The Michael J. Fox Foundation Announces $1.5 Million in Funding to Advance Development of Drug Targets for Disease-Modifying Parkinson's Disease Treatments

http://www.prnewswire.com/news-relea...-78151902.html

NEW YORK, Nov. 30 /PRNewswire-USNewswire/ -- The Michael J. Fox Foundation for Parkinson's Research (MJFF) today announced $1.5 million in total awards to six research teams working to develop potentially disease-modifying therapies for Parkinson's disease. The funding was awarded under the Novel Approaches to Drug Discovery for Parkinson's Disease program, made possible by funding from Elan Corporation, plc (NYSE: ELN), a neuroscience-based biotechnology company.

The Novel Approaches program is an important component of MJFF's overall strategy of providing critical resources to under-funded areas of the drug development pipeline. Novel Approaches seeks to advance the development of therapeutic targets that already have some promising initial data, while engaging industry partner Elan as a potential follow-on funder for those projects with the greatest potential to bring new, transformative treatments to people living with PD.

Inhibition of brain-dependent nitric oxide (NO) over-production by isoform-selective NO synthase (NOS) inhibitors
John Andrews, PhD, NeurAxon, Toronto, Ontario, Canada
Development of HSF1 effectors as Parkinson's disease therapeutics
William Janzen, PhD, and Maria Sippola-Thiele, PhD, Chaperone Therapeutics, Durham, North Carolina
Optimizing metalloporphryins for clinical development
Manish Patel, PhD, University of Colorado, Denver, Colorado
Optimization of alpha synuclein 5'UTR directed translation blockers as novel drugs for Parkinson's disease
Jack Rogers, PhD, Mental Health Research Institute of Victoria, Melbourne, Australia
Cerium oxide nanoparticles in treatment of Parkinson's disease
Beverly Rzigalinski, PhD, Virginia College of Osteopathic Medicine, Blacksburg, Virginia
Novel JNK inhibitors as therapeutic agents for Parkinson's disease
Bobby Thomas, PhD, Weill Medical College of Cornell University, New York, New York and Maurizio Pellecchia, PhD, Burnham Institute for Medical Research, La Jolla, California

stakeholders making decisions for us.......it looks good i guess.......

someone let me know if i have something included that is incorrect...p
http://michaeljfox.org/research_MJFF...ountry=&State=
&Last_Name=&Institution=&Grant_Funded_Year=&search .x=19&search.y=7

Novel Approaches to Drug Discovery for Parkinson's Disease 2009
HSF1 Effectors

Objective/Rationale:

This project will focus on the development of small molecule therapeutics to treat Parkinson’s disease by advancing lead compounds that modulate protein chaperones. Protein chaperones are proteins that guide the correct protein folding in cells and also function as the cellular quality control mechanism for correct protein folding. Chaperone’s compounds work by stimulating HSF1, a key regulator of protein chaperones, to restore normal protein balance in diseased neurons.

Title:
Cerium Oxide Nanoparticles for Treatment and Prevention of Alzheimer's Disease, Parkinson's Disease, and Disorders Associated with Free Radical Production and/or Mitochondrial Dysfunction

United States Patent Application 20090092671



Porphyrins which are combined with a metal ion. The metal is bound equally to all four nitrogen atoms of the pyrrole rings. They possess characteristic absorption spectra which can be utilised for identification or quantitative estimation of porphyrins and porphyrin-bound compounds.
(12 Dec 1998)

Novel Approaches to Drug Discovery for Parkinson's Disease 2009
Objective/Rationale:

Oxidative stress is a well-defined therapeutic target for Parkinson’s disease (PD) and antioxidant therapy is one of the most promising neuroprotective strategies for its treatment. Metalloporphyrins are synthetic catalytic antioxidants that mimic the body’s own antioxidant defensive enzymes i.e. superoxide dismutases and catalase. The goal of this proposal is to determine if a newly developed glyoxylate (AEOL112) series of metalloporphyrins designed to penetrate blood brain barrier shows promise for treatment of PD.


http://michaeljfox.org/research_MJFF...s_3.cfm?ID=583

Int Immunopharmacol. 2006 Jun;6(6):987-96. Epub 2006 Feb 9.
JNK inhibitor SP600125 reduces COX-2 expression by attenuating mRNA in activated murine J774 macrophages.

Nieminen R, Lahti A, Jalonen U, Kankaanranta H, Moilanen E.
The Immunopharmacology Research Group, University of Tampere Medical School, and Tampere University Hospital, Research Unit, FIN-33014, Tampere, Finland.
Inducible prostaglandin synthase (cyclooxygenase-2, COX-2) is highly expressed in inflammation. The signaling mechanisms involved in the up-regulation of COX-2 are not known in detail. In the present study we investigated the role of c-Jun NH2-terminal kinase (JNK), a member of the mitogen-activated protein kinase (MAPK) family in COX-2 expression and prostaglandin (PG) E2 production in murine J774 macrophages activated by bacterial lipopolysaccharide (LPS). LPS caused a transient activation of JNK which was followed by increased COX-2 expression. Anthra(1,9-cd)pyrazol-6(2H)-one (SP600125), an inhibitor of JNK, inhibited phosphorylation of c-Jun with an IC50 of 5-10 microM. At the same concentrations SP600125 suppressed also LPS-induced COX-2 protein levels and PGE2 production. SP600125 did not alter LPS-induced COX-2 mRNA levels when measured 3 h after addition of LPS, whereas mRNA levels were significantly reduced in SP600125-treated cells when measured 24 h after addition of LPS. LPS-induced COX-2 mRNA levels reduced faster in cells treated with SP600125 than in control cells. Cycloheximide (that is known to activate JNK) enhanced COX-2 expression and its effect was inhibited by SP600125. The present results suggest that JNK pathway is involved in the up-regulation of COX-2 expression possibly by a mechanism related to the stability of COX-2 mRNA.

PMID: 16644485 [PubMed - indexed for MEDLINE]

partner
http://www.elan.com/rd/research_areas/

Elan’s approach to Parkinson’s disease is focused on molecules that may be involved in the formation of Lewy bodies, which are considered the hallmark of Parkinson’s disease. Elan scientists have identified unusual forms of alpha-synuclein, a major component of Lewy bodies, in human Parkinson’s disease brain tissue, which has led to a series of therapeutic targets that are the current focus of our new drug discovery efforts.

Autoimmune Diseases

wrong thread sorry