Studies of in vivo amyloid beta-peptide

Studies of in vivo amyloid beta-peptide



Since Beta Amyloid plaque is widely believed today to be a contributor to Alzheimer's disease (see reference) and Nattokinase has been shown to favorably influence that process, along with safely helping prevent excessive blood clotting, we now have major reasons to add Endokinase to our Beyond Chelation program. Nattokinase has also been safely used with Essential Daily Defense and Boluoke to replace Coumadin in a patient with a mechanical heart valve.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
http://www.gordonresearch.com

http://www3.interscience.wiley.com/journal/118002007/abstract

Wiley Interscience

Review
Redox proteomics studies of in vivo amyloid beta-peptide animal models of Alzheimer's disease: Insight into the role of oxidative stress

Rukhsana Sultana 1 2, D. Allan Butterfield, Professor 1 2 3 * 1Department of Chemistry, University of Kentucky, Lexington, KY, USA 2Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA 3Center of Membrane Sciences, University of Kentucky, Lexington, KY, USA
D. Allan Butterfield 
*Correspondence to D. Allan Butterfield, Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA Fax: +1-859-257-5876 Funded by:
NIH; Grant Number: AG-05119, AG-10836

ABSTRACT
Alzheimer's disease (AD) http://www.dreddyclinic.com/findinformation/aa/alzheimersdisease.php is an age-related neurodegenerative disease. AD is characterized by the presence of senile plaques, neurofibrillary tangles, and synaptic loss. Amyloid -peptide (A ), a component of senile plaques, has been proposed to play an important role in oxidative stress in AD brain and could be one of the key factors in the pathogenesis of AD. In the present review, we discuss some of the AD animal models that express A , and compare the proteomics-identified oxidatively modified proteins between AD brain and those of A models. Such a comparison would allow better understanding of the role of A in AD pathogenesis thereby helping in developing potential therapeutics to treat or delay AD.