Please use this identifier to cite or link to this item:
|Title:||Neuroprotection and peptide toxins|
|Keywords:||Disorders of the nervous system|
|Source:||Rajendra, W., Armugam, A., Jeyaseelan, K. (2004). Neuroprotection and peptide toxins. Brain Research Reviews 45 (2) : 125-141. ScholarBank@NUS Repository. https://doi.org/10.1016/j.brainresrev.2004.04.001|
|Abstract:||Neurodegeneration induced by excitatory neurotransmitter glutamate is considered to be of particular relevance in several types of acute and chronic neurological impairments ranging from cerebral ischaemia to neuropathological conditions such as motor neuron disease, Alzheimer's, Parkinson's disease and epilepsy. The hyperexcitation of glutamate receptors coupled with calcium overload can be prevented or modulated by using well-established competitive and non-competitive antagonists targeting ion/receptor channels. The exponentially increasing body of pharmacological evidence over the years indicates potential applications of peptide toxins, due to their exquisite subtype selectivity on ion channels and receptors, as lead structures for the development of drugs for the treatment of wide variety of neurological disorders. This review comprehensively highlights the overview of the diversity in the molecular as well as neurobiological mechanisms of different peptide toxins derived from venomous animals with particular reference to neuroprotection. In addition, the potential applications of peptide toxins in the diagnosis and treatment of neurological disorders such as neuromuscular disorders, epilepsy, Alzheimer's and Parkinson's diseases, gliomas and ischaemic stroke and their future prospects in the diagnosis as well as in the therapy are addressed. © 2004 Elsevier B.V. All rights reserved.|
|Source Title:||Brain Research Reviews|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Feb 13, 2018
WEB OF SCIENCETM
checked on Jan 15, 2018
checked on Feb 18, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.