This is not the first time I’ve written about why coffee is so great here in science.casual, and I do so because 1) it is, 2) it just is, and 3) as a scientist, coffee is in my blood. I’m speaking metaphorically, but I would not be at all surprised if I was speaking literally at this point. This week’s Featured Article is yet another reason to celebrate coffee, other than that it’s winter in the Northern Hemisphere and it’s cold outside – Yan et al. assert that coffee may be able to protect the brain from developing Parkinson’s disease and certain types of dementia. Talking about Parkinson’s is probably going to be a bummer, but it’s something we have to do in truly appreciate this bit of research (I’ll keep it short, though). Pull up a chair, grab your coffee (and probably a pastry – I love you people), and let’s talk about the brain for a bit.
The target of this research are Lewy bodies, abnormal protein aggregates in nerve cells of the brain that can be found by taking tissue samples of the brain. These show up as the dark spots shown in the image above above, and for a while research has shown that these show up at places where neurons (‘brain cells’) have been dying out; it’s not clear whether these cause the brain cells to die out, though. That’s still a bad thing, as damage to different areas of the brain can cause a different host of Bad Things, such as tremors, sleep disorders, or even lowered blood pressure. Since we’re not entirely clear on how these bodies form or whether they cause brain cells to die, perhaps by preventing the formation of these bodies we can knock out one possible cause behind neural degeneration.
Still with me? Good, now pardon me while I get some dragon energy.
Anyway, Yan et al. suggest that although caffeine plays a protective role in a reduced risk of Parkinson’s disease, there may be other compounds in coffee that may be helping it in its role. This suggestion comes from a lot of reading (this is research, come on) in which studies have found that caffeine didn’t have an impact on the progression of Parkinson’s disease, but even decaf has protective properties, albeit in fruit flies (by the way, before you ask, they are commonly used in models of Parkinson’s disease). They want to demonstrate that one compound in particular, eicosanoyl-5-hydroxytryptamide (we’ll call it EHT, as they have in the Featured Article, from now on), works with caffeine to disrupt the production of α-synuclein, the key component of Lewy bodies that are indeed associated with Parkinson’s disease and other forms of dementia. EHT is found in the waxy coating of coffee beans, which you’ve no doubt seen when you look at them before they’re ground, and I’m pretty sure that this waxy coating also contributes to the ‘sheen‘ you get on top of French-pressed coffee.
Let’s get to the methods – isolating compounds from a mixture of stuff is big, serious business, and there are companies that make a tidy profit from separating, making and selling reagents. Biochemical researchers could even order antibodies. That’s what the authors were able to do, especially when it comes to caffeine, EHT, and a large assortment of antibodies. Yes, they had to test this on mice, genetically modified so that they can produce an excessive amount of α-synuclein, then were grouped for treatments with different combinations of water, caffeinated water, ‘mouse chow’ (really, that’s the term they use in their manuscript), and ‘mouse chow’ containing EHT. They were given behavioral tests to examine their brain functions, such has mazes, hanging from wires (relax, they fall into bedding material) and how they put together a new nest when moved to a different cage. This performance was based on ‘latency,’ the delay between actions caused by stimuli such as falling off the wire or running into a dead end in the maze (gamers in the audience: think lag). Their performance on the behavioral tests were compared to ‘wild type‘ mice, or mice that were not genetically modified. Finally (PUT DOWN THE PASTRY WARNING), the mice brains were removed for tissue study, which involved looking at neural degeneration, dopamine content, and so forth.
So, what did they find? Quite a bit, sure, but the big one is that EHT appears to indeed work with caffeine to protect the brain. Going by the behavioral study alone, the ‘control mice’ (water and ‘chow’, no caffeine nor EHT) were greatly impaired, especially when compared to the wild type mice. On the other hand, mice treated with caffeine and EHT had less lag than the control mice; they were still impaired compared to the wild types, but it shows that there is some improvement. These results also showed that caffeine and EHT work best together because while there wasn’t a lot of consistency in the differences between caffeine-only, EHT-only, and control mice, the caffeine-EHT mice outperformed them all across all tests. They repeated the test on the wild-type mice, after some were inoculated with something that allowed for the genetic expression of α-synuclein production and got similar results, which means that the caffeine-EHT duo still helps even if neural degeneration was something that started appearing relatively recently.
Tissue studies found that this improvement (or at least lack of impairment, depending how you look at your cup of coffee) has to do with how EHT and caffeine together prevents the formation of protein clumps, especially those containing α-synuclein, in neural tissue. Again, the authors concluded that they must be working together because there were less of these clumps in the EHT-caffeine treatment than in any other condition. Their synergy – finally, you can use a business buzzword unironically – allows for the regulation of PP2A, which in turn protect brain cells from degeneration, likely through the way it keeps cell division under control.
So there you have it – once again, coffee has come to save the day, this time aiming for your brain. Why? Because caffeine and EHT together prevents the formation of growths in the brain that may be killing off brain cells. I don’t have a coffee addiction, I’m practicing preventative medicine, and I SWEAR IF THIS IS DECAF I AM GOING TO SUE YOU FOR RECKLESS ENDANGERMENT YOU-
Anyway, it’s that time of the year for various winter holidays, mostly involving a lot of food, video games in my case, and also being very cold (if you’re in the Northern Hemisphere anyway – you lot in the other half get to holiday on the beach). So from all of us (which is just me and however many people my ego thinks I am) here at science.casual, here’s to a safe and restful holidays, whatever they may be, and above all:
Featured Article: Yan R, Zhang J, Park HJ, Park ES, Oh S, Zheng H, Junn E, Voronkov M, Stock JB, Mouradian MM. (2018) Synergistic neuroprotection by coffee components eicosanoyl-5-hydroxytryptamide and caffeine in models of Parkinson’s disease and DLB. Proceedings of the Natural Academy of Sciences: 201813365. DOI:
Featured Image: Flickr/Public Domain (Author: Pete, 2013)