Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...
Reexamination Certificate
2002-02-19
2002-11-26
Lilling, Herbert J. (Department: 1651)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Having -c-, wherein x is chalcogen, bonded directly to...
C424S725000, C514S290000, C514S423000, C514S425000, C546S098000, C548S530000, C548S539000, C548S543000, C548S544000, C548S555000
Reexamination Certificate
active
06486169
ABSTRACT:
BACKGROUND OF THE INVENTION
This invention relates to safe botanical drug of treatment and prevention of Alzhimer's disease. Specifically, this invention provides a safe botanical drug, including Huperzine (HUE) and Clausenamide (CLE).
DESCRIPTION OF PRIOR ART
Alzhimer's disease (AD) is the commonest form of dementia in the elderly. It manifests as a progressive loss of memory, particularly recent memories, and other cognitive functions, until patients eventually become completely dependent on cares.
It is estimated that AD affects about 4-5 million Americans. The incidence of AD and other dementia doubles every 5 years beyond the age of 65, and about 50% of the United States population over the age of 85 have symptoms of AD. Death occurs inevitably after 3-15 years. AD is predominantly a disease of the elderly and it is a major medical concern in view of the fact that about 33 million Americans are 65 and older, and this number is predicted to increase to 51 million by the year 2025. The annual economic cost of AD health care expenses and lost wages (for AD patients and their caregivers) is estimated at $80-100 billion.
Patients with AD have a large loss of neurons, in both cortical and subcortical regions. Brain weight is reduced by 30-40%. Many patients with AD have a large reduction of cholinergic neurons. It is known that choline acetyltransferase (CAT), which is caused by the loss of cholinergic nuclei and function. AD is characterized by progressive impairment of memory and cognitive functions and may lead to a completely vegetative state. There is much evidence for a marked decrease in choline acetyltransferase and other markers of cholinergic neuron activity and for changes in brain of AD. Eventually, cholinergic and perhaps other neurons die or are destroyed. Many methods of treatment of AD have been explored. Most attention has been focused on the cholinergic drugs because of the evidence for loss of cholinergic neurons noted above. Some drugs, for example, Tacrine and Donepezil used for treatment of AD. These two drugs are cholinesterase inhibitor. The drug apparently increases the release of acetylcholine. However, Tacrine has a significant hepatic toxicity. Also, Tacrine causes nausea and vomiting and Donepezil has shortest half-life. Also, Donepezil has some side effects of peripheroneural systems.
Other important factor of AD is the &bgr;A peptide that is found in the senile plaques and cerebrovascular deposits exist as aggregate with a fibrillar appearance. So far, the result of all drug for AD are very disappointed. There still is lacking an effective and safety drug, which will treat and prevent AD and without any side effect at same time.
DETAILED DESCRIPTION OF THE INVENTION
Recent development in molecular neuroscience aspects indicated that cholinergic neurons, CAT and the &bgr;-amyloid peptide (&bgr;A) have an important act in AD. Botanical drug for treatment and prevention of Alzhimer's disease (BTA) is a new safe botanical drug. BTA contains HUE or CLE or HUE combined with CLE. HUE is an acetylcholinesterase inhibitor and the intention is to increase cholinergic transmission by preventing the breakdown of Ach liberated from the remaining cholinergic neurons. Also, HUE decreases &bgr;A.
HUE produces pharmaceutical effects by inhibiting the action of acetylcholinesterase, which hydrolyzes acetylcholine to choline and acetic acid. HUE increases the concentration of endogenous acetylcholine in brain. Therefore, patients with AD treated by HUE showed some symptomatic improvements of AD.
CLE increases long-term potentiation and improves memory and biochemistry reactivity in neuron.
Chemical structure of HUE and CLE are shown as below:
REFERENCES:
patent: 4731456 (1988-03-01), Hartwig
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