University of South Florida

The United States Government As Represented by the Department of Veterans Affairs

Gary W Arendash

Huntington Potter

Jun Tan

Chuanhai Cao

Timothy Boyd

Steven Bennett

Michael J Mullan

Thomas Nadackal Thomas

Lars Nilsson

Zhiming Suo

Fiona C Crawford

The subject invention concerns materials and methods for treating a person or animal having cognitive impairment. In one embodiment, the method comprises administering an effective amount of one or more inflammatory mediator(s), for example, fms-related tyrosine kinase 3 (Flt3) ligand, interleukin-6 (IL-6), macrophage migration inhibitory factor (MIF), interleukin-1 (IL-1), interleukin-3 (IL-3), erythropoietin (EPO), vascular endothelial growth factor A (VEGF-A), hypoxia-inducible transcription factor (HIF-1alpha), insulin like growth factor-1 (IGF-1), tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), granulocyte/macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF), Stem Cell Factor (SCF), Darbepoetin (ARANESP), and metalloproteinases, to an animal or person in need of treatment.

Methods of treating cognitive impairment

A method of treating and preventing a neurological disorder, such as Alzheimer's disease, in a subject in need thereof by positioning an electromagnetic field emitting source proximal to the subject and exposing the subject to an electromagnetic field having a predetermined frequency (preferably &#x2248;300-3,000 MHz) for a predetermined absorption period (preferably greater than &#x2248;3 days). Each individual treatment (comprising exposure to the predetermined frequency for the predetermined absorption period) is continued at a predetermined schedule for a predetermined treatment period. The EMF can have a specific absorption rate up to about 8 W/kg. The methodology enhances cognition in the subject and/or treats/prevents the underlying neurological disorder or a symptom thereof.

Prevention and treatment of brain diseases and disorders related to abnormal protein aggregation through electromagnetic field treatment

The invention includes a method of treating and preventing a neurological disorder, such as Alzheimer's Disease, in a subject in need thereof by positioning an electromagnetic field emitting source proximal to the subject and exposing the subject to an electromagnetic field having a predetermined frequency for a predetermined absorption period. Preferably, each individual treatment (comprising exposure to the predetermined frequency for the predetermined absorption period) is continued at a predetermined schedule (preferably daily) for a predetermined treatment period. The predetermined frequency, according to a preferred embodiment, is about 918 MHz with a specific absorption rate (SAR) of about 0.25 W/kg+/&#x2212;2 dB. The predetermined absorption period of this preferred embodiment is about one hour. The treatment period is long-term, being greater than about 6 months and preferably between about 7 and 9 months.

Prevention and treatment of alzheimer'S disease through electromagnetic field exposure

A transgenic animal, preferably a mouse, that expresses human antichymotrypsin (ACT) in brain tissues is provided, together with animal tissue-derived cell lines and progeny animals of said transgenic animal. Progeny are obtained by mating the transgeny animal with select animal strains used as models of Alzheimer's disease, related neurological disorders, or amyloidogenic diseases. Methods utilizing the parent and progeny animals and cells derived therefrom are disclosed for testing compounds for use as anti-inflammatory drugs, inhibitors of amyloidogenesis, and/or inhibitors of tau protein pathology associated with Alzheimer's disease, in the treatment of a variety of neurological diseases.

Transgenic animal and methods

A method is disclosed for treating and preventing diseases, wherein at least one of the causes of the disease is .beta.-amyloid peptide induced change in free radical production resulting in vascular endothelial dysfunction and vasoactivity, by antagonizing vascular free radicals in excess of functional equilibrium. An animal model for the disease is also disclosed.

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Prescott, AZ, United States of America

Gary W Arendash