Life-extension drugs

Life-extension drugs

Alzheimer's disease and dementia


 Alzheimer Disease

Alzheimer’s disease, also known as presenile dementia, is a progressive form of dementia occurring in middle age, which is associated with diffuse degeneration of the brain. Dementia is a chronic disorder of the mental processes due to organic brain disease and organic loss of intellectual functions. It is marked by memory disorders, changes in personality, deterioration in personal care and impaired reasoning ability.

Brain protectors. About the future Alzheimer disease.

What is the central mystery of Alzheimer's? The two main abnormalities of the disease are microscopic lesions called plaques and tangles, which occur in the brains of patients. This is how the disease was first recognized, in 1906. We want to know if these abnormalities are the result of the disease process or if they are abnormalities that cause the disease. That's been the number-one question in the field for a long time, and there's a lot of debate and disagreement about it—are the plaques and tangles cause or effect?
Biochemist PETER DAVIES began investigating Alzheimer's disease in the 1970s, long before its full impact became clear. By 2030 roughly 7.5 million Americans will have this debilitating neurodegenerative disorder. Already Alzheimer's costs the country $148 billion a year; we urgently need to find the cause—and a cure. For years the prevailing theory was that memory loss was caused by protein fragments, so-called plaques and tangles, that accumulate in the brain. Davies, now at the Litwin-Zucker Center for the Study of Alzheimer's Disease and memory disorders, changes in personality, deterioration in personal care and impaired reasoning ability. in Manhasset, New York, suspects a different culprit. His hunch is that the mechanisms controlling cell division have gone wrong— somewhat like what happens in cancer—and that plaques and tangles are the result. In the quest for answers, Davies has led hundreds of studies and examined more than 6,000 brains.
Alois_Alzheimer If we have known about Alzheimer's since 1906, why do we still not understand it? By the time we get to look at the brain of a patient with Alzheimer's, it's really end-stage disease. Alzheimer's is an agonizingly slow process, so by the time we get to study the disease itself during its late stages, all kinds of things have gone on that may be just consequences of disease rather than causal.
What is the most pressing issue today in the field of Alzheimer's research? It's really an issue of what comes first, the chicken or the egg. The majority of people in this field today believe that the plaques, made of a protein fragment calledtbeta-amyloid_geptide (BAP), come first, and that the accumulation of this material causes the rest of the disease. We call them the BAPtists. The other side of the disease is the tangle, made of a protein called tau. TAUists believe that this protein comes first. If you are a BAPtist, you believe that the amyloid is the most important, so you work on ways to prevent or block the production or formation of amyloid in the brain.
But you don't think Alzheimer's is caused by either plaques or tangles, right? nerve cells I believe these abnormalities are results of the disease process. We have looked at cancer cell processes in Alzheimer's disease to see if they might have the ability to cause the disease and the plaques and tangles that are such striking features. I know it sounds off, that Alzheimer's disease might be similar to brain cancer. But this came from work in my laboratory and others that suggested that nerve cells in affected regions of the Alzheimer brain looked like they were trying to divide. Several of the proteins characteristic of cancer cells seem to show up in these nerve cells, and this is very abnormal. One research group [led by a former student] made mice with adult brain cells and forced them with a viral gene to turn on cell-division machinery. What happened was dramatic: The mice showed the same evidence that cell division mechanisms were turned on, and then showed cell death, tangles and plaques—a lot like Alzheimer's disease. We are trying to find out exactly how and why the nerve cells in the Alzheimer's brain decide to turn on their cell division system.
How will knowing the cause of Alzheimer's change the way we treat it? Right now the treatment we have is for the symptoms of the disease rather than the disease itself. We really want to slow down the progress of the disease at an early stage. If we understand the process, hopefully we can slow it down, prevent it, or stop it by interfering with the lesion formations. Let's say I understand precisely what is going wrong in the brain of a patient. The next thing I want to do is figure out how to accurately diagnose the disease very early, because that way I could save a patient who still had some functioning. I don't want a treatment that simply stops the process in late stages and leaves me with an incapacitated patient. We're working on ways to accurately diagnose the disease early. That's not a trivial matter. If we were working on something that wasn't quite so uniquely human, it might be an easier task.
When will we have a cure? This is an incredibly exciting time right now because the research community has more than 600 clinical trials going. Hopefully one of them is going to hit. There are a variety of creative approaches, from drugs to monoclonal antibodies, and it's hard to overstate the importance of that. If the beta-amyloid hypothesis is correct, then the clinical trials we are doing right now might stop or prevent this disease. One of the hundreds of trials in the field is actually going to provide an effective treatment for this disease; that's my hope, anyway.
People say that Alzheimer's will soon swamp the health care system. Do you agree? This is an epidemic in a very real sense. Alzheimer's will kill you, but it will take its sweet time doing it. You start with a kind of memory impairment where you forget where you put your car keys, but you end up with somebody completely nonfunctional, unable to speak or recognize their own kids. We're not doing nearly enough. I don't think this has really dawned on the health care system yet. The pharmaceutical industry is heavily invested in Alzheimer`s now, but it took a long time to get that attention. In 2050 there will be some-Thing like f6~million patients with the disease. There's no way we can afford that. Most of those patients will end up in a nursing home costing at least $40,000 a year. Multiply that by 16 million. There's no health care system in the developed world that can afford that. It's outrageous.

Products: Anti-Alzheimer's, Anti-Dementia Agents

TextAricept (Generic Name: Donepezil) is an oral drug used for the treatment of Alzheimer’s disease. It belongs to the drug classification termed cholinesterase inhibitors which also include tacrine (Cognex). It is deemed by scientists that Alzheimer’s disease may be due to a deficiency in chemicals, specifically neurotransmitters, used by nerves which are inside the brain to communicate with each other. Aracept prevents acetylcholunesterase, an enzyme that causes the obliteration of one neurotransmitter which is acetylcholine. This results in more concentrations of acetylcholine in the brain. This condition is deemed to be the cause of the improvement observed during the treatment with Donepezil. Every now and then, this drug is being utilized by healthy individuals as a brain booster. It is found to be effective in memory enhancement and aids in learning. : Continue reading...

antiagingCentrophenoxine is chemically different from the typical nootropics, but on the basis of pharmacological properties and therapeutic effects, is ranked in this group. It was discovered in 1959 in France and since then it proved to be an effective drug applied for prevention as well as treatment of brain disorders in both young and old people. The drug acts as an inhibitor of free radicals. It improves cognitive function, has a mild stimulating effect on the CNS, activates metabolism, and improves synaptic transmission in the hypothalamus and other brain regions. Increases the content of acetylcholine in the synaptic terminals and increases the density of cholinergic receptors. The drug has an expressing anti-aging effect. It is reported that the application of Centrophenoxine has a positive effect on treatment of a wide range of brain-related disorders including Alzheimer disease and senile dementia. It’s not recommended to patients with paranoid and hallucinatory symptoms as it might cause worsening of delusional and hallucinatory phenomena and provoke occurrence of fear and anxiety.

Centrophenoxine is said to be an effective drug for the treatment concerning brain related disorders in people of different age groups. The drug, as per the studies, improves the thought process as it has a stimulating effect on the central nervous system that improves human metabolism. Consumption of Centrophenoxine assists in improving the synaptic transmission in brain regions especially hypothalamus. Moreover, other than this, it helps in improving acetylcholine content in synaptic terminals and augments the density of cholinergic receptors. The brain related disorders in which Centrophenoxine is used include problems like Alzheimer disease and senile dementia, other than these Centrophenoxine has an expressing anti-aging effect. Continue reading...

Memantin makes part of a class of medications called NDMA receptor antagonist which works by decreasing the abnormal activity of the brain and it is used to treat the symptoms of Alzheimer's disease. It can help people with Alzheimer's disease to perform daily activities easily and think clearly, but taking this drug will not stop the progression of the disease. This medicine may cause side effects such as: dizziness, confusion, extreme tiredness, headache, sleepiness, pain anywhere in the body. If you develop any of these side effects you must inform your doctor immediately.


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Alzheimer's disease and dementia
Alzheimer's disease and dementia

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