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

By BiotechDaily International staff writers
Posted on 22 Jul 2014
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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.”

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