Coffee is by far the most widely and highly consumed herbal extract. Numerous epidemiological studies indicate that coffee consumption affords reduced risk of Parkinson's disease (PD). This association has been attributed to caffeine, but coffee is much more than just caffeine and the finding that caffeine may be neuroprotective in no way obviates the possibility that other components in coffee may play a synergistic role with caffeine. We have recently isolated a lipid-like component of coffee, EHT, and found it to have a protective effect in mouse models of PD. Biochemical and neuropathological analyses demonstrate that dietary supplementation with EHT leads to decreased ?-synuclein phosphorylation and aggregation, a robust anti-inflammatory effect, and protection against oxidative stress. Studies indicate that the actions of caffeine stem from its antagonism of adenosine A2A receptor signaling, but downstream neuroprotective mechanisms remain to be established. The proposed research will elucidate the molecular mechanisms of neuroprotection mediated by caffeine and EHT as well as their synergy through in vitro biochemical analyses, cell based molecular experiments and in vivo studies in mouse models of PD. The ultimate goal of this work is to develop a dietary supplement(s) or medical food that would slow the progression or prevent the development of neurodegenerative disorders such as PD.
Coffee, which by far is the most widely and highly consumed herbal extract worldwide, has been linked to reduced risk of developing Parkinson's disease. While this effect has been attributed largely to caffeine, coffee has many more components than just caffeine. This project focuses on understanding the mechanisms by which certain coffee constituents protect brain cells. The ultimate goal of this work is to develop a dietary supplement(s) that would slow the progression or prevent the development of neurodegenerative disorders including Parkinson's disease.
|Oh, Stephanie E; Mouradian, M Maral (2017) Regulation of Signal Transduction by DJ-1. Adv Exp Med Biol 1037:97-131|
|Park, Hye-Jin; Lee, Kang-Woo; Oh, Stephanie et al. (2017) Protein Phosphatase 2A and Its Methylation Modulating Enzymes LCMT-1 and PME-1 Are Dysregulated in Tauopathies of Progressive Supranuclear Palsy and Alzheimer Disease. J Neuropathol Exp Neurol :|
|Phukan, Geetika; Shin, Tae Hwan; Shim, Jeom Soon et al. (2016) Silica-coated magnetic nanoparticles impair proteasome activity and increase the formation of cytoplasmic inclusion bodies in vitro. Sci Rep 6:29095|
|Park, Hye-Jin; Lee, Kang-Woo; Park, Eun S et al. (2016) Dysregulation of protein phosphatase 2A in parkinson disease and dementia with lewy bodies. Ann Clin Transl Neurol 3:769-780|
|Aung, Latt Latt; Mouradian, M Maral; Dhib-Jalbut, Suhayl et al. (2015) MMP-9 expression is increased in B lymphocytes during multiple sclerosis exacerbation and is regulated by microRNA-320a. J Neuroimmunol 278:185-9|
|Chaudhuri, Amrita Datta; Kabaria, Savan; Choi, Doo Chul et al. (2015) MicroRNA-7 Promotes Glycolysis to Protect against 1-Methyl-4-phenylpyridinium-induced Cell Death. J Biol Chem 290:12425-34|
|Potts, Lisa F; Uthayathas, Subramaniam; Greven, Alexander C M et al. (2015) A new quantitative rating scale for dyskinesia in nonhuman primates. Behav Pharmacol 26:109-16|
|Potts, Lisa F; Park, Eun S; Woo, Jong-Min et al. (2015) Dual ?-agonist/?-antagonist opioid receptor modulation reduces levodopa-induced dyskinesia and corrects dysregulated striatal changes in the nonhuman primate model of Parkinson disease. Ann Neurol 77:930-41|
|Lee, Kang-Woo; Woo, Jong-Min; Im, Joo-Young et al. (2015) Apoptosis signal-regulating kinase 1 modulates the phenotype of ?-synuclein transgenic mice. Neurobiol Aging 36:519-26|
|Kabaria, Savan; Choi, Doo Chul; Chaudhuri, Amrita Datta et al. (2015) Inhibition of miR-34b and miR-34c enhances ?-synuclein expression in Parkinson's disease. FEBS Lett 589:319-25|
Showing the most recent 10 out of 16 publications