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patient in intensive care unit
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SPIEGEL:
Mr. Heneka, people who have had to go to the hospital because of an infection have a higher risk of developing Alzheimer's later in life.
This is shown by a recent study in the journal PLOS Medicine.
Can infectious diseases cause dementia?
Michael Heneka
: There are now many studies that show a connection.
Experimental studies have also shown that inflammation can lead to changes in learning and memory performance.
But the relationships between infections, the immune processes they trigger, and dementia are likely to be multifaceted.
On the one hand, an infection can accelerate degenerative processes that are already taking place in the brain.
Sometimes the mental decline could also be re-initiated.
Or normal aging processes in the brain could be transformed into pathological degenerative processes by the infection.
MIRROR:
How does something like that work?
Heneka:
First of all, a severe infection – and, as the current study also showed, these infections in particular increase the risk of dementia – causes temporary or permanent damage to organs such as the kidneys, liver or thyroid gland.
This organ damage alone can have a lasting negative effect on brain function.
Above all, however, the blood-brain barrier becomes more permeable in the event of an infection, messenger substances from the immune system and also immune cells can cross from the blood into the brain and there influence the activity of the so-called microglia, the brain's own immune cells.
SPIEGEL:
Wasn't the dogma that there was a strict separation between the immune system and the brain always valid?
Heneka:
This dogma is long outdated.
We now know that the microglia play a key role in the development of Alzheimer's - and we have been able to observe live in the brains of mice how an infection can accelerate this process.
SPIEGEL:
You have to explain that.
Heneka:
Protein deposits, the so-called amyloid plaques, are found in the brains of Alzheimer's patients years before the onset of the disease.
The microglia, i.e. the immune cells of the brain, try to remove the amyloid from the brain.
With the help of laser scanning microscopy, we were able to look directly into the brains of mice and observe what happens to the microglia cells when an infection takes place in the body: The mice were downright paralyzed - the immune system of the brain was temporarily paralyzed by the infection in the body.
Thus, the amyloid load on the brain continued to increase.
Because the microglia are not able to completely remove the amyloid plaques over the long term, the reaction of these immune cells in the Alzheimer's brain continues at some point like a smoldering fire,
and at a certain point, the negative effects outweigh the negative ones.
Inflammatory messengers damage the sensitive nerve cells, and inflammatory proteins drive amyloid clumping and spreading.
SPIEGEL:
Are infections with certain pathogens particularly harmful?
Heneka:
As far as we know, no.
Viruses, bacteria, even fungi can increase the risk of dementia.
However, the prerequisite is that the infection is severe.
If you have a cold, you have nothing to fear in this regard.
SPIEGEL:
What about a Sars-CoV-2 infection?
It can also lead to problems with concentration and memory.
Heneka:
Yes, in Bonn we noticed as early as the summer of 2020 that our memory clinic was filling up with patients who had been diagnosed with Covid.
We were surprised that these were mainly patients whose infection had been comparatively mild.
Some had experienced the loss of their sense of smell as their only symptom.
I still don't have a plausible explanation for this.
In order to find out more, we started a study with corona patients, whom we examined neurologically very thoroughly.
The results have not yet been published, but an initial analysis of the MRI scans we performed on them shows a reduction in volume in the areas of the brain that are important for memory.
SPIEGEL:
Could it be that the corona pandemic will generate a wave of dementia patients?
Heneka:
I think that's conceivable, I even fear it.
However, we will only really know this in a few years, maybe even decades.
It would be important to conduct long-term studies now, because there is a great deal that is still unknown in this area.
For example, the question of whether there are risk genes for neurological consequential damage from Covid disease and what kind of genes they are.
However, it is not surprising that there is an accumulation of neurological disorders during a pandemic: after the Russian flu there was an increase in psychoses, and after the Spanish flu there was an increase in movement disorders.
This also shows how much infectious diseases can affect brain function.
Finding out more about it is important simply because this was certainly not the last pandemic,
SPIEGEL:
A lot is now known about the role of the immune system in the development of Alzheimer's.
Are drugs already being developed on the basis of these findings?
Heneka:
Definitely, there are now a number of companies working on such drugs.
But I think it's important to research and think things through very thoroughly.
The immune system not only contributes to the development of Alzheimer's through the smoldering fire in the brain, but is probably also able to protect the brain.
We conducted a long-term study in which we were able to detect an inflammatory signal in the cerebrospinal fluid years before the onset of dementia.
But the stronger this signal, the less pronounced the memory loss afterwards.
So if you rush to develop an Alzheimer's drug that suppresses the immune response in an unfavorable way, it could also have negative effects.
A lot of research is certainly still needed, and the topic will keep us busy for a long time.