Peripheral alpha-Defensins 1 and 2 are Elevated in Alzheimer's Disease
AuthorWatt, AD; Perez, KA; Ang, C-S; O'Donnell, P; Rembach, A; Pertile, KK; Rumble, RL; Trounson, BO; Fowler, CJ; Faux, NG; ...
Source TitleJournal of Alzheimer's Disease
University of Melbourne Author/sMasters, Colin; Barnham, Kevin; Villemagne, Victor; REMBACH, ALAN; Faux, Noel; Ang, Ching-Seng; Perez, Keyla; O'DONNELL, PAUL ANTHONY; Pertile, Kelly; Rumble, Rebecca; ...
AffiliationFlorey Department of Neuroscience and Mental Health
Medicine (Austin & Northern Health)
MHRI Department of Neuroscience in Mental Health
Biochemistry and Molecular Biology
Pharmacology and Therapeutics
Document TypeJournal Article
CitationsWatt, A. D., Perez, K. A., Ang, C. -S., O'Donnell, P., Rembach, A., Pertile, K. K., Rumble, R. L., Trounson, B. O., Fowler, C. J., Faux, N. G., Masters, C. L., Villemagne, V. L. & Barnham, K. J. (2015). Peripheral alpha-Defensins 1 and 2 are Elevated in Alzheimer's Disease. JOURNAL OF ALZHEIMERS DISEASE, 44 (4), pp.1131-1143. https://doi.org/10.3233/JAD-142286.
Access StatusOpen Access
Biomarkers enabling the preclinical identification of Alzheimer's disease (AD) remain one of the major unmet challenges in the field. The blood cellular fractions offer a viable alternative to current cerebrospinal fluid and neuroimaging modalities. The current study aimed to replicate our earlier reports of altered binding within the AD-affected blood cellular fraction to copper-loaded immobilized metal affinity capture (IMAC) arrays. IMAC and anti-amyloid-β (Aβ) antibody arrays coupled with mass spectrometry were used to analyze blood samples collected from 218 participants from within the AIBL Study of Aging. Peripheral Aβ was fragile and prone to degradation in the AIBL samples, even when stored at -80°C. IMAC analysis of the AIBL samples lead to the isolation and identification of alpha-defensins 1 and 2 at elevated levels in the AD periphery, validating earlier findings. Alpha-defensins 1 and 2 were elevated in AD patients indicating that an inflammatory phenotype is present in the AD periphery; however, peripheral Aβ levels are required to supplement their prognostic power.
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