By CIBA Foundation Symposium
Degeneration of sensory receptors or of the nerves innervating them results in a sensory deficit. numerous innovations were attempted for selling regrowth of sensory receptors, fairly within the eye and ear. the most recent info from experimental reports in animals are offered within the ebook together with purposes of BDNF and CNTF within the eye and epidermal development consider the ear.
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Extra resources for Ciba Foundation Symposium 196 - Growth Factors as Drugs for Neurological and Sensory Disorders
Has this been measured? Vaught: Yes, we’ve evaluated that, and you are correct. Greene: If we consider David Kaplan’s published data on the repsonse of TrkA to NGF, there’s an initial large increase in receptor autophosphorylation that seems to significantly down-regulate within several hours. Perhaps just an initial short-term activation is a good thing, and a long ‘off period without NGF followed by another ‘on’ period with N G F might be a good thing from a biological and clinical perspective.
EfJicacy of CNTF, BDNF and CNTF-BDNF combinations in animal models of motor neuron disease The potent actions of CNTF and BDNF in promoting the survival of cultured motor neurons and the ability of either factor to rescue developing motor neurons from naturally occurring cell death, or axotomy-induced cell death in the neonate, has prompted a lot of interest in the therapeutic potential of these factors in the treatment of human motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies.
I was never too intrigued by these molecules, because at the concentrations used they are extremely toxic. Are you pursuing these? Vaught; The 4-methyl catechol was simply a tool. The idea there was rather than trying to administer N G F directly to the brain, which is difficult, a small molecule would turn on the expression of NGF. We are presently a t a point of decision where we have a molecule that, given orally, crosses the blood-brain barrier and turns on N G F message, increases N G F protein, causes Trk phosphorylation and reverses both biochemical and behavioural deficits from a partial fimbria-fornix lesion.