Health and Medicine
PUBLISHED
It’s one of the most feared health conditions we humans face, and the problem is only set to grow.
By 2050, a recent forecast says, nearly 25 million people around the world could develop dementia each year. That’s a huge increase on previous estimates and begs the urgent question: what can we do about it?
As with many of the big dilemmas in science, people are divided on the best way to approach the issue and the most urgent priorities for research. We didn’t want to ask just one expert for their take; instead, we’re bringing you three different perspectives from scientists addressing this question from a range of angles.
Fernando Gonzalez Ortiz, MD, PhD is a doctor and neuroscientist at the University of Gothenburg who specializes in blood-based biomarkers for the detection of neurological disease.
Dr Anna Mallach is an Edmond and Lily Safra Research Fellow at Imperial College London and Emerging Leader at the UK Dementia Research Institute who studies how the brain’s glia cells contribute to neurodegeneration.
Dr Ben Goult is Professor of Mechanistic Cell Biology at the University of Liverpool. His research into how cells store and use information has led to the proposal of the MeshCODE framework, which suggests that networks of proteins may act as mechanical information processing systems inside cells.
Together, they can help guide us through the possible future directions of research into this burgeoning public health crisis.
Alzheimer’s disease is one type of dementia. But could there also be different types of Alzheimer’s disease that need different treatments?
Fernando Gonzalez Ortiz: I think that that is really interesting, because there are groups focusing on understanding the different subtypes of Alzheimer’s disease based on the proteomic profile of individuals.
That’s what we call precision medicine – not only saying, “here’s a patient with Alzheimer’s disease,” but also based on their proteomic profile, individuals with Alzheimer’s disease might have more vascular impairment, or more [of] an inflammatory response.
I think that definitely in the future in addition to more biomarkers, we will have biomarkers that will also help us to profile individuals according to [these subtypes].
I can definitely see a future where we have Alzheimer’s subtypes and treating patients in general based on these.
Anna Mallach: Dementia is a symptom, Alzheimer’s disease is one disease, but there are other diseases that also lead to dementia symptoms.
There’re very clear ways you can think about diseases [like Alzheimer’s and Parkinson’s], but ultimately the molecular picture is a lot more mixed. People with Alzheimer’s disease often also have pathologies related to Parkinson’s and vice versa.
We want to move away from the stereotypical [idea of] this is the “Alzheimer’s brain” and this is the “Parkinson’s brain”. It’s a whole mixed bag of all the pathologies.
What can we learn from other medical fields that might be applied to dementia research?
FGO: I think that the oncology field is a field that we can learn so much from.
In the oncology field, you are working also with biomarkers, and these biomarkers are, in a way, more specific than the biomarkers that we use in Alzheimer’s disease. [Cancer scientists] are using biomarkers that are not present in patients unless they have a tumor producing these biomarkers […] but they are not basing their diagnosis and their whole conception of cancer just on these biomarkers.
The oncology field is fascinating and I’m always checking what they do because they're great!
AM: What I found really interesting were the results coming out of the Huntington’s field.
Huntington's disease is ultimately a genetic disease, so we know what we know that if you have an expansion repeat of long enough length, you will get Huntington's disease. Up until now, diagnosis required you to start developing some sort of symptoms. There's been a push to [use genetic data] to define an earlier stage of Huntington's, which is presymptomatic Huntington's.
What that ultimately means is that at that point, the patients have a diagnosis and then drug trials can start [more easily].
If we can effectively shift diagnosis towards saying, okay, these people have a 95 percent likelihood of developing Alzheimer’s disease, [drug trials are] a much easier case to make and [this] ultimately benefits the patients.
Ben Goult: I think what we learn in one field, at the minute, doesn’t transpose over onto another quite as efficiently as it could. And a lot of the time, you’re working on something and then you Google and look in the other field, and they kind of had a lead on that 10 years ago or something!
So, maybe AI trying to crosslink ideas or synthesize new thoughts from data – that might lead to new routes. But I still think there’s some massive gaps in our understanding at the fundamental level.
If we were to sit down and have this conversation again in five or 10 years’ time, where would you like things to have progressed to?
BG: [I’d like more people to] appreciate the importance of the mechanical structure and integrity of the neurons. If we look at neurons in culture, everything looks very dynamic – it looks organised at one level but [also] quite disorganised.
You could easily imagine that the brain is a highly organised structure, but that’s also quite controversial because it doesn’t necessarily always look like that.
The mechanical forces and the mechanical properties of the brain are really essential, and I think they might be new avenues for treatment.
I think I'd like to say in five years’ time, we'll have a new set of ideas which extend beyond amyloid plaques, which I think have been thoroughly disproved as being the main cause of this now with all these drug failures which are happening all the time.
FGO: If I would have to guess, I would say that in the coming years we will have a different view on what [the] biomarkers are capable of. I think that right now, the dominant idea is that these biomarkers can do everything. Not only [can they] diagnose, but they are also prognostic and they can tell you [about] the response to therapies.
But then, when you put these biomarkers in a real-life setting, it’s really messy.
So, I think that in the coming years, what we will see is that we will realize that these biomarkers are great, but they cannot be disconnected from clinical syndromes, clinical evaluation. I think that we will realize [these markers have] important limitations in real-life settings.
AM: Another question is, what do we make of the data? We’re generating enormously large datasets, and now it slowly becomes a problem of analysis – like, what do we do with that?
I think the next decade in dementia research is going to be really interesting because we will slowly have the abilities to ask the really important questions.
Curious to know more? Listen to the full interviews here on IFLScience's The Big Questions podcast. You can listen to this episode and subscribe to the podcast on all your favorite podcast apps: Apple Podcasts, Spotify, Podbean, Amazon Music, and more.
