Abstract: Embodiments of this invention include methods for increasing the amount of the enzyme tyrosine hydroxylase (TH) in the central nervous system (CNS) of mammals in need of an increase in TH. Methods include the use of the tripeptide, gly-pro-glu (GPE) to increase TH in the CNS. GPE can increase the amount of TH and/or decrease the loss of TH in conditions characterized by a loss of dopamine, such as Parkinson's disease and CNS injury. GPE may act to increase the expression of TH or by inhibiting a decrease in TH expression within the CNS or by inhibiting the loss of TH-containing neurons within the CNS. By increasing the amounts of TH in the CNS, GPE can increase the amount of the neurotransmitter, dopamine, in areas of the CNS responsible for adverse symptoms of neural injury or disease.

Abstract: A method for treatment or prophylaxis of a patient suffering from functional symptoms of Parkinson's disease, especially as a consequence of damage to dopaminergic neurons, by administering to the patient a neuroprotective amount of a peptide selected from the tripeptide gly-pro-glu (GPE) and analogs and mimetics thereof, preferably GPE. The GPE will usually be administered subsequent to the onset of Parkinson's disease but prior to the damage of said dopaminergic neurons.

Abstract: The tripeptide glycine-proline-glutamine (GPE) may be administered before, or usually after, injury to reduce damage to the central nervous system. GPE appears useful for neuronal rescue particularly but not exclusively within the hippocampus. Advantages of GPE include: (a) that it crosses the blood-brain barrier, so is effective by injected peripheral administration, (b) it is unlikely to challenge the immune system, (c) it is cheap, and (d) its therapeutic ratio is high. GPE may also be infused into the CSF. It may be administered prior to parturition or elective brain or cardiac surgery. Transdermal routes may be useful for chronic neural disorders. The CNS of mammals (including foetal mammals) after trauma including hypoxic/ischaemic experimental insults showed reduced damage under GPE protection as measured by histological assessment of cell damage or death and regional shrinkage.

Abstract: Embodiments of this invention include methods for increasing the amount of the enzyme tyrosine hydroxylase (TH) in the central nervous system (CNS) of mammals in need of an increase in TH. Methods include the use of the tripeptide, gly-pro-glu (GPE) to increase TH in the CNS. GPE can increase the amount of TH and/or decrease the loss of TH in conditions characterized by a loss of dopamine, such as Parkinson's disease and CNS injury. GPE may act to increase the expression of TH or by inhibiting a decrease in TH expression within the CNS or by inhibiting the loss of TH-containing neurons within the CNS. By increasing the amounts of TH in the CNS, GPE can increase the amount of the neurotransmitter, dopamine, in areas of the CNS responsible for adverse symptoms of neural injury or disease.

Abstract: This invention relates to methods of regulating the effect of tyrosine hydroxylase (TH). In particular it relates to increasing the effective amount of TH in the central nervous systems (CNS) for the purpose of increasing TH-mediated dopamine production in the treatment of conditions such as Parkinson's disease.

Abstract: This invention relates to the use of the tripeptide Gly-Pro-Glu (GPE) or analogs thereof for the treatment of conditions of the central nervous system (e.g. cerebral vasculitis) in which the amount of the neural enzymes nitric oxide synthetase (NOS) and/or glutamic acid decarboxylase (GAD) is reduced.

Abstract: A method for treatment or prophylaxis of a patient suffering from functional symptoms of Parkinson's disease, especially as a consequence of damage to dopaminergic neurons, by administering to the patient a neuroprotective amount of a peptide selected from the tripeptide gly-pro-glu (GPE) and analogs and mimetics thereof, preferably GPE. The GPE will usually be administered subsequent to the onset of Parkinson's disease but prior to the damage of said dopaminergic neurons.

Abstract: The tripeptide glycine-proline-glutamine (GPE) may be administered before, or usually after, injury to reduce damage to the central nervous system. GPE appears useful for neuronal rescue particularly but not exclusively within the hippocampus. Advantages of GPE include: (a) that it crosses the blood-brain barrier, so is effective by injected peripheral administration, (b) it is unlikely to challenge the immune system, (c) it is cheap, and (d) its therapeutic ratio is high. GPE may also be infused into the CSF. It may be administered prior to parturition or elective brain or cardiac surgery. Transdermal routes may be useful for chronic neural disorders. The CNS of mammals (including foetal mammals) after trauma including hypoxic/ischaemic experimental insults showed reduced damage under GPE protection as measured by histological assessment of cell damage or death and regional shrinkage.

Abstract: Disclosed herein is a method for protecting dopaminergic neurons of a mammal against death resulting from Parkinson's disease. The method comprises administering a neuroprotective amount of the tripeptide Gly-Pro-Glu.

Abstract: The present invention relates to a method of treating pancreatic disorders and insufficiency by administering a medicament comprising IGF-I or IGF-II.

Abstract: The present invention relates to the use of iGF-II or effective analogues thereof for the manufacture of a medicament for prevention or treatment of nutritional or gastrointestinal disorders and for promoting human or animal neonatal growth. It also relates to composition comprising exogenous human or animal IGF-II or effective analogues thereof in a therapeutically effective amount together with a pharmaceutically acceptable carrier or diluent or foodstuff, preferably in admixture with artificial or natural milk or colostrum. The invention may be applied both in man and in animals.

Abstract: Fetal growth is promoted and fetal growth retardation is reduced in mammals by increasing in a maternal host during pregnancy the active concentration of IGF-1 and /or IGF-2 and/or analogues thereof. The active concentration of IGF-1 and/or IGF-2 and/or analogues thereof may be increased either by directly administering to the maternal host IGF-1 and/or IGF-2 and/or analogs thereof or by administering another compound which, upon being so administered, causes an increase in the active concentration of IGF-1 and/or IGF-2 and/or analogues thereof in the maternal host.