Method for treating or preventing Alzheimer's disease

Abstract

Disclosed is a method for treating or preventing Alzheimer's disease by restricting the level of metabolizable carbohydrate in the diet and / or administering to the patient an effective amount of an agent which reduces serum insulin levels.

Description

CROSS REFERENCE TO RELATED APPLICATIONS

[0001] The present application is a continuation of PCT / US98 / 04731 filed Mar. 12, 1998. The present application also claims the benefit of U.S. provisional application 60 / 039,607. The contents of each of these two applications are fully incorporated by reference herein.BACKGROUND OF THE INVENTION

[0002] 1. Field of the Invention

[0003] The present invention is in the field of medicinal chemistry. In particular, the present invention is related to a sunrising new method to treat or prevent Alzheimer's disease by dietary restriction of carbohydrates and / or administration of an agent which causes reduction in serum insulin levels.

[0004] 2. Related Art

[0005] According to a recent review by Mairin B. Brennan published in Chemical and Engineering News 75(3):29-35 (1997), roughly 4 million people in the United States have Alzheimer's disease. Inherited or not, the disease manifests itself with progressively impaired memory leading to mental confusi...

Examples

example 1

Insulin Stimulates the Expression of AD7c-NTP, a Protein which causes Neurons to Exhibit Neuronal Sprouting and Apoptosis

[0038] Insulin is an important mediator of growth and differentiation in CNS neurons. Insulin stimulated differentiation of PNET2 cells was associated with rapid (within 10 minutes) but transient increases in the levels of the 39 kD, 18 kD and 15 kD NTP species, followed by sustained increases in synthesis and steady state levels of all five NTP species. In contrast, the failure of insulin to induce differentiation of PNE-T1 cells was associated with absent insulin modulation of NTP.

[0039] Analysis of the signal transduction pathways demonstrated that the insulin-induced up-regulation of NTP molecules in PNET2 cells was mediated through phosphorylation of the insulin receptor substrate-1 (IRS-1) and the insulin receptor β subunit (IRβs) itself. In PNET1 cells, the lack of insulin responsiveness was associated with impaired insulin-mediated tyrosyl phosphorylatio...

CROSS REFERENCE TO RELATED APPLICATIONS

[0001] The present application is a continuation of PCT / US98 / 04731 filed Mar. 12, 1998. The present application also claims the benefit of U.S. provisional application 60 / 039,607. The contents of each of these two applications are fully incorporated by reference herein.BACKGROUND OF THE INVENTION

[0002] 1. Field of the Invention

[0003] The present invention is in the field of medicinal chemistry. In particular, the present invention is related to a sunrising new method to treat or prevent Alzheimer's disease by dietary restriction of carbohydrates and / or administration of an agent which causes reduction in serum insulin levels.

[0004] 2. Related Art

[0005] According to a recent review by Mairin B. Brennan published in Chemical and Engineering News 75(3):29-35 (1997), roughly 4 million people in the United States have Alzheimer's disease. Inherited or not, the disease manifests itself with progressively impaired memory leading to mental confusi...

Examples

example 1

Insulin Stimulates the Expression of AD7c-NTP, a Protein which causes Neurons to Exhibit Neuronal Sprouting and Apoptosis

[0038] Insulin is an important mediator of growth and differentiation in CNS neurons. Insulin stimulated differentiation of PNET2 cells was associated with rapid (within 10 minutes) but transient increases in the levels of the 39 kD, 18 kD and 15 kD NTP species, followed by sustained increases in synthesis and steady state levels of all five NTP species. In contrast, the failure of insulin to induce differentiation of PNE-T1 cells was associated with absent insulin modulation of NTP.

[0039] Analysis of the signal transduction pathways demonstrated that the insulin-induced up-regulation of NTP molecules in PNET2 cells was mediated through phosphorylation of the insulin receptor substrate-1 (IRS-1) and the insulin receptor β subunit (IRβs) itself. In PNET1 cells, the lack of insulin responsiveness was associated with impaired insulin-mediated tyrosyl phosphorylatio...