In recent months, a range of studies have been published that provide scientific evidence to back up the idea that brain and gut are in constant dialogue and influence each other. Researchers at the University of California, Los Angeles (UCLA), for example, have discovered a relationship between specific kinds of bacteria found in the gut and structural and functional changes in the brain. In addition, new research has been published regarding the role of the microorganisms that live inside us in the progression of conditions such as Parkinson’s and Alzheimer’s.
Agustín Ruiz, MD, is Director of Research at Fundación ACE -a private non-profit organisation that researches Alzheimer’s and other kinds of dementia located in Barcelona (Spain)—studies the role of the microbiota in our brain health, specifically investigating its relationship with neurodegenerative diseases such as dementia.
Ruiz took part in a science conference on microbiota called BDebate, an initiative promoted by the ‘la Caixa’ social project fund and Biocat, – the organization that coordinates and promotes the healthcare and life sciences sector in Catalonia-, held at the Cosmocaixa science museum in Barcelona in early July.
Parkinson’s affects the body as a whole and, importantly, is related to gut motility disorders and interaction with the microbiota
Do the gut and brain talk to each other?
Of course they do. All the body’s systems communicate with each other and, in fact, the nervous system is everywhere. Consequently, communication takes place, and not only through the nerves that reach the gut, but also directly through circulating factors that travel through the blood, hormonal factors, etc.
In the past decade, we have started to discover relationships between health and the microbiota, including associations between some diseases and the microorganisms that live in the gut.
Until recently, we did not think that diseases such as Parkinson’s were “systemic”; in other words, that they affected the organism as a whole. Now, the concept has undergone radical change. Parkinson’s has an impact on the organism as the whole and, importantly, it is related to intestinal motility disorders and interaction with the microbiota. The microorganisms that live in the gut can emit factors into the blood that can lead to very remote inflammation. There is a lot of research being undertaken that looks for the pro- or anti-inflammatory effect of our gut bacteria.
Are these just correlations or are there data that prove a causal effect?
Very sophisticated experiments are being carried out using murine models of different diseases. Their microbiota is replaced with the microbiota of healthy or diseased subjects to try and see the direct effect of the microbiome on different disease models. That is how the “long-distance” relationships with neurological diseases are being shown. And we are starting to get empirical data, not just purely epidemiological statistical relationships.
This is transforming the field and characterising the microbiome for all diseases. At Fundación Ace, for instance, we are involved in programmes to characterise the microbiome and its relationship with the cognitive aspect.
Which came first: the chicken or the egg? Do the alterations in the microbiota appear first and lead to the disease, or does the disease lead to alterations in the microbiota?
In this case, mutualism occurs. The microbiome really does have an influence on many aspects of human physiology and vice versa. There are also genetic studies that show that, depending on the genomic profile of the subjects, their microbiome is different. It seems that our genes select or purge the bacteria they are not interested in for this mutualism. Our genome can predict part of the microbiome’s composition and our microbiome can modulate, for instance, our immune system or our neuroendocrine system.
Obviously, modifying the microbiome also means that modifications can be made in the pro- or anti-inflammatory profile of a subject, subsequently affecting the development, modulation or prevention of some diseases. That is our hope.
How can the microbiota be modified: with a faecal transplant or perhaps through diet, probiotics or exercise?
In the case of Alzheimer’s disease, for instance, genetic studies over the past 10 years have led us to verify the neuro-inflammatory hypothesis. We have observed that many genes linked to the disease are also linked to inflammatory processes, not only in the central nervous system but also in the peripheral nervous system and the inflammatory profile in our blood.
If the modification of peripheral inflammatory factors can actually change the course of Alzheimer’s disease, they can probably be controlled through changes in the microbiota; that is one of our hopes. That is why we are looking very closely at these processes of interaction between nervous system diseases or neurodegenerative disease and changes in the microbiota.
In the future, will we be able to use the microbiota to prevent Alzheimer’s or other diseases that are associated with changes in the composition of the microbes in our gut?
This is one of our ideas. If we manage to identify a pro-inflammatory microbiota profile and can replace that with another microbial composition that is more stable and less pro-inflammatory, perhaps we can reduce the inflammation in the central nervous system and in other parts of the body. That way, we would reduce the pathological effect of the process, allowing us to prevent the appearance of neuroinflammatory processes that take place remotely.
This is our hope for prevention, but it may also help us control the process. For now, we are starting to save material from patients with Alzheimer’s for the whole process, from the healthy subject to a subject who complains of memory problems, subjects who are already showing slight cognitive decline before the onset of dementia, with the aim of comparing their microbiota profiles and seeing if we can come across a clue about how to intervene.
The problem is that the disease also leads to a drastic change in people’s behaviour. People’s diets are less rich, for instance, because they start to forget recipes. They stop using lots of ingredients because they do not remember how to prepare them. The disease also somehow unsettles their microbiota. And that must be taken into consideration.