Organic compounds -- part of the class 532-570 series – Organic compounds – Oxygen containing
Patent
1991-07-11
1993-09-07
Cintins, Marianne M.
Organic compounds -- part of the class 532-570 series
Organic compounds
Oxygen containing
568524, 568667, 568668, C07C 3508
Patent
active
052430944
DESCRIPTION:
BRIEF SUMMARY
The present invention relates to derivatives of long chain hydrocarbon fatty alcohols as well as pharmaceutical compositions containing these derivatives, and the use of the latter, in particular as cytotrophic and cytoprotective medicines.
It is generally admitted that the nervous tissue of adult mammals cannot be regenerated following a lesion. This lack of the capacity to regenerate itself may be due to a failure of signals capable of inducing regeneration or to an irreversible lesion which leads to neuronal death (A. J. AGUAYO, in: A. BIGNAMI, F. E. BLOOM, C. L. BOLTS and A. ADELOYE eds, CNS Plasticity and Repair, Raven Press (N.Y.) (1985) pp 31-40). However, neuronal death may be prevented by protecting the nervous tissue from the consequences of ischemia or by providing it with a favourable micro-enviroment, in particular of neurotrophic or neuroprotective substances; these substances might also promote regeneration of the nervous tissue if they are administered before death occurs.
The neurotrophic factors are agents capable of promoting the survival of neurons and of stimulating neuronal differentiation (J. R. PEREZ-POLO, in J. E. BOTTENSTEIN and G. SATO eds, Cell Culture in the Neurosciences, Plenum Publishing Corp. (1985) pp 95-123). The activation of cellular metabolism may result in the formation of a network of axons oriented towards the target to be innervated. The demonstration of neurotrophic factors may be made in vitro with the aid of cultures of nerve cells (G. BARBIN, I. SELAK, M. MANTHORPE, and S. VARON; NEUROSCIENCE 12: 33-43 (1984)). Cultures of dissociated cells from various regions of the central nervous system (CNS) have made it possible to show the effect of these neurotrophic factors on the survival of the neurons and on their maturation.
Moreover, an experimental lesion to the median septum in the rat leads to a considerable loss of cholinergic neurons (D. M. ARMSTRONG et al., COMP. NEUROL. 264: 421-436 (1987); F. H. GAGE et al., BRAIN RES. 268: 27-37 (1983)). Certain diseases such as Alzheimer's or Parkinson's disease, Huntington's chorea or amyotrophic lateral sclerosis are the consequence of the progressive disappearance of certain neurons (J. T. COYLE et al., SCIENCE, 219: 1184-1190 (1983); J. B. MARTIN, NEUROLOGY 34: 1059-1072 (1984); M. D. YAHR and K. J. BREGMANN, NEUROLOGY vol., Raven Press (N.Y.) (1985)). Some studies have suggested that this loss of neurons could be prevented by the administration by the intracerebroventricular route of neurotrophic factors such as NGF (Nerve Growth Factor) or FGF (Fibroplast Growth Factor) (L. F. KROMER, Science 235: 214-216 (1987); K. J. ANDERSON et al., Nature 332-360-361 (1988); T. HAGG et al., Exp. Neurol. 101: 303-312 (1988)).
Neuronal death may also be linked to the presence of neurotoxic substances. Certain excitatory amino acids have an excitotoxic action on the neurons; when they are injected into the brain of rats, they cause degeneration of certain zones (J. T. COYLE and R. SCHWARCZ, in: Handbook of Chemical Neuroanatomy, Elsevier, Amsterdam (1983) pp 508-527). This phenomenon is similar to that of the neuronal degeneration observed in the hippocampal area in man and which is called hippocampal sclerosis (Meldrum, Clin. Sci. 68: 112-113 (1985)). This type of lesion may be reproduced by intracerebral injections of excitotoxic substances, such as ibotenic acid. It has been suggested that the loss of hippocampal neurons which is observed in Alzheimer's disease and subsequent to a cerebral ischemia might be linked to the high density of glutamate receptors present on these neurons (S. M. ROTHMANN and J. W. OLNEY, Ann. Neurol.; 19: 105-111 (1986)). Neurotoxic amino acids may also induce lesions at a distance by the intermediary of glutamatergic projections and which resemble the lesions observed in epilepsy (J. V. NADLER et al., Nature 271: 676-677 (1978) and in Huntington's chorea (J. T. COYLE and R. SCHWARZCZ, Nature 263: 244-246 (1976)). The excitotoxins might also be implicated in the genesis of ischemic lesions; ischemia in
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Cintins Marianne M.
Hydorn Michael B.
Medafor
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