Neuren Pharmaceuticals Limited

Auckland Uniservices Limited

Genentech, Inc.

Neuronz Limited

Pharmacia Ab

Nestec S.a.

Societe Des Produits Nestle S.a.

Chiron Corporation

Pharmacia & Upjohn Aktiebolag

Kabi Pharmacia Ab

University of Southampton

Agresearch Limited

Peter David Gluckman

Jian Guan

Christopher E Williams

Catherine Mace

Irma Silva Zolezzi

Keith Malcolm Godfrey

Cyrus Cooper

Margaret Anne Brimble

Karoly Nikolics

Tajrena Alexi

David J Mellor

Anna Skottner

Ross Graham Clark

Frank Casper Tortella

Frank Sieg

Karoly Nikolich

Linda Fryklund

Gregory Brian Thomas

Xi-Chun May Lu

Anthony Joseph Williams

Roy Mark Kimble

Barbara Madeleine Johnston

Nicole Susan Bassett

Bernhard H Breier

Jane Elizabeth Harding

Geoffrey R Ambler

Rita V M Krishnamurthi

Christopher Williams

Mary-Anne Woodnorth

Douglas Wilson

Jed A Hartings

Divina Gryder

Michael Dragunow

Ashmit Kumar Anand

Arjan Scheepens

Stella R Milsom

Mark Adrian Hanson

Graham Charles Burdge

Karen Ann Lillycrop

Joanne Lesley Slater-Jefferies

Allan Michael Sheppard

The present invention generally relates to the early prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children. For example, the present invention relates to the prevention of over-weight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children through appropriate nutrition for women desiring to get pregnant and/or during pregnancy and/or lactation. Embodiments of the present invention relate to vitamin B12 for use in the prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in the off-spring, wherein the vitamin B12 is administered to an overweight and/or obese women desiring to get pregnant and/or to the over-weight and/or obese mother during pregnancy and/or lactation and to maternal food compositions that can be used for this purpose.

Maternal vitamin B12 administration for the prevention of increased adiposity, overweight or obesity in the offspring especially offspring overweight and/or obese mothers

The present invention generally relates to the early prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children. For example, the present invention relates to the prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children through appropriate nutrition for women desiring to get pregnant and/or during pregnancy and/or lactation. Embodiments of the present invention relate to the Vitamin B6 for use in the prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in the offspring, wherein the vitamin B6 is administered to women desiring to get pregnant and/or to the mother during pregnancy and/or lactation and to maternal food compositions that can be used for this purpose.

Maternal vitamin B6 administration for the prevention of increased adiposity, overweight or obesity in the offspring

The present invention generally relates to the early prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children. For example, the present invention relates to the prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in infants or children through appropriate nutrition for women desiring to get pregnant and/or during pregnancy and/or lactation. Embodiments of the present invention relate to vitamin B12 for use in the prevention of overweight, obesity, excessive fat accumulation and/or associated metabolic disorders in the offspring, wherein the vitamin B12 is administered to an overweight and/or obese women desiring to get pregnant and/or to the overweight and/or obese mother during pregnancy and/or lactation and to maternal food compositions that can be used for this purpose.

This invention provides compounds, compositions and methods for treating a cognitive disorder or memory disorder in animals that result from aging or other neurodegenerative condition. In particular, compounds of this invention can stimulate neural cell growth, increased amounts of cells containing a key enzyme needed for production of the cholinergic neurotransmitter, and can improve memory and cognitive function in animals who have experienced a loss of memory or cognitive function.

Cognitive enhancement and cognitive therapy using glycyl-L-2-methylprolyl-L-glutamic acid

A method of treating injuries to or diseases of the central nervous system that predominantly effects glia and/or non-cholinergic neuronal cells characterized in that it comprises the step of increasing the active concentration(s) of insulin-like growth factor 1 and/or analogues thereof in the central nervous system of the patient. The present invention also provides therapeutic compositions comprising insulin-like growth factor 1 and/or analogues thereof for administration to a patient at or following a neural insult, which compositions are useful in minimizing damage to the central nervous system that would otherwise occur following the insult.

IGF-1 to improve neural outcome

Aspects of this invention include the use of G-2MePE to treat patients with brain injury characterized by non-convulsive seizures. G-2MePE is useful in treating brain injuries caused by traumatic brain injury, stroke, hypoxia/ischemia and toxic injury.

Treatment of non-convulsive seizures in brain injury using G-2-methyl-prolyl glutamate

This invention provides analogs and peptidomimetics of glycyl-L-prolyl-L-glutamic acid (GPE). In particular, this invention relates to GPE analogs and peptidomimetics that are anti-apoptotic, anti-necrotic and have neuroprotective effects. These agents are useful in treating neurodegeneration and behavioural disorders caused by toxins, traumatic brain injury and autoimmune disorders of the brain, such as multiple sclerosis and in reducing seizures.

Effects of glycyl-2 methyl prolyl glutamate on neurodegeneration

The invention relates to neuroprotection and to medicaments for use therein. Neuroprotection is induced by activation of neural growth hormone receptors, primarily using medicaments comprising growth hormone, growth hormone analogs or ligands which are functionally equivalent. Such medicaments may also include one or more secondary neuroprotective agents.

Neuroprotective effect of growth hormone

The invention relates to GPE analogs, particularly GPE analogs capable of inducing an equivalent physiological effect to GPE within a patient. Such GPE analogs include peptides where the Gly of Gly-Pro-Glu is replaced by any of Ala, Ser, Thr, or Pro; where the Pro of Gly-Pro-Glu is replaced by any of Ala, Ser, Thr, or Gly; and where the Glu of Gly-Pro-Glu is replaced by any of Asn, Asp, or Gln. The GPE analogs of the invention have application in any method of therapy or prophylaxis in which GPE has application. These applications include the treatment of acute brain injury and neurodegenerative disease, including but not limited to injury or disease in the CNS. The GPE analogs will normally be administered as part of a pharmaceutical composition or preparation.

GPE analogs

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.

Regulation of tyrosine hydroxylase by GPE

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.

Methods to improve neural outcome

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.

Use of GPE to protect glial cells or non-dopaminergic cells from death from neural injury or disease

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.

Regulation of tyrosine hydroxylase

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.

Regulation of neural enzymes

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Auckland, New Zealand

Peter David Gluckman