(252d) Dispersion of Amyloid Beta Peptide Fiber Via Cactus Mucilage As a Potential Disruptor of Alzheimer's Disease Plaques | AIChE

(252d) Dispersion of Amyloid Beta Peptide Fiber Via Cactus Mucilage As a Potential Disruptor of Alzheimer's Disease Plaques

Authors 

Peng, T. - Presenter, University of South Florida
Guo, F. - Presenter, University of South Florida
Veisi, Z. - Presenter, University of South Florida
Alcantar, N. A. - Presenter, University of South Florida
Toomey, R. - Presenter, University of South Florida

Alzheimer’s disease (AD) is the primary cause of senile dementia worldwide. It is a neurodegenerative disorder defined as the loss of memory and language skill, collapse of the cognitive function, and distortion of social behavior. It is the America’s Sixth Leading Cause of Death. As of today, the onset mechanisms of Alzheimer’s disease and cure are yet to be known. Three hallmarks are commonly recommended by studies: extra and intracellular accumulation of amyloid beta peptide plaques, formation of intracellular neurofibrillary tangles, and inevitable neuronal death. This research is focused on using cactus mucilage to induce the dispersion of Amyloid Beta (Aβ) peptide fibers and eventually interrupt one of the proposed onset mechanisms-- kinetic formations of Aβ plaques and possibly Alzheimer’s disease. Cactus mucilage is a biomaterial comprised of mainly sugars and carbohydrates extracted from cactus plants. It has been used as food source in some South America countries because of its beneficial characteristics such as renewable, biodegradable, accessible and inexpensive. There are two different extractions can be obtained from the cactus plants by applying different methods: Gelling extraction (GE) and Non-gelling extraction (NE).  Previous research has found that both cactus mucilage extractions are effective dispersants of heavy aliphatic and aromatic molecules such as crude oil. In this study, Aβ monomeric species have been incubated along with GE and NE  in vitro. The changes in the kinetic formation of the Aβ fibers were monitored by attenuated total reflectance Fourier transform infrared (ATR-FTIR) spectroscopy.  Different concentrations and types of mucilage fractions were used to determine the changes induced by cactus mucilage in the secondary structures of the Aβ peptides during and after the incubation process. Different techniques, including  optical microscopy, atomic force microscopy, and transmission electron microscop, were used to capture the physical exploration and visualization of the different processes of aggregation and dispersion in terms of adhesion, size evolution, and distribution of the peptide. In addition, the Du Noüy ring method test was used to evaluate the surface tension of the fiber/mucilage complex and the effectiveness of the dispersion. Experimental analysis of ATR-FTIR spectra and the topology results of the Aβ fibers indicate that the addition of  cactus mucilage has an effect on the surface energy of normal Aβ fibers and oligomers. We have also observed that the kinetic formation of Aβ fibers is slightly disturbed by the presence of mucilage extract. These positive experimental results could possibly provide basic information of an alternative effective method of treatment for Alzheimer’s plaques.

 

Reference: Jimenez, J. (2010). Effects of Monoclonal Anti-Abeta Antibodies on the Amyloid Beta Peptide Fibrillogenesis and their Involvement in the Clearance of Alzheimer's Disease Plaques.University of South Florida Scholar Commons. Retrieved April 20, 2015.