Neuroprotection
Neuroprotection is the effect of any chemical, biological molecule or medical practice which has a protective effect in the nervous system against neurodegenerative disease or brain injury. This effect may take the form of protection of neurons from apoptosis or degeneration.
Currently, there is a broad interest in applying neuroprotection in the prevention and treatment of a number of diseases of the central nervous system such as Alzheimer's, Parkinson's, schizophrenia, and stroke.[1]
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[edit] Types
A variety of neuroprotection agents have been identified that work through one or more of the following mechanisms of action:[1]
- Anti apoptotic – caspase inhibitors
- Antiinflammatory
- Antioxidant (e.g., minocycline)
- Glutamate toxicity blocking agents – glutamate receptor antagonists, NMDA receptor antagonists (e.g., acamprosate), GABAA receptor agonists
- Trophic factors – CNTF, IGF-1, VEGF, GDNF
- Anti protein aggregation agents
- Increasing energy availability (e.g., creatine)
[edit] Therapeutic hypothermia
Animal studies have shown that cooling the ischemic brain can provide neuroprotection. This technique's is called therapeutic hypothermia. By decreasing temperatures from 34 to 30 degrees Celsius, damage from global forebrain ischemia in rats can be significantly reduced. 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. In addition, after hypothermia treatment during focal ischemia, there was a significant reduction of infarct volume.[2]
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.[3] One device used to induce therapeutic hypothermia was called the Arctic Sun.
[edit] Miscellaneous
A 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 neuroprotection.[4]
[edit] See also
[edit] References
- ^ a b Djaldetti R, Lev N, Melamed E (August 2003). "Neuroprotection in progressive brain disorders". Isr. Med. Assoc. J. 5 (8): 576–80. PMID 12929297. http://www.ima.org.il/imaj/ar03aug-10.pdf.
- ^ Dietrich WD, Busto R, Alonso O, Globus MY, Ginsberg MD (July 1993). "Intraischemic but not postischemic brain hypothermia protects chronically following global forebrain ischemia in rats". J. Cereb. Blood Flow Metab. 13 (4): 541–9. doi:10.1038/jcbfm.1993.71. PMID 8314910.
- ^ Li PA, He QP, Miyashita H, Howllet W, Siesjö BK, Shuaib A (July 1999). "Hypothermia ameliorates ischemic brain damage and suppresses the release of extracellular amino acids in both normo- and hyperglycemic subjects". Exp. Neurol. 158 (1): 242–53. doi:10.1006/exnr.1999.7088. PMID 10448438.
- ^ Clark D, Dedova I, Cordwell S, Matsumoto I (May 2006). "A proteome analysis of the anterior cingulate cortex gray matter in schizophrenia". Mol. Psychiatry 11 (5): 459–70, 423. doi:10.1038/sj.mp.4001806. PMID 16491132.
[edit] Further reading
- Kewal K. Jain (2011). The Handbook of Neuroprotection. Totowa, NJ: Humana Press. ISBN 1-61779-048-6.
- Tiziana Borsello (2007). Neuroprotection Methods and Protocols (Methods in Molecular Biology). Totowa, NJ: Humana Press. pp. 239. ISBN 1-58829-666-0.
- Christian Alzheimer (2002). Molecular and cellular biology of neuroprotection in the CNS. New York: Kluwer Academic / Plenum Publishers. ISBN 0-306-47414-X.
