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Method for treatment of neurodegenerative diseases and the effects of aging

a neurodegenerative disease and aging-related technology, applied in the field of neurodegenerative diseases and aging-related diseases, can solve the problems of weakness and impairment of physical functions, impaired mental functions, and conventional treatments that offer little in the way of true relief, and achieve the effects of increasing the neuronal metabolism of tele-methylhistamin

Inactive Publication Date: 2008-01-03
DELACK ELAINE A
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

Neurodegenerative conditions, which include diseases of autoimmunity, strike an increasing number of individuals each year, and for many of these conditions conventional treatments offer little in the way of true relief.
As a group, however, these conditions are characterized by weakness and impaired physical functions, and, sometimes, impaired mental functions as well.
Debilitation is often progressive, and, as stated, conventional treatments and therapies have been limited in their success.
The prevailing theory has been that some agent causes the myelin sheath to be attacked by the immune system, resulting in destruction of the myelin and creation of lesions.
While interferon has demonstrated some positive results when treating remissive-relapsive type MS, it has proven almost entirely ineffective against the chronic-progressive type.
Another treatment method that has yielded a limited degree of success involves the injection of adenosine monophosphate.
This material is not readily absorbed, in part because it is ordinarily available only in an oil-based solution, and is not “friendly” to the patient's tissues.
The tissues have a tendency to wall off the material and form a small abscess capsule around it, and with each injection the material becomes harder and harder to absorb.
In order for the material to be absorbed, most patients must walk vigorously on a treadmill for 20-30 minutes or engage in other strenuous exercise, or else the material will simply remain at the injection site with the result that the patient becomes extremely sore and the symptoms do not improve.
Most people suffering from MS, however, are not mobile and are simply incapable of engaging in such exercise.
Consequently, while many individuals experience significant benefits at the beginning of adenosine monophosphate treatments, these results eventually fade as the person's body becomes unable to absorb the material.
Jonez's work, however, this distinction (between histamine H1 and histamine H2) was not fully appreciated.
In any event, the amounts of histamine phosphate that are involved in McMichael's treatment are far too small to have any significant impact on overall levels of histamine H2 in the body.
Some of these conditions have been conventionally approached on a similar basis to the autoimmune theories described above, and again with limited success.
Most other approaches have been similarly disappointing, and in many instances progression of the neurodegenerative conditions has simply been accepted as inevitable.

Method used

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  • Method for treatment of neurodegenerative diseases and the effects of aging
  • Method for treatment of neurodegenerative diseases and the effects of aging
  • Method for treatment of neurodegenerative diseases and the effects of aging

Examples

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example one

[0050] A 39 year old, 144-pound female patient clinically diagnosed as suffering from multiple sclerosis was treated in accordance with the method of the present invention. The patient had suffered from Multiple Sclerosis for approximately 12 years prior to treatment, and exhibited symptoms indicating that the disease had advanced to the chronic-progressive phase. Approximately 0.069 milligrams of histamine phosphate solution (Eli Lily & Co., see above) were administered subcutaneously three times daily, accompanied by simultaneous oral administration of approximately 200 milligrams of caffeine in aqueous solution. Clinically significant improvements were observed within 24 hours, and full mobility was regained in about 5 two days. The patient subsequently continued the treatment regimen, with no additional exacerbation episodes having occurred to date.

example two

[0051] Ten patients participating in clinical trials were treated in accordance with the present invention. The patients were selected from a larger group of candidates on the following basis: [0052] (a) Each was clinically diagnosed as suffering from multiple sclerosis; [0053] (b) Each was diagnosed as being in the “chronic-progressive” phase of the disease, so as to minimize the possibility of erroneous results due to spontaneous remission; and [0054] (c) Each was assessed as exhibiting physical deterioration in the range from about 5.0 to 7.5 on the MS Expanded Disability Status Scale (EDSS), so that the disability would be severe enough that an improvement in condition would be clinically noticeable, but not so severe that the musculatory structure would have atrophied to the point where no improvement could be observed even if neurological damage was reversed.

[0055] Transdermal patches were used to administer the treatment compositions, as opposed to the subcutaneous / oral regi...

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Abstract

A method for treatment of neurodegenerative disease conditions stemming from multiple sclerosis, aging, autoimmune diseases and fibromyalgia. A compound effective to increase neuronal metabolism of histamine to a histamine H2 agonist is administered in an amount sufficient to stimulate production of cyclic AMP at a level which is sufficient to maintain myelin against undergoing self-degeneration. The compound is selected from the group consisting of histamine M-methyltransferase, monoamineoxidase-A, monoamineoxidase-A agonists and histamine H3 antagonists. The histamine M-methyltransferase may be administered to increase neuronal metabolism of histamine to tele-methylhistamine, whereas the monoamineoxidase-A or monoamineoxidase-A agonist may be administered so as to increase neuronal metabolism of telemethylhistamine to an H2 agonist. Separately or in conjunction with the others, the histamine H3 antagonist may be administered so as to inhibit metabolism of the telemethylhistamine to an H3 agonist, thereby increasing metabolism of the telemethylhistamine to an H2 agonist. The increased histamine H2 agonist levels reduce demyelination and the symptoms that are associated with these conditions.

Description

RELATED APPLICATIONS [0001] This application is a divisional of U.S. patent application Ser. No. 09 / 887,832, filed on Jun. 21, 2001, now U.S. Pat. No. 7,232,830, which is a continuation-in-part application of Ser. No. 09 / 340,277, filed on Jun. 25, 1999, now U.S. Pat. No. 6,277,402, which claimed the benefit of U.S. Provisional Patent Application No. 60 / 090,832, filed on Jun. 26, 1998.BACKGROUND [0002] a. Field of the Invention [0003] The present invention relates generally to methods for the treatment of neurological conditions, and, more particularly, to a method for alleviating / controlling symptoms associated with neurodegeneration and similar conditions stemming from multiple sclerosis, aging, autoimmune diseases and other causes, by administration of compositions which induce an increased presence of histamine H2 and cyclic AMP in the body. [0004] b. Related Art [0005] Neurodegenerative conditions, which include diseases of autoimmunity, strike an increasing number of individual...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): A61K38/44A61K38/45A61P25/28A61P37/00A61K31/417A61K31/475A61K31/52A61K31/66
CPCA61K31/417A61K31/475A61K31/52A61K31/66A61K38/44C12Y104/03004A61K38/45C12Y201/01008A61K31/415A61K2300/00A61P25/28A61P37/00
Inventor DELACK, ELAINE A.
Owner DELACK ELAINE A
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