Alzheimer's Research and Treatment
Examining the Roots and Research of a Neurodegenerative Disease
Jul 23, 2007
Alzheimer's disease may have to do with actions of proteins in the brain. Abnormal protein formation, accumulation of protein plaques, presence of tangled microtubules in brain cells and interactions between amyloid proteins and amyloid enzymes could all play a role.
A peptide is a sequence of 10 to 100 amino acids that link with other peptides to form a polypeptide strand. That strand then folds into a convoluted protein structure, but under certain conditions - which remain unknown to science - polypeptides can fold abnormally. Researchers are discovering how such protein misfolding may lead to Alzheimer's disease.
According to the American Health Assistance Foundation, the "formation of amyloid plaques and neurofibrillary tangles are thought to contribute to the degradation of the neurons (nerve cells) in the brain and the subsequent symptoms of Alzheimer's disease."
A postmortem diagnosis of Alzheimer's disease can be determined by the presence of dense accumulations of insoluble amyloid protein plaques between neurons. Inside diseased brain cells can be found tangles of insoluble protein microtubules, called neurofibrillary tangles. Such microtubules normally carry nutrients from one part of the cell to another, but in a diseased cell, they collapse and get twisted up. Normally, damaged microtubules would be broken down, and eliminated as waste.
The main element of amyloid plaque build-up in Alzheimer's sufferers is a peptide known as amyloidβ. Aβ is composed of a sequence of 39-43 amino acids. Research has determined that various mutations in the original protein that Aβ separates from affect the amount of amyloid plaque build-up, and that Aβ42 is the main constituent. It has also been determined that Aβ40 is involved in the process, but that it may play a different role. Evidence suggests that Aβ40 may actually counteract Aβ42 aggregation, since the "ratio of Aβ42⁄Aβ40, rather than total amount of Aβ, correlates with the load of characteristic [of Alzheimer's Disease] plaques in the brain," according to research done at Rensselaer Polytechnic Institute.
In one study, it was determined that macrophages, which help eliminate debris from brain tissue, do not operate efficiently in elderly patients with Alzheimer's. These weak immune cells can not keep up with the amounts of amyloid proteins produced by the brain.
Then the researchers treated these weak macrophages with a chemical composition found in ground turmeric root - specifically bisdemethoxycurcumin - which strengthened the immune cells, making them more effective in the elimination of amyloid protein deposits.
Scottish scientists have very recently discovered that brain cell damage can be caused by the interaction between amyloidβ and an enzyme named amyloidβ alcohol dehydrogenase. This reciprocal action causes a release of neurotoxic substances. Based on their new findings, these researchers developed an "inhibitor that can prevent amyloid attaching to it in a living model."
It should be noted: the theory suggesting that amyloid plague causes Alzheimer's disease is acceptable to most researchers, but still remains inconclusive. But research seems to be getting closer to effective preventive treatments for this infamous neurodegenerative disease.
