Troy, N.Y. -- Researchers at Rensselaer Polytechnic Institute are challenging current thinking on the causes and prevention of Alzheimers disease, offering a new hypothesis that could be the key to preventing this form of dementia. The researchers have found that a specific imbalance between two peptides may be the cause of the fatal neurological disease that affects more than five million people in the United States.
"We have found that two peptides, AB42 and AB40, must be in balance for normal function," said Chunyu Wang, lead researcher and assistant professor of biology at Rensselaer. "They are like the Yin and Yang in Taiji, an ancient Chinese philosophy. When the peptides are produced in the correct proportions, the brain is healthy; but when that delicate balance is changed, pathological changes will occur in the brain and the persons memories become hazy, leading to eventual dementia."
Wang expects that this imbalance could be the main factor in the progression of Alzheimers disease. If correct, the addition of AB40 may stop the diseases development. Wang notes that further research is needed, but his preliminary results challenge the current mode of thinking about how these peptides contribute to the progression of the disease.
The research will be published in the June edition of the Journal of Molecular Biology.
Peptides are formed by the linking of different amino acids. The two peptides that Wang investigated were both Amyloid B-peptides (AB) specifically those composed of 40 and 42 amino acids, called AB40 and AB42. These two peptides have been previously found in deposits, called senile plaques or amyloid plaques, in brains afflicted with Alzheimers disease. These plaques, mainly composed of AB42 fibrils, are a hallmark of Alzheimers disease.
Prior research has uncovered that increased levels of AB42 become toxic to brain cells when individual molecules of AB42, or monomers, combine to form oligo
Contact: Gabrielle DeMarco
Rensselaer Polytechnic Institute