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Surprising findings for beer and Alzheimer’s related brain lesions

Could beer have some positive effects on the brain and memory? Eloise, who recently crowdfunded on Walacea has just had a manuscript accepted for publication and she explains about her journey to get there and gives us a few insights into her recent taste of the media limelight in Finland

beer-intro

Image: Thinkstock

Can scientists be media personalities?

In keeping with the idea that scientists can also be media personalities, I’ve just received an email to be interviewed for a women’s magazine here in Finland. Yes, it’s true. I’m not really sure of the positive fluffy role model image that I could provide, but they are interested in hearing about my crowdfunding adventure. As a colleague earlier said to me “It’s not bad if a scientist is in the news in a positive light”. Well….ok, I’ll go with it.

But I should backtrack a little. I had my manuscript accepted for publication a while back and this week was the early view publication release. Now, that’s nothing to rejoice at in the world of science – although let’s be fair, I haven’t had an article published in four years, so I’m pretty ecstatic about the whole thing – but I believed the concept would appeal to the general population, so thought I’d jump on the bandwagon of press release accompanying research method.

beerandlesionsmanuscript

Well…it certainly has appealed to the public. An article on the University’s website (coupled with an English version – these guys are really getting to know me now!), plus an article in the local paper. Not to sound too arrogant or anything, but that’s kinda THE DREAM….for a scientist. To get your research read by every day people thinking you’re on the way to a cure for such and such a disease. Because let’s be honest, as scientists we all believe our research is finding the ultimate answer to this or that.

I do know however, how the media take your results and rewrite them the way that makes it seem like you HAVE found the cure. Boy have they done that. How many times do we have to read about the next ‘cure for cancer’ or something? Well that’s kind of what they did with my research. But I’m still excited about it, and if you’re interested in actually hearing more about it from my perspective rather than the media’s, I’ll attempt to explain the research itself and the implications.

I was given an older autopsy series to work with on this topic, (compared to the one I usually work with) which had brain lesion data (information about whether the individual had amyloid beta aggregations or plaques) and alcohol consumption data. Amyloid beta aggregations are thought to be the cause behind Alzheimer’s disease. The protein accumulates in clumps and is believed to cause the death of neutrons, which leads to the associated memory loss. The alcohol consumption information involved types of alcohol drunk and an estimate of how much (note this is retrospective data, which is less strong than data collected in real time). The alcohol data came from relatives of the deceased, so to be fair, it’s not entirely rock-solid info. However, it’s interesting enough to show some insight into how these people lived. You’d be amazed at how much you can divulge on a person’s habits when you really think about it.

One final point is that the cohort is a non-demented cohort, meaning that none of them are cognitively impaired, although some had the brain lesions. This could mean that they would have developed dementia if they had lived longer, or may alternatively suggest that these lesions can occur without dementia and there is something else required to cause Alzheimer’s disease.

beerandlesions

Fig 2 shows that beer drinkers had less than half the amount of amyloid beta-immunoreactivity compared with non-beer drinkers. Amyloid-beta aggregations are strongly associated with Alzheimer’s disease.

I’ll focus on our most interesting results to keep it simple. We measured the amyloid beta aggregations as a dichotomous variable (present or not) and had a look whether any alcohol amounts or types were statistically associated with the brain lesions. In one of those beautiful eureka moments, the statistical program I use (SPSS, in case you’re wondering) spat out a nice significant result. Beer drinkers were less likely to have amyloid beta aggregations in their brains than drinkers of other types of alcohol.

So does that mean beer is good for you?

Yes, it is possible that beer could be good for you! But before we go jumping to extravagant conclusions, let me bring you back down to the ground. This was quite a small study (125 males – which means the results cannot be assumed to apply automatically to women – sorry ladies!) and when we investigated further it seemed that age had a large part to do with the effect. But this isn’t the end of the story. I have another larger cohort with similar information (with both males and females) where I will look to see if I can find similar results.

Of course it will also be nice to back up our results with a substantial theory as to how and why we found this result. Our thinking is that beer has a number of nutrients that are involved in important mechanisms in keeping cells functioning well. So another step will be to see if we can measure certain metabolites to corroborate our story, of which I’ve made a new collaboration to tackle this topic, through the sharing of my research!

So yeah, beer could potentially be good for your brain. But as I should point out all things should be enjoyed in moderation and a full healthy diet with exercise should be paramount to living a healthy long life!

Read the full article here: http://onlinelibrary.wiley.com/doi/10.1111/acer.13102/abstract

Project Update: Using 3D Cameras To Improve The Lives Of African Children

Shifting perspectives 365 by Ricgard Bailey. Andrea/Flickr CC BY-NC 2.0

Certain conditions are associated with characteristic facial features, but less is known about these in African children compared with other populations. Shifting perspectives 365 by Richard Bailey. Andrea/Flickr CC BY-NC 2.0

Kicking off the year to a great start, January saw the launch of a campaign on Walacea which sought funds for a project hoping to improve the diagnosis of a number of different conditions in African children, therefore ultimately quality of life and access to treatment, too. The campaign was a deserved success, with the team raising the £2,750 needed for the project to commence. No time wasted, the funds were immediately put to use, and we’re delighted to share with you an exciting update on the project’s progress so far!

But first things first, a bit of background on the science. In general, the earlier a particular condition is diagnosed, the better it can be managed or treated. In developing areas, such as Africa, poor access to health care and a lack of understanding about certain conditions means that diagnoses are often made too late, or not at all, thus affected individuals don’t get the potentially life-saving treatments they need.

For instance, Down syndrome is one of around 700 conditions that has associated characteristic facial features which help in the initial diagnosis, before confirmation by genetic testing. While these are well-recognised in European infants, they differ across populations and are hard to identify in some, such as black Africans, thus delaying the provision of medicines for associated health problems, such as heart defects.

That’s why Dr Vinet Coetzee and colleagues embarked on their current project, which aims to identify the facial features linked with various conditions in African children, including Down syndrome, and use this information to aid diagnosis. To do this, they needed funds to build an accurate 3D camera to image and compare the facial dimensions of those with and without these conditions.

Within only a month and a half of collecting the funds, the team build their camera system and used it for the first time in April at the Down syndrome sports day at Centurion High School, Pretoria. “It was a super busy day but well worth it,” said Coetzee. “Many parents were interested and in the end we recruited, interviewed and took photos of 20 children and young adults with Down syndrome.

“We started compiling the first 3D images from the day. They look fairly good, but we want to improve them further.” For instance, they need to optimise the position of the camera so that more detailed information can be gathered on the sides of the face, Coetzee said. They also found that the kids were really interested in the equipment, so to not let curiosity kill the camera, they need to do some child-proofing!

As a project that has the potential to change the lives of so many, it’s great to see that it’s already making headway. We’re all hoping this will be the first of many positive updates that might not have been possible without the generosity of the supporters who dug deep in their pockets to help make this research a reality. So we thank you once again for joining the campaign, and backing science you believe in!

Alzheimer’s Reversed In Mice: What Does This Mean For Us?

Alzheimers

Image credit: *Ann Gordon/Flickr CC BY-SA 2.0

An increasing burden on public health across the globe, Alzheimer’s is an intensely studied disease and promising research often hits the headlines. Just the other day, for instance, a study published in the prestigious journal PNAS kicked up a storm in the media because of the potential implications of the results: that Alzheimer’s could be reversed. 

One of Walacea’s successful crowdfunding campaigns is an Alzheimer’s project, and interestingly there are some links between this research and the recently published study. We therefore decided to catch up with the scientist behind the former, postdoctoral researcher Dr Eloise Mikkonen, to chat about both pieces of research and what we could learn from them, and whether the hype is justified. 

But first things first, what did the new study find? Researchers from Hong Kong and Glasgow universities managed to reverse the memory problems of mice with Alzheimer’s-like disease, in addition to reducing the build-up of toxic clumps of protein, called beta-amyloid plaques, which are characteristic of the condition. 

They achieved this by giving them injections of a molecule called IL-33, a signalling protein produced naturally by the body which plays various important roles in mediating immune system responses. The rationale for testing this out as a potential treatment stems from the fact that the brains of people with Alzheimer’s commonly show lower than normal levels of IL-33, and several different mutations in the gene that makes IL-33 have been linked with Alzheimer’s.  

The team thinks that the injections changed the activity of a type of immune cell called microglia, which are the brain and spinal cord’s primary defence system, boosting their ability to gobble up beta-amyloid and putting them in anti-inflammation mode. That’s an important find, as work by Mikkonen and others has found that inflammation plays a role in the progression of Alzheimer’s, something that she intends to scrutinize further in her crowdfunded research. 

But as is often the case with science, things aren’t quite as black and white as they may first seem. As Mikkonen explains: “Genetic investigations of Alzheimer’s disease have revealed that inflammation plays a role, but it isn’t clear as to how. It could be that some inflammatory factors decrease and others increase, and there needs to be a certain pattern which leads to Alzheimer’s disease. 

“It should be noted that some inflammatory factors are beneficial in certain diseases, whilst being detrimental in others… all in the same body at the same time!”

Mikkonen also points out that mice don’t naturally produce the proteins which result in the characteristic brain lesions seen in Alzheimer’s, so the animals have to be mutated for this kind of study. We should therefore be cautious about jumping to conclusions in humans, a message that the researchers have actually been quite clear about. That said, animals models are incredibly useful tools in medical research, so we shouldn’t dismiss this as irrelevant. 

Another important issue Mikkonen raises is that removing the beta-amyloid plaques could actually release toxic molecules into the brain, and therapies that have attempted to do this before have failed. In addition, her work has shown that these plaques are surprisingly common in non-demented individuals. 

“Does this mean that if they lived long enough, they would eventually develop Alzheimer’s?” Mikkonen ponders. “Or do they have some additional protective factor that we don’t know about that differs from those that succumb to the disease?”

These are questions that she seeks to address in her research, which will involve analysing one of the biggest brain samples in the world, totalling more than 1,300 people. Fewer than 30 of these individuals had memory problems or early stages of dementia, so Mikkonen will look for the presence or absence of brain lesions linked with Alzheimer’s and attempt to identify certain genetic factors or lifestyle choices which could influence the risk of developing them. 

So far, the campaign has exceeded its fundraising goal by more than £1,000. As a result, she has introduced stretch goals which, if met, will allow further rounds of data analysis to look for potential links between disease progression and various factors, like exercise and blood type. Each set of analysis costs £1,000, so do something amazing and dig deep for this brilliant cause! 

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