Reduction of Lewy Body Pathology by Oral Cinnamon
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ORIGINAL ARTICLE
Reduction of Lewy Body Pathology by Oral Cinnamon Sumita Raha 1 & Debashis Dutta 1 & Avik Roy 1 & Kalipada Pahan 1,2 Received: 21 August 2020 / Accepted: 31 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract α-Synucleinopathies in a broader sense comprise of several neurodegenerative disorders that primarily include Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). These disorders are well characterized by the accumulation of aggregated insoluble α-synuclein (α-syn) protein known as Lewy bodies. Till date no effective cure is available to reduce the burden of Lewy body. The present investigation underlines the importance of a naturally used spice and flavoring agent viz. cinnamon in reducing α-syn deposits in transgenic mice expressing mutant A53T human α-syn. Upon oral administration, cinnamon markedly reduced the level of insoluble α-syn in nigra, hippocampus and brain stem of A53T mice. We also demonstrated that sodium benzoate (NaB), a metabolite of cinnamon, a widely used food additive and a FDA-approved drug for glycine encephalopathy, was also capable of reducing α-syn deposits in A53T mice. In addition, both cinnamon and NaB treatments showed improvement in their motor and cognitive functions. Glial activation plays an important role in the pathogenesis of various neurodegenerative disorders including PD, DLB and MSA, and we found suppression of microglial and astroglial activation in the nigra of A53T mice upon cinnamon treatment. Moreover, neuroprotective proteins like DJ-1 and Parkin are known to reduce the formation of Lewy bodies in the CNS. Accordingly, we observed upregulation and/or normalization of DJ-1 and Parkin in the nigra of A53T mice by treatment with cinnamon and NaB. Together, these results highlight a new therapeutic property of cinnamon and suggest that cinnamon and NaB may be used to halt the progression of αsynucleinopathies. Keywords α-synucleinopathy . A53T mice . Cinnamon . Sodium benzoate . Glial activation
Introduction α-Synuclein (α-syn) is the key molecule in the pathogenesis of synucleinopathy that leads to neurodegenerative diseases characterized by the abnormal accumulation of α-syn aggregates in neurons, nerve fibers or glial cells of which the main types are Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Of these, PD is the second most devastating progressive neurodegenerative Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11481-020-09955-2) contains supplementary material, which is available to authorized users. * Kalipada Pahan [email protected] 1
Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison St, Suite 310, Chicago, IL 60612, USA
2
Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, 820 South Damen Avenue, Chicago, IL 60612, USA
movement disorder caused by the death of dopaminergic neurons in the su
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