Summary: Researchers report that drinking coffee may lower the risk of developing Alzheimer’s and Parkinson’s disease. The study finds that compounds formed during roasting — particularly in dark roasts — show the strongest neuroprotective activity.
Source: Universal Health Network.
Approximately 500 billion cups of coffee are consumed worldwide each year.
A new study from the Krembil Brain Institute, part of the Krembil Research Institute, suggests that the benefits of coffee extend beyond increased alertness and energy. The research indicates that certain compounds produced during coffee roasting may help protect the brain from the protein changes linked to Alzheimer’s and Parkinson’s diseases.
“Coffee consumption does seem to have some correlation to a decreased risk of developing Alzheimer’s disease and Parkinson’s disease,” says Dr. Donald Weaver, Co-director of the Krembil Brain Institute. “We wanted to investigate which specific compounds are responsible and how they might influence age-related cognitive decline.”
Dr. Weaver’s team, including medicinal chemist Dr. Ross Mancini and biologist Yanfei Wang, compared three instant coffee extracts: light roast, dark roast, and decaffeinated dark roast. Their experiments examined how those extracts and individual coffee components affect the aggregation of proteins associated with neurodegenerative disease.
Early results showed that both caffeinated and decaffeinated dark roast extracts produced similar protective effects. “We observed early on that its protective effect could not be due to caffeine,” Dr. Mancini explains.
The researchers identified a group of molecules called phenylindanes, formed during the roasting process, as particularly important. Phenylindanes stood out because they inhibited aggregation of both beta-amyloid and tau proteins — the two major proteins implicated in Alzheimer’s disease — as well as showing activity relevant to Parkinson’s-related protein changes. “Phenylindanes are a dual inhibitor of amyloid-beta and tau aggregation. That was surprising and noteworthy,” Dr. Weaver says.
Because phenylindane levels rise with roasting, dark roast coffee showed greater inhibitory activity against these pathological protein assemblies than light roasts in the laboratory tests. The team emphasizes that identifying a naturally occurring compound with dual activity is an important step, but not a claim that coffee is a cure.
“The next steps are to determine how beneficial these compounds are in living systems and whether they can reach the bloodstream and cross the blood-brain barrier,” Dr. Mancini notes. Dr. Weaver adds that the fact these compounds are natural is an advantage: “Nature often produces complex molecules more efficiently than synthetic chemistry. If these compounds prove useful, they could potentially be extracted or optimized for therapy.”
Researchers caution that much more work is required before any therapeutic conclusions can be drawn. The current study translates epidemiological observations into laboratory evidence that specific coffee components can interfere with the molecular processes linked to Alzheimer’s and Parkinson’s disease, but it does not establish that drinking coffee will prevent or treat these conditions.
Funding: Supported by the Krembil Foundation and Canada Research Chair funding.
Source: Reported by Heather Sherman for Universal Health Network. Published by NeuroscienceNews.com. Image source: public domain.
Original Research: Mancini, R. S., Wang, Y., & Weaver, D. F. “Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation.” Frontiers in Neuroscience. Published October 12, 2018. DOI: 10.3389/fnins.2018.00735
Universal Health Network. “Drinking Coffee May Reduce Alzheimer’s and Parkinson’s Risks.” NeuroscienceNews. November 2, 2018.
Abstract
Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation
Coffee consumption has been linked to a lower risk of Alzheimer’s disease (AD) and Parkinson’s disease (PD), but the mechanisms behind potential neuroprotection are not fully understood. This study tested whether brewed coffee extracts and selected coffee components could inhibit aggregation of amyloid-beta (Aβ) and tau (key proteins in AD) and affect α-synuclein aggregation (linked to PD). The research examined three instant coffee extracts (light roast, dark roast, decaffeinated dark roast) and six coffee components: caffeine, chlorogenic acid, quinic acid, caffeic acid, quercetin, and phenylindane.
Using fluorescence assays to measure fibrillization and ELISA-based tests for oligomerization, the study found that all instant coffee extracts inhibited Aβ and tau fibrillization at certain concentrations, while promoting α-synuclein oligomerization above 100 μg/mL. Dark roast extracts were more potent Aβ oligomerization inhibitors (IC50 approximately 10 μg/mL) compared with light roast (IC50 = 40.3 μg/mL). Pure caffeine had no effect on Aβ, tau, or α-synuclein aggregation. Some coffee components inhibited Aβ fibrillization at 100 μM, and quercetin inhibited Aβ oligomerization (IC50 = 10.3 μM). Notably, phenylindane was a potent inhibitor of both Aβ and tau fibrillization and inhibited Aβ oligomerization (IC50 = 42.1 μM).
These results suggest that phenylindanes formed during roasting—and present in higher amounts in dark roasts—are plausible contributors to coffee’s observed association with reduced risk of neurodegenerative disease. Identification of phenylindane as a dual inhibitor of both Aβ and tau aggregation represents a novel finding and a potential mechanistic explanation for some of the protective effects linked to coffee consumption.