Features | Partner Sites | Information | LinkXpress
Sign In
GLOBETECH PUBLISHING LLC
GLOBETECH MEDIA
GLOBETECH PUBLISHING LLC

Cinnamon Feeding Blocks Development of Parkinson's Disease in Mouse Model

By BiotechDaily International staff writers
Posted on 22 Jul 2014
Image: Molecular rendering of the crystal structure of parkin (Photo courtesy of Wikimedia Commons).
Image: Molecular rendering of the crystal structure of parkin (Photo courtesy of Wikimedia Commons).
A team of neurological researchers has identified a molecular mechanism by which cinnamon acts to protect neurons from damage caused by Parkinson's disease (PD) in a mouse model of the syndrome.

Investigators at Rush University (Chicago, IL, USA) have been exploring the novel use of cinnamon in upregulating the enzymes Parkin and DJ-1 and protecting dopaminergic neurons in the MPTP mouse model of PD. Recently they found that oral feeding of cinnamon (Cinnamonum verum) powder produced sodium benzoate (NaB) in the blood and brains of the mice.

Parkin is a protein which in humans is encoded by the PARK2 gene. The precise function of this protein is unknown; however, the protein is a component of a multiprotein E3 ubiquitin ligase complex which in turn is part of the ubiquitin-proteasome system that mediates the targeting of proteins for degradation. Mutations in this gene are known to cause a familial form of Parkinson's disease known as autosomal recessive juvenile Parkinson's disease (AR-JP). How loss of function of the parkin protein leads to dopaminergic cell death in this disease is unclear. The prevailing hypothesis is that parkin helps degrade one or more proteins toxic to dopaminergic neurons.

DJ-1 is a protein which in humans is encoded by the PARK7 gene. DJ-1 belongs to the peptidase C56 family of proteins. It acts as a positive regulator of androgen receptor-dependent transcription. It may also function as a redox-sensitive chaperone, as a sensor for oxidative stress, and it apparently protects neurons against oxidative stress and cell death.

In the current study, which was published in the June 20, 2014, online edition of the Journal of Neuroimmune Pharmacology, the investigators found that the proinflammatory cytokine IL-1beta decreased the level of Parkin/DJ-1 in mouse astrocytes. However, the cinnamon metabolite NaB abrogated IL-1beta-induced loss of these proteins. These findings at the molecular level paralleled improved clinical appearance of the PD mice following cinnamon feeding.

“Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of PD,” said senior author Dr. Kalipada Pahan, professor of neurology at Rush University. “It is known that some important proteins like Parkin and DJ-1 decrease in the brain of PD patients.”

“Cinnamon is metabolized in the liver to sodium benzoate, which is an FDA-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia,” said Dr. Pahan. “Cinnamon has been used widely as a spice throughout the world for centuries and is also widely used as a food preservative due to its microbiocidal effect. This could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients.”


Related Links:
Rush University



Channels

Genomics/Proteomics

view channel
Image: In mice, mitochondria (green) in healthy (left) and Mfn1-deficient heart muscle cells (center) are organized in a linear arrangement, but the organelles are enlarged and disorganized in Mfn2-deficient cells (right) (Photo courtesy of the Rockefeller Press).

Cell Biologists Find That Certain Mitochondrial Diseases Stem from Coenzyme Q10 Depletion

A team of German cell biologists has linked the development of certain mitochondrial-linked diseases to depletion of the organelles' pool of coenzyme Q10 brought about by mutation in the MFN2 gene, which... Read more

Biochemistry

view channel

Possible New Target Found for Treating Brain Inflammation

Scientists have identified an enzyme that produces a class of inflammatory lipid molecules in the brain. Abnormally high levels of these molecules appear to cause a rare inherited eurodegenerative disorder, and that disorder now may be treatable if researchers can develop suitable drug candidates that suppress this enzyme.... Read more

Lab Technologies

view channel
Image: The FLUOVIEW FVMPE-RS Gantry microscope (Photo courtesy of Olympus).

New Multiphoton Laser Scanning Microscope Configurations Expand Research Potential

Two new configurations of a state-of-the-art multiphoton laser scanning microscope extend the usefulness of the instrument for examining rapidly occurring biological events and for obtaining images from... Read more

Business

view channel

Roche Acquires Signature Diagnostics to Advance Translational Research

Roche (Basel, Switzerland) will advance translational research for next generation sequencing (NGS) diagnostics by leveraging the unique expertise of Signature Diagnostics AG (Potsdam, Germany) in biobanks and development of novel NGS diagnostic assays. Signature Diagnostics is a privately held translational oncology... Read more
 
Copyright © 2000-2015 Globetech Media. All rights reserved.