Targeting Parkinsons Disease 

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As an industry-focused preclinical meeting, the Targeting Parkinson’s Disease conference will address major challenges in current drug development while identifying significant contributions to technology and target optimization by leading researchers. As a complex neurodegenerative movement disorder, Parkinson’s disease can be approached from multiple angles in drug discovery. One can look at disease modification or symptomatic improvement; create models that mimic specific disease states or genetically engineer models to elicit progressive degeneration.  Advances in imaging, biomarker development, and genetics (such as LRKK2 and alpha-synuclein) are playing a crucial role in the accelerated discovery of new targets and the development of lead compounds.



12:30 pm Registration

1:55 Chairperson’s Opening Remarks



David Weiner, M.D., Vice President, Head, Early Clinical Development & Neurology Global Clinical Development Unit; U.S. Site Head, Medical Science and Innovation, EMD Serono, Inc.

Mouse Models 

2:30 Mitopark Mice: A Model of Progressive Dopamine Depletion and Parkinsonism

Susan E. Browne, Ph.D., Director, Neuropharmacology, Merck Research Labs

A new player recently entered the arena of Parkinson's disease (PD) research. MitoPark mice offer several advantages over conventional in vivo models of PD.  First, they undergo gradual impairment of the central dopaminergic system, due to mitochondrial damage selectively targeted to dopamine neurons. Consequently, mice develop a series of motor defects resembling those typical of Parkinsonism, including bradykinesia, tremor, and catalepsy. We will discuss the progressive phenotypes that distinguish MitoPark mice, and their potential as tools in PD drug development.

3:00 Alpha-synuclein Overexpressing Mouse Models of Parkinson’s Disease

Anita Sidhu, Ph.D., Professor & Head, Laboratory of Molecular Neurochemistry, Georgetown University

3:30 Networking Refreshment Break in the Exhibit Hall

4:30 The Rotenone Model of Parkinson’s Disease

J. Timothy Greenamyre, M.D., Ph.D., Professor & Vice-Chair of Neurology; Director, Pittsburgh Institute for Neurodegenerative Diseases; UPMC Endowed Chair & Chief, Movement Disorders, University of Pittsburgh  

While recent genetic studies have provided evidence for systemic mitochondrial impairment in PD, the first proof-of-concept came years earlier from rotenone-treated rats. The rotenone model of PD accurately reproduces many features of the human disease, including nigrostriatal degeneration and DOPA-responsive behavioral deficits, aggregation of endogenous alpha-synuclein with Lewy pathology, and microglial activation. It also recapitulates the gastrointestinal pathology and functional deficits seen in the human disease. Moreover, epidemiological studies have shown that rotenone is a bona fide risk factor for human PD. As such, the rotenone model may have substantial value for pre-clinical testing.   

5:00 PD Genetic Mouse Models of LRRK2l

Youren Tong, Ph.D., Instructor in Neurology, Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School

Dominantly inherited mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson’s disease (PD), but how these mutations cause the disease is unclear. To investigate the pathogenic mechanism underlying LRRK2 mutations and the normal physiological role of LRRK2, we generated LRRK2 knockin (R1441C) and knockout mouse models. The results from our multidisciplinary analyses of the LRRK2 mouse models will be discussed.

5:30 End of Day


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