Abstract
Oxidative stress has been strongly associated with Parkinson disease (PD) aetiology. We investigated the effects of blueberry extract (BBE) supplementation on α-synuclein induced phenotypes in a Drosophila melanogaster model of PD. Enhanced α-synuclein expression in D. melanogaster dopaminergic (DA) neurons can reduce lifespan and we have performed longevity assays to measure the effects of BBE on D. melanogaster survival. Flies expressing α-synuclein in their DA neurons fed BBE had up to an 8 day, or 15%, greater median lifespan than those fed a standard control diet. In addition, BBE improved α-synuclein-induced developmental defects in the Drosophila eye. Our biometric analyses revealed that individuals fed BBE had less atypical ommatidia as well as an increased number of mechanosensory bristle cells than those fed a control diet. We propose that BBE, rich in naturally occurring antioxidants, promotes the survival of neurons in tissues with increased levels of α-synuclein through a protective cell survival mechanism.
Highlights
Parkinson disease (PD) is the second most common progressive neurodegenerative disorder and is only surpassed in frequency by Alzheimer disease [1]
In this study we describe the restorative effects of blueberry extract (BBE) concentrate on a Drosophila model of PD
We report a reduced lifespan in flies when α-synuclein expression is enhanced in the DA neurons (Figure 1(a))
Summary
Parkinson disease (PD) is the second most common progressive neurodegenerative disorder and is only surpassed in frequency by Alzheimer disease [1]. E. Staveley paminergic (DA) neurons in the substantia nigra pars compacta (SNc) and the presence of intra-neuronal inclusions known as Lewy bodies (LB) in surviving cells. Staveley paminergic (DA) neurons in the substantia nigra pars compacta (SNc) and the presence of intra-neuronal inclusions known as Lewy bodies (LB) in surviving cells Affected individuals have both motor and non-motor symptoms ranging from bradykinesia, resting tremor, and muscular rigidity to dementia, depression and olfactory dysfunction. The human α-synuclein gene (SNCA) encodes a 140 amino acid peripheral membrane protein that localizes to the pre-synaptic region of neurons [3] Both point mutations and duplications of its gene locus result in autosomal-dominant PD, the latter causing a more severe early-onset form of the disease. Both LBs and Lewy neurites, located in the perikarya and neuronal processes, respectively, stain positively for α-synuclein. α-synuclein is associated with both sporadic and familial PD and seems to play a critical role in its origin
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
