12 January - 20 June 2016

Drinking coffee may protect from neurological conditions

While consumption of coffee has previously been liked to decreased risk of developing neurological diseases such as Alzheimer’s and Parkinson’s disease, mechanisms by which this may happen are not fully understood. A new study conducted by researchers at the Krembil Brain Institute, Canada, and published in Frontiers in Neuroscience, has attempted to investigate these mechanisms and suggests that the answer lies in compounds released during the roasting process.

While consumption of coffee has previously been liked to decreased risk of developing neurological diseases such as Alzheimer’s and Parkinson’s disease, mechanisms by which this may happen are not fully understood. A new study conducted by researchers at the Krembil Brain Institute, Canada, and published in Frontiers in Neuroscience, has attempted to investigate these mechanisms and suggests that the answer lies in compounds released during the roasting process.

Weaver et al. investigated three types of coffee: light roast, dark roast and decaffeinated dark roast and used ELISA methods to generate results. Co-author Dr Ross Mancini is quoted in a press release as saying that “the caffeinated and decaffeinated dark roast both had identical potencies in our initial experimental tests. So we observed early on that its protective effect could not be due to caffeine”. The researchers then began to investigate the effect of roasting coffee beans. Mancini identified a group of compounds formed during roasting, known as phenylindanes, which give coffee its bitter flavour. Interestingly, this compound was targeted due to maple syrup sharing the same property and previous studies showing it reduces the clumping of two protein fragments, Amyloid-Beta and Tau. These are toxic proteins, of which excessive aggregation in the brain is directly correlated with the incidence of Alzheimer’s and Parkinson’s disease.

Weaver et al. showed benefits with all coffee types tested. The light and dark roast blends both successfully inhibited Amyloid-Beta fibril formation at the same level while with the suppression of Tau formation, a dark roast blend was more potent than a light roast blend independent of whether the coffee was caffeinated or not thus suggesting that the roasting process has a part to play.

In conclusion, Weaver et al reiterate that they have identified the phenylindane component of roasted coffee as being “responsible for the observed aggregation inhibition activity of the coffee extracts toward Aβ and tau.” They also note that having these compounds produced naturally is much easier than having to synthesise them and that while the research is promising, before phenylindanes can be used as a treatment option, much more research needs to be performed. Mancini is quoted as saying “What this study does is take the epidemiological evidence and try to refine it and to demonstrate that there are indeed components within coffee that are beneficial to warding off cognitive decline. It's interesting, but are we suggesting that coffee is a cure? Absolutely not”

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