Parkinson’s disease is a degenerative disorder of the central nervous system in which dopamine generating cells in the substantia nigra die. This then affects the motor system with regards to movement related activities, such as, shaking, rigidity, difficulty in walking and slowness in walking.
Two proteins in the brain act to protect neurons in the substantia nigra from cell death. The first is Protein deglycase DJ-1 (DJ-1) which protects neurons against oxidative stress and cell death The second is Parkin which helps degrade one or more proteins toxic to dopaminergic neurons. The loss of function of the Parkin protein leads to dopaminergic cell death, which then can lead to Parkinson’s disease. Parkin and DJ-1 are known to stimulate and support the survival of existing dopaminergic neurons. It has been identified that Parkin and Protein deglycase DJ-1 decrease in the brain of Parkinson’s patients. 1
An interesting article published in the Journal of Neuroimmune Pharmacology in September 2014 entitled Cinnamon Treatment Upregulates Neuroprotective Proteins Parkin and DJ-1 and Protects Dopaminergic Neurons in a Mouse Model of Parkinson’s Disease explored a novel use of cinnamon in upregulating Parkin and DJ-1 and protecting dopaminergic neurons in a MPTP mouse model of Parkinson’s.
The authors from Rush University Medical Center’s Department of Neurological Sciences, Kalipada Pahan and Saurabh Khasnavis found that after oral feeding, ground cinnamon (Ceylon cinnamon (Cinnamonum verum)) is metabolized into sodium benzoate, which then enters into the brain, which then: 2
- Stops the loss of Parkin and Protein deglycase DJ-1
- Protects neurons
- Normalizes neurotransmitter levels
- Improves motor functions in mice with Parkinson’s
The authors also found that the oral treatment of MPTP-intoxicated mice with cinnamon powder and sodium benzoate: 3
- Reduces the nigral expression of iNOS
- Blocks nigral loss of Parkin and DJ-1
- Protects the nigrostriatal axis
- Restores locomotor activities
They suggested that cinnamon may be used to protect dopaminergic neurons in the nigra of Parkinson’s patients.
The authors of the study used True Cinnamon or Ceylon cinnamon (Cinnamonum verum) rather than using Chinese cinnamon (Cinnamomum cassia). They stated that “Although both types of cinnamon are metabolized into sodium benzoate, by mass spectrometric analysis, we have seen that Ceylon cinnamon is much more pure than Chinese cinnamon as the latter contains coumarin, a hepatotoxic molecule.” 4
The use of Ceylon cinnamon “could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients.” 5
Ceylon cinnamon contains a major compound named cinnamaldehyde, which is converted into cinnamic acid by oxidation. In the liver, this cinnamic acid is β-oxidized to benzoate that exists as sodium salt (NaB) or benzoyl-CoA. 6
The authors concluded their study by stating, “Now we need to translate this finding to the clinic and test ground cinnamon in patients with PD. If these results are replicated in PD patients, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease.” 7
It is important to note that if one is to consume a teaspoon or less of Ceylon cinnamon or True cinnamon (Cinnamonum verum) daily, it should be consumed in liquid or in food, and never in its dry form directly in the mouth as this could cause choking. Also make sure that it is Ceylon cinnamon or True cinnamon (Cinnamonum verum) that is consumed and not Chinese cinnamon (Cinnamomum cassia), as Chinese cinnamon can be hepatotoxic in large quantities and on a frequent basis.
A common method of consuming Ceylon cinnamon or True cinnamon (Cinnamonum verum) is to mix it in a smoothie with fruit and protein powder.
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