Researchers at UAB and University of Stockholm have created a computer modelling of the structural malfunctioning of the ApoE4 protein when it enters into contact with the Amyloid beta molecule, the main cause of Alzheimer's disease. The research, published in PLoS Computational Biology, supports experimental evidence that links ApoE4 with this pathology and opens up new exploration possibilities in understanding and fighting against the disease. The research proposes a three-dimensional model which simulates the interaction between the peptide Amyloid beta and the different forms of Apolipoprotein E (ApoE) and offers a first molecular base for the comprehension of this phenomenon. Three possible ApoE forms exist in humans: ApoE2, ApoE3 and ApoE4.
ApoE3 is the most common form, while ApoE4 is very closely linked to Alzheimer's disease. The developed model structurally reaffirms the experimental observations which link ApoE4 to this pathology. Researchers have observed that this protein tends to lose its functional structure in presence of the peptide Amyloid beta; this however does not occur with the ApoE2 and ApoE3 forms. According to researchers, these differences are due to subtle divergences between the structures of each form and would explain the different responses of carriers of forms 3 and 4 in the presence of Amyloid beta molecules. The loss of the structure reveals the possibility of new explorations aimed at better understanding and fighting against Alzheimer's disease.
More information:
http://www.uab.es/servlet/Satellite/latest-news/news-detail/new-advance-in-the-study-of-alzheimer-s-disease-1096476786473.html?noticiaid=1266391646189
More information:
http://www.uab.es/servlet/Satellite/latest-news/news-detail/new-advance-in-the-study-of-alzheimer-s-disease-1096476786473.html?noticiaid=1266391646189