris and glutei.CONCLUSIONSIntercostal, ilioinguinal, and iliohypogastric nerves are suitable donors to transfer to the gluteal and femoral nerves after SCI to restore some hip and knee motor functions.


2012 ◽  
Vol 29 (5) ◽  
pp. 957-970 ◽  
Author(s):  
Cameron Lutton ◽  
Yun Wai Young ◽  
Richard Williams ◽  
Adrian C.B. Meedeniya ◽  
Alan Mackay-Sim ◽  
...  

2015 ◽  
Vol 30 (3) ◽  
pp. 645-658 ◽  
Author(s):  
Dominic Schomberg ◽  
Gurwattan Miranpuri ◽  
Tyler Duellman ◽  
Andrew Crowell ◽  
Raghu Vemuganti ◽  
...  

Clinics ◽  
2012 ◽  
Vol 67 (10) ◽  
pp. 1219-1224 ◽  
Author(s):  
AF Cristante ◽  
TE Barros ◽  
RM Marcon ◽  
OB Letaif ◽  
ID Rocha

2021 ◽  
Vol 16 (7) ◽  
pp. 1273
Author(s):  
Antonio Ibarra ◽  
Raúl Silva-García ◽  
Dulce Parra-Villamar ◽  
Liliana Blancas-Espinoza ◽  
Elisa Garcia-Vences ◽  
...  

2021 ◽  
Author(s):  
Floriane Bretheau ◽  
Adrian Castellanos-Molina ◽  
Benoit Mailhot ◽  
Maxime Kusik ◽  
Dominic Belanger ◽  
...  

Abstract Spinal cord injury (SCI) triggers neuroinflammation, and subsequently secondary degeneration and oligodendrocyte (OL) death. We report that the alarmin interleukin (IL)-1α is released by damaged microglia after SCI. Intra-cisterna magna injection of IL-1α in mice rapidly induced neutrophil infiltration and OL death throughout the spinal cord, mimicking what is seen at sites of SCI. These effects were abolished by co-treatment with the IL-1R1 antagonist anakinra, as well as in IL-1R1-knockout mice which showed enhanced locomotor recovery after SCI. Conditional restoration of IL-1R1 expression in astrocytes or endothelial cells (ECs), but not in OLs or microglia, restored IL-1α-induced effects, while astrocyte- or EC-specific Il1r1 deletion reduced OL loss. Conditioned medium derived from IL-1α-stimulated astrocytes is toxic for OLs; further, IL-1α-stimulated astrocytes generate reactive oxygen species (ROS) and blocking ROS production in IL-1α-treated or SCI mice prevented OL loss. Thus, after SCI, microglia release IL-1α, which induces astrocyte- and EC-mediated OL degeneration.


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