Abstract
Drosophila melanogaster provides a powerful genetic model system in which to investigate the molecular mechanisms underlying neurodegenerative diseases. In this review, we discuss recent progress in Drosophila modeling Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis (ALS), Huntington’s Disease, Ataxia Telangiectasia, and neurodegeneration related to mitochondrial dysfunction or traumatic brain injury. We close by discussing recent progress using Drosophila models of neural regeneration and how these are likely to provide critical insights into future treatments for neurodegenerative disorders.
Highlights
Drosophila as a Model System for Studies of Human DiseaseThe common fruitfly Drosophila melanogaster has been used as a genetic model system for more than 100 years
Over the past three decades, a variety of human diseases have been modeled in Drosophila, including many affecting the nervous system [2,3,4]
Recent studies in Drosophila have demonstrated that paraquat exposure leads to deregulated innate immune responses [90]. It remains unclear whether deregulation of the innate immune response is a primary contributor to neurodegeneration following paraquat exposure; activation of the innate response has been linked to neurodegeneration in other contexts (e.g., [93])
Summary
The common fruitfly Drosophila melanogaster has been used as a genetic model system for more than 100 years. Drosophila possess extensive homology with humans at the genetic level making them a useful model for investigation of the cellular and molecular processes underlying development and disease [2]. Multiple rigorous assays to score neurodegeneration can be used in Drosophila, providing reliable measurements for the effects of the disease process. Such assays include examination of eye morphology and retinal structures by light microscopy, vacuolization of the central brain using histological staining, lifespan analysis, locomotor performance measurements using a climbing assay as well as assessment of neuromuscular junction morphology to determine potential synaptic abnormalities [18,19]. Wlikeeclyonfcultuudreewdiitrhecsotimones of the lDikreolsyopfuhtiulareneduirreocdtieognesnoefrtahteioDnrfioseolpdhitlhaanteiunrcoludedgeeuneseraotifotnhfisiepldowtheartfiunlclmudoedeulsteooifntvheisstpigoawteernfuelural regemnoedraetlioton iannvdeshtiogwatethneesuersatlurdeigeesnmeraaytiolenadantdo chloinwictahlleysereslteuvdainest tmhearyapleeaudtictos. clinically relevant therapeutics
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
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 call
