NEUROPROTECTION

(Redirected from Neuroprotective)
The term 'neuroprotection' means mechanisms within the nervous system which protect neurons from apoptosis or degeneration, for example following a brain injury or as a result of chronic neurodegenerative diseases. The word derives from the words "neuron" (Greek for nerve cell) and "protection" (Latin for "saving").
Currently, there is a broad interest in how apoptosis and neuroprotection act on the brain in situations as different as growing up and learning or being ill (stroke, schizophrenia, Parkinson's disease).
A recent post-mortem study of the anterior cingulate cortex of persons with schizophrenia found increased levels of cellular signaling proteins, primarily PEBP, that may lead to increased levels of neuroprotection. (Clark, 2006)

Contents

Glaucoma

Brain Cooling

References

Glaucoma

Neuroprotection is also a concept used in ophthalmology regarding glaucoma. The only neuroprotection currently proven in glaucoma is intraocular pressure reduction. However, there are theories that there are other possible areas of neuroprotection, such as protecting from the toxicity induced by degenerating nerve fibres from glaucoma. Cell culture models show that retinal ganglion cells can be prevented from dying by certain pharmacological treatments. However, no large clinical studies have been completed for neuroprotection in glaucoma.

Brain Cooling

Animal studies have shown that cooling the ischemic brain can provide neuroprotection. Myron Ginsberg, MD, Director of the Cerebral Vascular Disease Research Center and Co-Director of the Neurotrauma Research Center at the University of Miami School of Medicine in Florida led studies using rats as subjects. These studies showed that by decreasing temperatures from 34 to 30 degrees Celsius, damage from global forebrain ischemia can be significantly reduced. Dr. Ginsberg said the experiments resulted in a "virtually complete preservation of pyramidal cell layer" in the CA1 hippocampus, and there was significant neuroprotection exhibited in the central and dorsal striatum, as well. Dr. Ginsberg also noted that after hypothermia treatment during focal ischemia there was a significant reduction of infarct volume.
Ashfaq Shuaib, MD, FRCPC, Director of Neurology at the University of Alberta Hospital in Edmonton, led studies which showed that post-ischemic hypothermia can provide neuroprotection, as well, given that it is of a sufficient duration and degree. 48 hours of 32 to 34 degree hypothermia of rats, initiated two and a half hours after the initiated onset of middle cerebral artery occlusion, preserved the rats' ability to retrieve food pellets in a "staircase test" of independent forelimb reaching ability.

References

★ Clark, D., Dedova, I. Cordwell, S., Matsumoto, I. (2006). A proteome analysis of the anterior cingulate cortex gray matter in schizophrenia. ''Molecular Psychiatry, 11'', 459–470.

★ http://www.neurologyreviews.com/apr01/nr_apr01_brain.html