New study: Implantable capsule might help prevent Alzheimer's
To see a loved one suffer because of this crippling disease is truly heartbreaking. As a human being, it is in our nature to protect our families and loved ones against this pain. But there is no way to stop illness from taking over. Our only way to cope for now is to learn how to be experts in managing this condition.
In line with this, a recent discovery might prove to be beneficial in managing Alzheimer's disease. The study suggests the use of an implantable capsule.
Researchers from the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland published the findings in the journal Brain. They disclosed the information how the implant mechanism would work. Once the capsule has been implanted under the skin, it will emit antibodies to the brain which will be responsible for the activation of the immune system in order to eliminate beta-amyloid protein.
Beta-amyloid protein facilitates the progression of the disease. What it does is it bundles the protein together and creates plaques that collect in between the spaces of nerve cells. This alters the ability of the cells to survive.
The scientists are constantly in search of methods to solve the problems with the plaques, and they have an interesting idea how to. The idea is to mark the beta-amyloid proteins with antibodies which in turn would prompt the immune system to destroy them before they transform into plaques.
But the process is still not in its finest form; the treatment should be done in the early stages of the disease for it to be deemed effective. This means multiple injections that might have side effects.
Aebischer claims that the implantable capsule is another method for a safer treatment.
The macroencapsulation device has the following measurements: 27 mm in length, 12 mm wide and 1.2 mm thick. The device is composed of genetically engineered cells from muscle tissue that releases increased levels of antibodies which identify and target beta-amyloid proteins in the brain. These cells must also be compatible with the patient's to prevent any rejection from the immune system.
The capsule will discharge the antibodies into the bloodstream. From this, they will go to the brain to hunt and tag beta-amyloid protein. This will call the immune system to attack.
Aebischer and the team conducted an experiment on mouse models with early onset of Alzheimer's. These were evaluated for 39 weeks.
The brains depicted reduced levels of beta-amyloid protein and plaques. This is indicative that the experiment prevented the plaque formation. The mice also had lower phosphorylation of the tau protein which accounts for tangle formation inside the nerve cells.
The study authors find that the research is something that provides a helpful concept in formulating an effective approach for Alzheimer's and other neurodegenerative diseases.
Dr. David Tal has more than twenty years of clinical experience. He strongly believes that medical treatment can improve the life of Alzheimer's and memory loss patients of any age. His participation at the Age Matters Clinic allows him to share his knowledge with patients and their families.
Saturday, 23 April 2016
Sunday, 17 April 2016
New Cancer Drug Holds Promising Results For Treatment Against Alzheimer's
As we age, there is an apparent increased risk factor for Alzheimer s disease. What can we do about it? How can we help our loved ones who are exhibiting early symptoms? These questions would arise eventually and we have no way of stopping this disease.
However, a team of scientists conducted an observation of the disease and after noticing its effects, found that there is a certain anti-cancer drug that combats the disease before it even starts. The disease forms crystallized protein clumps which get clogged up and eventually kill the brain cells. The main function of the drug is to prevent the plaques from forming; that is if disseminated early enough to affected individuals.
Based on the Science Advances journal, the scientists studied that the lymphoma treatment drug bexarotene aims to prevent primary nucleation which initiates a response resulting to protein clumps and amyloid plaques.
Although this is a huge breakthrough, the scientists claim that the drug is not a cure for the disease. The drug strengthens the defenses of the human body against the affected proteins in the brain. It decreases the risk factor, but not eliminate the disease entity.
A professor in chemistry at the University of Cambridge and senior author Michele Vendruscolo clarifies that as we get older, our natural defenses against plaques become vulnerable. The professor states though that if the mechanisms of the natural defenses are understood, they might be able to design drugs that act in the same way.
Professor Vendruscolo, as well as other researchers from University of Cambridge, University of Groningen and Lund University, was able to facilitate an experiment that involves giving bexarotene to nematode worms that were genetically modified to exhibit signs of Alzheimer s.
The scientists' findings proved that the drug was effective in suppressing the first phases of plaque formation. However, it was ineffective once the disease symptoms are already present.
When this phase happens, natural proteins change into the wrong shape and latch to other proteins. This creates the amyloid fibrils and oligomers which causes brain damage for patients with Alzheimer s.
The study showcases what happens for each stage in Alzheimer s disease. It reveals the outcome as well if a stage is interrupted or turned off.
A thorough search of a library of 10,000 small molecules was all it took for the scientists to discover the bexarotene. The molecules were compiled when the scientists searched for compounds that interact with amyloid beta (a sticky protein molecule that is vital in the plaque formation for Alzheimer s.)
Professor Chris Dobson, co-author from the chemistry department at University of Cambridge, says that the unsuccessful previous trials do not necessarily mean that it is the wrong molecule. Failure may be attributed to the timing of delivery. The professor explains, "Even if you have an effective molecule, if you target the wrong step in the process, you can actually make things worse by causing toxic protein assemblies to build up elsewhere."
The head of research for Alzheimer s in the UK, Dr. Rosa Sancho, says that the clinical trial involving humans was not a success. Based on Dr. Sancho, the worms experiment will be effective if given in the early stages of Alzheimer s.
Dr. David Tal has more than twenty years of clinical experience. He strongly believes that medical treatment can improve the life of Alzheimer's and memory loss patients of any age. His participation at the Age Matters Clinic allows him to share his knowledge with patients and their families.
However, a team of scientists conducted an observation of the disease and after noticing its effects, found that there is a certain anti-cancer drug that combats the disease before it even starts. The disease forms crystallized protein clumps which get clogged up and eventually kill the brain cells. The main function of the drug is to prevent the plaques from forming; that is if disseminated early enough to affected individuals.
Based on the Science Advances journal, the scientists studied that the lymphoma treatment drug bexarotene aims to prevent primary nucleation which initiates a response resulting to protein clumps and amyloid plaques.
Although this is a huge breakthrough, the scientists claim that the drug is not a cure for the disease. The drug strengthens the defenses of the human body against the affected proteins in the brain. It decreases the risk factor, but not eliminate the disease entity.
A professor in chemistry at the University of Cambridge and senior author Michele Vendruscolo clarifies that as we get older, our natural defenses against plaques become vulnerable. The professor states though that if the mechanisms of the natural defenses are understood, they might be able to design drugs that act in the same way.
Professor Vendruscolo, as well as other researchers from University of Cambridge, University of Groningen and Lund University, was able to facilitate an experiment that involves giving bexarotene to nematode worms that were genetically modified to exhibit signs of Alzheimer s.
The scientists' findings proved that the drug was effective in suppressing the first phases of plaque formation. However, it was ineffective once the disease symptoms are already present.
When this phase happens, natural proteins change into the wrong shape and latch to other proteins. This creates the amyloid fibrils and oligomers which causes brain damage for patients with Alzheimer s.
The study showcases what happens for each stage in Alzheimer s disease. It reveals the outcome as well if a stage is interrupted or turned off.
A thorough search of a library of 10,000 small molecules was all it took for the scientists to discover the bexarotene. The molecules were compiled when the scientists searched for compounds that interact with amyloid beta (a sticky protein molecule that is vital in the plaque formation for Alzheimer s.)
Professor Chris Dobson, co-author from the chemistry department at University of Cambridge, says that the unsuccessful previous trials do not necessarily mean that it is the wrong molecule. Failure may be attributed to the timing of delivery. The professor explains, "Even if you have an effective molecule, if you target the wrong step in the process, you can actually make things worse by causing toxic protein assemblies to build up elsewhere."
The head of research for Alzheimer s in the UK, Dr. Rosa Sancho, says that the clinical trial involving humans was not a success. Based on Dr. Sancho, the worms experiment will be effective if given in the early stages of Alzheimer s.
Dr. David Tal has more than twenty years of clinical experience. He strongly believes that medical treatment can improve the life of Alzheimer's and memory loss patients of any age. His participation at the Age Matters Clinic allows him to share his knowledge with patients and their families.
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