CNS Injury:
Acute central nervous system (CNS) injuries consist (of) stroke, traumatic brain injury, and spinal cord injury. Early brain injury is a main cause of disability and death for patients of stroke or traumatic brain injury. The procedure of initial brain damage after stroke and trauma are compound, and endure inperfectly understood. A spinalcord injury damage to any part of the spinal cord or nerves at the end of the spinal canal often causes permanent changes in strength, sensation and additional body tasks below the place of the trauma.
Repair and Inhibition:
It associates to the regrowth or repair of nervous tissues, cells or cell products. Such mechanisms may include generation of new neurons, glia, axons, myelin, or synapses. Neuroregeneration differs between the peripheral nervous system (PNS) and the central nervous system (CNS) by the functional mechanisms involved, especially in the extent and speed of repair. If an axon is injured, the distal segment will undergo Wallerian degeneration, misplacing its myelin sheath. The primal segment can either die by apoptosis or undergo the chromatolytic reaction, which is an attempt at repair. In the Central Nervous System, synaptic stripping happens as glial foot procedures invade the deceased synapse.
Inhibition is the process whereby nerves can retard or prevent the functioning of an organ or part.
Excitation:
The electrical activity elicited in a neuron or muscle cell in response to an external stimulus, specifically the propagation of an action potential.
Title : A case of vile vindictive primary CNS vasculitis
George Diaz, Memorial Healthcare Systems, United States
Title : Novel important cellular responses, signaling mechanisms and therapeutic options in vascular dementia
Yong Xiao Wang, Albany Medical College, United States
Title : The role of beliefs, perception, and behavioural patterns in the evolution of psychophysical disorders
Ken Ware, NeuroPhysics Therapy Institute and Research Centre, Australia
Title : A multiscale systems biology framework integrating ODE-based kinetics and MD-derived structural affinities to model mBDNF–proBDNF-mediated bifurcation dynamics in CNS neurotrophin signaling
Krishna Moorjani, Boston University, United States
Title : A multiscale systems biology framework integrating ODE-based kinetics and MD-derived structural affinities to model mBDNF–proBDNF-mediated bifurcation dynamics in CNS neurotrophin signaling
Abhay Murthy, Boston University, United States
Title : A multiscale systems biology framework integrating ODE-based kinetics and MD-derived structural affinities to model mBDNF–proBDNF-mediated bifurcation dynamics in CNS neurotrophin signalling
Ethan Liu, Boston University, United States