Grant: Travel Awards - Institute Community Support
University of Toronto
$778.00
Transduction of wild type mice with AAV2-alpha-synuclein-GFP drives expression of alpha-synuclein in the brain stem region that controls muscle atonia during REM sleep.
FY 2014-15
Summary
Rapid eye movement (REM) sleep is the stage of sleep during which dreaming occurs and the body is paralyzed. Control of this paralysis relies on an area of the brain stem called the subcoeruleus (SubC). When the SubC stops functioning, paralysis is lost and dreams are violently acted out, a condition known as REM sleep behavior disorder (RBD). The brain pathology of RBD is poorly understood, however greater insight into this disease is crucial. The vast majority of RBD patients (>80%) eventually develop synucleinopathies, which are a type of neurodegenerative disease defined by toxic buildup of a protein called alpha-synuclein, the most prominent of which is Parkinson's disease. Adeno-associated virus (AAV) can be used to increase the amount of a desired protein in cells. Using AAV2-alpha-synuclein, we are the first to show that alpha-synuclein expression can be driven in the SubC, which demonstrates a possible mechanism for the development of RBD. This provides a link between RBD and synucleinopathic neurodegenerative diseases, and is a vital tool for future research to better understand the development of both. By focusing on the brain stem region controlling paralysis during REM sleep, an area which appears to be affected early in the development of neurodegenerative diseases, our findings also provide an animal model for investigation into possible preventative treatments for Parkinson's disease and related disorders.
Department
Program
Travel Awards - Institute Community Support
Recipient
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
324334
Name
McKenna Dillon
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Canadian Sleep Society
Projecttitle
Transduction of wild type mice with AAV2-alpha-synuclein-GFP drives expression of alpha-synuclein in the brain stem region that controls muscle atonia during REM sleep.
Programtype2
Undefined
Orgnameinp2
University of Toronto
Cihramount2
$778
Cihrequipment2
$0
Programname2
Travel Awards - Institute Community Support
Keyworddelim
Alpha-Synuclein; Parkinson'S Disease; Rem Sleep; Rem Sleep Behavior Disorder; Subcoeruleus
Abstract
Rapid eye movement (REM) sleep is the stage of sleep during which dreaming occurs and the body is paralyzed. Control of this paralysis relies on an area of the brain stem called the subcoeruleus (SubC). When the SubC stops functioning, paralysis is lost and dreams are violently acted out, a condition known as REM sleep behavior disorder (RBD). The brain pathology of RBD is poorly understood, however greater insight into this disease is crucial. The vast majority of RBD patients (>80%) eventually develop synucleinopathies, which are a type of neurodegenerative disease defined by toxic buildup of a protein called alpha-synuclein, the most prominent of which is Parkinson's disease. Adeno-associated virus (AAV) can be used to increase the amount of a desired protein in cells. Using AAV2-alpha-synuclein, we are the first to show that alpha-synuclein expression can be driven in the SubC, which demonstrates a possible mechanism for the development of RBD. This provides a link between RBD and synucleinopathic neurodegenerative diseases, and is a vital tool for future research to better understand the development of both. By focusing on the brain stem region controlling paralysis during REM sleep, an area which appears to be affected early in the development of neurodegenerative diseases, our findings also provide an animal model for investigation into possible preventative treatments for Parkinson's disease and related disorders.
Competitiondate
201501
Approvedterm2
1 yr 0 mth
Pinamesdelim
McKenna, Dillon
Approvedterm
1 an 0 mois
Cihrcontribution2
Inst of Circ &Respiratory Hlth~ $778~ $0~