Summary: A new study reports caffeine plus another compound found in the waxy coating of coffee beans may help protect the brain against Parkinson’s disease.
Source: Rutgers University.
Rutgers scientists have found a compound in coffee that may team up with caffeine to fight Parkinson’s disease and Lewy body dementia – two progressive and currently incurable diseases associated with brain degeneration.
The discovery, recently published in the Proceedings of the National Academy of Sciences, suggests these two compounds combined may become a therapeutic option to slow brain degeneration.
Lead author M. Maral Mouradian, director of the Rutgers Robert Wood Johnson Medical School Institute for Neurological Therapeutics and William Dow Lovett Professor of Neurology, said prior research has shown that drinking coffee may reduce the risk of developing Parkinson’s disease. While caffeine has traditionally been credited as coffee’s special protective agent, coffee beans contain more than a thousand other compounds that are less well known.
The Rutgers study focused on a fatty acid derivative of the neurotransmitter serotonin, called EHT (Eicosanoyl-5-hydroxytryptamide), found in the bean’s waxy coating. The researchers found that EHT protects the brains of mice against abnormal protein accumulation associated with Parkinson’s disease and Lewy body dementia.
In the current research, Mouradian’s team asked whether EHT and caffeine could work together for even greater brain protection. They gave mice small doses of caffeine or EHT separately as well as together. Each compound alone was not effective, but when given together they boosted the activity of a catalyst that helps prevent the accumulation of harmful proteins in the brain. This suggests the combination of EHT and caffeine may be able to slow or stop the progression of these diseases. Current treatments address only the symptoms of Parkinson’s disease but do not protect against brain degeneration.
Mouradian said further research is needed to determine the proper amounts and ratio of EHT and caffeine required for the protective effect in people.
“EHT is a compound found in various types of coffee but the amount varies. It is important that the appropriate amount and ratio be determined so people don’t over-caffeinate themselves, as that can have negative health consequences,” she said.
According to the U.S. Department of Health & Human Services, Parkinson’s disease is a brain disorder that can lead to shaking, stiffness and difficulty with walking, balance and coordination. Nearly one million people in the United States are living with Parkinson’s disease. Lewy body dementia, one of the most common forms of dementia, affects more than one million people in the United States. It causes problems with thinking, behavior, mood, and movement.
Funding: The study was funded by the National Institutes of Health.
Source: Neal Buccino – Rutgers University
Publisher: Organized by NeuroscienceNews.com.
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Original Research: Open access research for “Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB” by Run Yan, Jie Zhang, Hye-Jin Park, Eun S. Park, Stephanie Oh, Haiyan Zheng, Eunsung Junn, Michael Voronkov, Jeffry B. Stock, and M. Maral Mouradian in PNAS. Published December 3 2018.
Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB
Hyperphosphorylated α-synuclein in Lewy bodies and Lewy neurites is a characteristic neuropathological feature of Parkinson’s disease (PD) and Dementia with Lewy bodies (DLB). The catalytic subunit of the specific phosphatase, protein phosphatase 2A (PP2A) that dephosphorylates α-synuclein, is hypomethylated in these brains, thereby impeding the assembly of the active trimeric holoenzyme and reducing phosphatase activity. This phosphatase deficiency contributes to the accumulation of hyperphosphorylated α-synuclein, which tends to fibrillize more than unmodified α-synuclein. Eicosanoyl-5-hydroxytryptamide (EHT), a fatty acid derivative of serotonin found in coffee, inhibits the PP2A methylesterase so as to maintain PP2A in a highly active methylated state and mitigates the phenotype of α-synuclein transgenic (SynTg) mice. Considering epidemiologic and experimental evidence suggesting protective effects of caffeine in PD, we sought, in the present study, to test whether there is synergy between EHT and caffeine in models of α-synucleinopathy. Coadministration of these two compounds orally for 6 mo at doses that were individually ineffective in SynTg mice and in a striatal α-synuclein preformed fibril inoculation model resulted in reduced accumulation of phosphorylated α-synuclein, preserved neuronal integrity and function, diminished neuroinflammation, and improved behavioral performance. These indices were associated with increased levels of methylated PP2A in brain tissue. A similar profile of greater PP2A methylation and cytoprotection was found in SH-SY5Y cells cotreated with EHT and caffeine, but not with each compound alone. These findings suggest that these two components of coffee have synergistic effects in protecting the brain against α-synuclein−mediated toxicity through maintenance of PP2A in an active state.