Ghrelin in the diagnosis of cns disorders
AssigneeSwansea University
InventorJeffrey Stephen DAVIES
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Abstract
An inhibitor of ghrelin de-acylation (GDAi) such as an APT1 inhibitor for use in the treatment or prophylaxis of physiological or pathophysiologicial conditions that are mediated by acylated ghrelin (AG) and un-acylated ghrelin (UAG) in mammals. Such conditions include CNS disorders such as Alzheimer's disease and Parkinson's disease. Peripheral administration of the inhibitors is a useful method of treatment for such conditions. Also, the ratio of AG to UAG (as well as the GDA enzyme content or GDA enzyme activity) can be a useful biomarker that may be used as the basis of diagnostic techniques.
Claims26
A method for diagnosing or detecting a predisposition to a CNS disorder, or for staging a CNS disorder, or for measuring the rate of progression of a CNS disorder, which method comprises measuring the ratio of acylated to un-acylated ghrelin in a biological sample, and relating the result to the presence or absence of CNS disorder or a predisposition thereto, or to the stage of progression of the CNS disorder, or relating the changing result to the rate of progression of a CNS disorder, respectively.
-3. (canceled)
A method for diagnosing or detecting a predisposition to a CNS disorder, which method comprises either measuring the amount of ghrelin de-acylation enzyme;
- or measuring the total ghrelin de-acylation activity of a biological sample;
- and relating the result to the presence or absence of CNS disorder or a predisposition thereto.
-15. (canceled)
The method of claim 29 which further inhibits APT2.
The method of claim 28 wherein the physiological or pathophysiological condition is a Central Nervous System (CNS) disorder.
-20. (canceled)
The method of claim 28 wherein the inhibitor is selected from a lactone derivative or a boron-based compound.
(canceled)
The method of claim 28 wherein the inhibitor is a specific binding partner for APT1.
-27. (canceled)
A method for preventing or treating a physiological or pathophysiological condition that is mediated by acylated ghrelin (AG) and un-acylated ghrelin (UAG) in mammals, which method comprises the peripheral administration to a patient in need thereof an effective amount of an inhibitor of ghrelin de-acylation.
(canceled)
Dependencies are inferred from the claim text.