The chemical compounds in coffee – especially the phenylindans that arise during the roasting of coffee beans – seem to prevent the harmful aggregation of amyloid beta and tau, which are known to play key roles in Parkinson's disease and Alzheimer's disease, the researchers say.
Caffeine, on the other hand, did not affect the accumulation of protein in this early laboratory study, and the researchers noticed that coffee consumption did not provide any protection against alpha-synuclein aggregation.
Research, "Phenylindans in coffee brewing inhibit beta and Tau amyloid aggregation, "It was published in Frontiers in Neuroscience.
It is suggested that consumption of coffee reduces the risk of developing diabetes, various cancers and neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Despite the evidence available, it is not clear how exactly coffee can help prevent cognitive impairment associated with age.
Previous studies have reported that caffeine, the main bioactive compound of coffee, can reduce the risk of Parkinson's disease in both men and women who have not used hormone replacement therapy. There has also been a reduction in the death of nerve cells in the brain substantia nigra – the area of the brain most affected by Parkinson's disease – in mouse models of the disease.
However, recent data also suggest that long-term consumption of caffeine may exacerbate the behavioral and mental symptoms associated with anxiety in dementia patients, counteracting its potential beneficial effects.
These contrasting results emphasize the need to identify those coffee components that may be neuroprotective.
Researchers led by Donald Weaver, PhD, co-managing the Brain Institute of the Kremlin, assessed the potential of coffee chemical components to inhibit the accumulation of proteins that can cause neurodegenerative diseases such as Alzheimer's and Parkinson's disease, in particular: beta-amyloid, tau and alpha-synuclein.
The team began by investigating three types of soluble coffee – a light roast, dark baking and a dark decaffeinated roast – in terms of its ability to prevent protein aggregation. They tested the instant coffee, adding it to one of these three proteins in vitro (Laboratory vessel).
"The effect of caffeine content would be assessed by comparing the activity of caffeinated and decaffeinated dark roasted coffee extracts." In addition, because different baking levels are known to affect the composition of brewed coffee, a comparison of light and dark roasted coffee extracts was also carried out, the researchers wrote.
The dark roast coffee showed the greatest inhibitory effect in relation to the accumulation of tau protein. Interestingly, the level of caffeine in each type of coffee had no effect on the aggregation ability of tau, amyloid beta and alpha-synuclein.
"It surprised us that the caffeine content did not affect the inhibition of aggregation, and hence Post-hoc analysis of pure caffeine, "the researchers said in the study:" There was no effect on fibril growth compared to vehicle control, consistent with the results for caffeine against decaffeinated coffee extracts. "
Further experiments have shown that all coffee extracts can prevent aggregation of beta amyloid and tau protein at a concentration of 200 μg / ml. Dark roasted coffee (with or without caffeine) was seen as stronger in preventing oligomerization – the chemical form that proteins can take – beta amyloid than a light roast extract.
All types of coffee as instant mixtures, however, showed the ability to promote alpha-synuclein aggregation above 100 mg / ml.
To better understand these findings, the team investigated the activity of the six main chemical components of coffee – caffeine, chlorogenic acid, quinic acid, caffeic acid, quercetin and phenylindan.
Researchers found that most of these compounds – except caffeine and quinic acid for beta-amyloid – and caffeine and caffeic acid for tau – prevented protein aggregation.
It was found that phenylindan has the strongest inhibitory activity, acting as a double inhibitor, preventing the formation of amyloid-beta aggregates by 99%, and tau tensions by 95.2%. Importantly, in subsequent experiments, phenylindans did not show "aggressive behaviors" toward alpha-synuclein, reports the report.
Phenylindans are formed during the roasting of coffee beans and occur at higher concentrations in dark roasted coffee, which have longer smoking times.
"For the first time, someone has been studying how phenylindan interacts with proteins responsible for Alzheimer's and Parkinson's disease," said Ross Mancini, a medical chemistry professor at the Krembil institute and the first author of the study. "The next step would be to investigate how beneficial these compounds are and whether they are able to enter the bloodstream or cross the blood-brain barrier."
The team is currently investigating whether phenylindans can reduce beta, tau and alpha-synuclein amyloid charges in cell and animal models of Alzheimer's and Parkinson's disease.
Scientists warn that their findings do not recommend excessive consumption of coffee.
'What is happening in this study is the collection of epidemiological evidence and an attempt to refine it and show that there are indeed coffee components that are beneficial in preventing cognitive decline,' said Weaver. "It's interesting, but are we suggesting that coffee is a medicine? Absolutely not."