Matthew Farrer

Professor

Research Classification

Neurological Diseases
Genetics of Neurological and Psychiatric Diseases
Neuronal Modeling
Neuronal Communication and Neurotransmission

Research Interests

Parkinson's disease
Dementia
Epilepsy

Relevant Degree Programs

 

Research Methodology

Confocal Imaging
Genome sequencing
electrophysiology
bioinformatics
Neuronal culture
Mouse models

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Postdoctoral Fellows
Any time / year round
2019

Research projects are devoted to 'precision' medicine, namely the development of novel therapeutics based on the genetic etiology of brain disorders. Over the past 20 years my group has identified many of the molecular causes of Parkinson's disease, some genetic forms of dementia and epilepsy, and has exploited that knowledge to make physiologic models with which to characterize subtle changes in brain function. Based on this innovation, and working in close collaboration with the Pharmaceutical industry, several drugs are now in clinical trials that have been designed to halt and/or prevent these diseases.

I support public scholarship, e.g. through the Public Scholars Initiative, and am available to supervise students and Postdocs interested in collaborating with external partners as part of their research.
I support experiential learning experiences, such as internships and work placements, for my graduate students and Postdocs.
I am open to hosting Visiting International Research Students (non-degree, up to 12 months).
I am interested in hiring Co-op students for research placements.

Graduate Student Supervision

Doctoral Student Supervision (Jan 2008 - May 2019)
Characterisation of the new vps35 p.d620n ki mouse model of parkinson's disease (2018)

No abstract available.

Identification of genetic modifiers in LRRK2 parkinsonism (2017)

Genetic studies have been extremely informative to the pathophysiology of PD. The most common pathogenic mutation discovered is LRRK2 p.G2019S which accounts for 30-40% of Parkinson disease (PD) in North African Arab Berbers, 18-30% in Ashkenazi Jews and 1-3% in Caucasians. Although LRRK2 p.G2019S parkinsonism is considered a monogenic form of disease, disease penetrance of motor symptoms is variable. We hypothesize that genetic factors can modulate the phenoconversion of LRRK2 p.G2019S which could lead to treatments that prevent onset or delay disease progression.Clinical characterization of LRRK2 p.G2019S carriers from Tunisia was performed by analysis of motor and non-motor features. Genetic analysis of age of onset as a genetic trait was performed in a cohort of Tunisian Arab Berbers with LRRK2 p.G2019S. Short-tandem repeat genotyping (4cM resolution) and non-parametric and model-based genome-wide linkage was evaluated in 41 multi-incident LRRK2 p.G2019S families. High-density locus-specific genotyping and association analyses were also performed in 232 unrelated LRRK2 p.G2019S carriers. Genome sequencing in a subset of 25 subjects informed imputation and haplotype analyses. Validation analysis used Sanger sequencing and Taqman genotyping on additional LRRK2 p.G2019S carriers originating from Algeria, France and Norway. Whole transcriptome, candidate gene and protein expression was assessed in striatum from 60 human brains.Significant linkage was identified on chromosome 1q23.3-24.3 (model-based LOD=4.99, D1S2768). In the chromosome 1q23.3-24. interval higher-resolution SNP genotyping, association and haplotype mapping nominated genetic variability within DNM3 as an age of onset modifier of disease penetrance (rs2421947 nominal p
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Master's Student Supervision (2010 - 2018)
The nigrostriatal dopamine system in the leucine-rich repeat kinase 2 G2019S knock-in mouse model of Parkinson's disease (2016)

Mutations on the leucine-rich repeat kinase 2 (LRRK2) gene are the most common variants responsible for idiopathic Parkinson’s disease (PD). Historically, PD is thought of as a late-stage neurodegenerative disease resulting from the loss of dopaminergic neurons in the substantia nigra pars compacta with the presence of Lewy pathology. Current treatments focus on the dopaminergic aspect of this disease, without addressing or successfully halting the underlying causes of this disease. The LRRK2 G2019S mutation is the single most common genetic risk factor for Parkinson’s disease and leads to increased kinase activity with subtle effects on the timing of nigrostriatal dopaminergic transmission. Here, using a genetically faithful G2019S knock-in (GKI) mouse model at multiple age points, although no differences were seen in monoamine, glutamate, or GABA release by in vivo microdialysis of the dorsolateral striatum, more temporally sensitive investigation revealed subtle release augmentation in mutants. Using fast-scan cyclic voltammetry to examine dopamine release and reuptake on a millisecond timescale in acute striatal slices at early (
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Publications

 
 

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