Alzheimers Research
A lot of research has already taken place over the years. Here are some of the results of such research. A research team from an Alzheimer's Disease Research Center under Dr. Lopez (Ref.1) analyzed the results of the treatments and the research of Alzheimers patients over 2 decades. They found that there were at least 6 subgroups where Alzheimers was associated with some other significant conditions.
The majority was the patients with Alzheimers disease due to cerebrovascular disease. Next there were the groups with Alzheimers due to alcoholism (15%), depression (7%), thyroid disorders (4%), a history of head trauma (6%), and due to pernicious anemia ( 6%, due to vitamin B12 deficiency).
The researchers found that over 20 years the first three subgroups, namely the ones with cerebrovascular disease, with depression and with Alzheimers due to alcoholism had a decreased life expectancy, whereas the others had a normal life expectancy.
There are many research papers that have described that the senile plaques, which are found on the cortex of brains of Alzheimer patients, are made up of beta-amyloid substance and of neurofibrillary tangles (don't worry if this is confusing).
To put it simple: This protein material is like glue, which prevents the neurons from working properly and causes the memory loss and the confusion so typical for Alzheimers patients. Over the years the question then arose where does this glue substance" beta-amyloid" come from? Ref. 2 points out that for many years it was thought that this abnormal protein would have come from the liver and was then deposited in the brain. There is now evidence presented in Ref. 2 that the beta-amyloid actually comes directly from the cells in the brain where it is found and also deposited. Ref. 3 showed that beta-amyloid is not useless at all. It actually has a very important antioxidant function in normal brains and keeps lipoproteins, an important chemical substrate of the brain, from getting oxidized.
The Alzheimers patient's brain appears to have a regulation problem where through some genetic or other mechanism, the autoregulation of amyloid-peptides and other similar peptides appears to have gotten lost. There seems to be an overproduction of these peptides until they no longer are soluble. The insoluble surplus of these beta-amyloids is then deposited as the glue-like senile plaques that clog up the patient's thinking. In Ref.4 the authors presented convincing evidence that low levels of a subtype of amyloid peptides was found to be lower in Alzheimer patients and in Lewy body dementia patients.
Ref. 5 showed, similar to the already mentioned Ref. 3, that this subtype of amyloid peptides prevents lipoproteins in the cerebrospinal fluids from being oxidized. Ref. 5 went further in describing the mechanism of how this is achieved. The authors suggest that this subgroup of amyloid peptides protects the very sensitive so-called "microtubules", an important cell component of nerve cells in the CNS, from being destroyed. If this protective system is not functioning, nerve cells are lost and this affects thinking, memorizing and other cognitive functions of the brain.
With the newer test methods it is now possible to depict these senile plaques at a stage when clinical symptoms are not present yet, which is very useful for early diagnosis in high risk families.
At a conference in Vancouver/BC (Ref. 16) Dr. Howard Feldman who is involved in several clinical trials involving newer treatments for Alzheimer patients reviewed the beneficial effects of a combination of Memantine and Donepezil. The medications seem to prevent the amyloid aggregate formation and thus allow the brain to function more normally. Once the senile neuritic plaques (the "gluey substance") have formed, an inflammatory reaction takes place that leads to neurodegeneration. This last stage is irreversible.
The key is to diagnose Alzheimers early with the above mentioned newer methods, to reduce or eliminate the inflammation and to prevent neurodegeneration from taking place. Cholesterol lowering drugs are a newer way to cut down on plaque formation, secretase inhibitors are another way. A-beta-vaccination has been successful in a mouse model to prevent Alzheimers, but in man 6% of subjects experienced encephalitis as a serious side-effect, so the vaccination approach has to be improved. Metal chelators are another new line of research to cut down on plaque formation as zinc and copper toxicity has been shown to play a role in this disease. There is also evidence that high insulin levels in the blood contribute to Alzheimers and this may be caused in turn from too much sugar intake.
All of the facts are not out yet about Alzheimers, but it is exciting to see the recent progress both in terms of early diagnosis and Alzheimers treatment. On the longterm prevention, as always in medicine, will prevail as the most effective method regarding diminishing the frequency of this disease.
|
|
