The Foundation supports research across basic, translational and clinical science to speed breakthroughs that can lead to the creation of new treatments and a better quality of life for people with Parkinson's disease.
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Previously funded studies appear chronologically, with the most recent appearing first.
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Target Validation, 2011Inhibition of LINGO-1 as a Novel Target for Regeneration in Pre-clinical PD Models
Objective/Rationale:
LINGO-1 inhibits growth responses in the central nervous system and LINGO-1 expression is increased when nerve cells are exposed to injury. We have shown that LINGO-1 expression... -
Target Validation, 2011Evaluation of ATP13A2 as a Molecular Target for Ameliorating Alpha-Synuclein-Induced Neurodegeneration in Pre-clinical Models of PD
Objective/Rationale:
Mutations in the alpha-synuclein gene cause autosomal dominant Parkinson’s disease. While mutant forms of alpha-synuclein are toxic when introduced into neurons and pre-clinical... -
MJFF Research Grant, 2011Generating Patient-Specific Induced Pluripotent Stem Cells to Study Parkinson's Disease
Objective/Rationale:
We have generated two lines of human dopamine neurons with parkin mutations and two lines from normal people using stem cells derived from their skin cells. Several interesting... -
Antibody Comparison, 2011Analysis of LRRK2 Antibodies
Objective/Rationale:
There is great hope that drugs targeting an enzyme termed LRRK2 may be useful in treating Parkinson’s disease (PD). There is therefore intense research taking place to better... -
Antibody Comparison, 2011LRRK2 Immunocytochemistry in Cultured Neurons
Objective/Rationale:
Several antibodies have been identified that recognize Leucine-Rich Repeat Kinase 2 (LRRK2), but uncertainty persists as to whether such antibodies are reliable in detecting ... -
Antibody Comparison, 2011Characterization of LRRK2 Monoclonal Antibodies in Pre-clinical Brain Tissue
Objective/Rationale:
Mutations in Leucine Rich Repeat Kinase 2 (LRRK2) are implicated in Parkinson’s disease in humans. At present we understand neither the normal nor the pathogenic role of LRRK2. We...
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