1. During well-learned tasks the brain prioritizes random movement activity.
The topic is a bit complicated, so let’s take it step by step. For a long time, scientists have been interested in two matters. The first is related how brain activity changes during a task and on identifying which regions, if any, might show activity associated with a certain task. The implicit assumption was that, during a task, the brain throws its full power at it and ignores everything else.
But think about it for a second. Don’t you seem to be focusing better when you’re chewing on that tasty pen? Or maybe when you tap your foot? Or pull on your hair? And aren’t all these movements also controlled by the brain? Well, that’s what Anne Churchland and her group also wondered.
To that end, they used mice. Much like humans, mice also show various movements unrelated to the task that needs to be performed. In this experiment, the researchers trained mice to respond when perceiving either an auditory or a visual stimulus. During the task, movements were tracked using video recordings and brain activity was recorded.
The results revealed that most of the neural activity was not associated with the stimulus detection task. Instead, it most reflected uninstructed movements the animals randomly performed, such as moving their paws. Additionally, as animals became better at the task, there was also a change in the pattern of uninstructed movements. Animals started performing them closer to the decision-making moment instead of at random times.
While these results need to be further replicated and extended to humans, one potential implication is that we might need to change the way we look at task-related brain activity by also looking at random uninstructed movements at the same time.
Additionally, it is currently unclear why so much brain activity is dedicated to random movements. The current hypothesis is that they play a critical role in cortical information processing. However, further research is necessary to elucidate the specific mechanisms behind this.
2. The Epstein-Barr Virus could be the leading cause for multiple sclerosis.
Multiple sclerosis (MS) is a demyelinating disease in which the myelin sheath, i.e. the protective cover of nerve cells, becomes damaged. This damage is accompanied by the formation of lesions called sclerae, as well as by increased inflammation.
Normally, the myelin sheath helps speed up signal transmission in your nervous system. When it becomes damaged, it can lead to a wide range of neurological symptoms, depending on where the lesions are localized. Some MS symptoms include blindness, dizziness, muscle weakness and pain, tingling, urinary problems etc.
There is currently no treatment for MS and the causes have remained largely mysterious. That is, until now. In a groundbreaking study, epidemiologist Alberto Ascherio and his group have found a very strong association between infection with the Epstein-Barr virus (EBV; the one which causes mononucleosis) and MS.
Asterio and his colleagues conducted a longitudinal study (that is, they observed people over a long period of time) on more than 10 million young adults in the US military over two decades. What they found was that the risk of developing MS after infection with EBV (but not other viruses) increased 32 times. To put it into perspective, that is higher than the association between smoking and lung cancer.
This could open the door towards new therapies against MS. But the results also need to be interpreted with caution, as this is after all a correlational study. Additionally, most people become infected with EBV at some point in their lives, but very few end up developing MS. So while the association between MS and EBV is so strong, the mechanisms behind it remain currently unclear.
One hypothesis is that EBV infection needs to be combined with a genetic predisposition, as well as environmental factors in order to cause MS. More research is necessary to disentangle the specific mechanisms behind this and to guide future therapies. But this seems to be the most promising lead we’ve had in terms of what causes MS, so it’s quite exciting to see what will come next.
3. Japanese scientists have manged to rejuvenate old neural stem cells.
Contrary to popular belief, the adult brain is still capable of producing new neurons (although, to be fair, this doesn’t happen everywhere, but only in two specialized regions). That means that the adult brain still has neural stem cells. Newly produced neurons are important for learning and memory.
Unfortunately, as we get older, the capacity of these neural stem cells for producing new neurons declines. That leads to declining learning and memory for older adults or, in other words, impaired cognitive functioning.
A simple fix to age-related cognitive decline would thus be convincing these neural stem cells to keep producing neurons even when we get old. But sadly, that’s much easier said than done.
Scientists have observed quite some time ago that, as these neural stem cells age, certain genes related to ageing were activated in them. But attempts to turn these genes back off in order to rejuvenate the cells have failed miserably. This was due to the fact that researchers manipulated one single gene at a time.
But Ryoichiro Kageyama and his group approached the problem differently: they first screened neural stem cells from both young and old mice to determine differences in gene expression. Then they tested several combinations of these genes.
In the end, they found one such combination which successfully made old neural stem cells start behaving again like young ones, i.e. dividing and producing lots of new neurons. Furthermore, the older mice whose neural stem cells were rejuvenated, showed improved cognitive functions (better memory and faster learning).
This study is important because it shows proof of concept: we can indeed rejuvenate neural stem cells and that leads to measurable cognitive performance improvements. In theory, this same technique could also be applied to treat neurodegenerative disorders, but it’s a long way from being applicable to humans.
4. Hospitalized Covid-19 patients have high levels of neurodegenerative biomarkers.
I know, we’re all quite sick of hearing “Covid this” and “Covid that”. But whether we like it or not, it looks like this virus is here to stay. And that means we should try to understand it as well as possible, so we can treat it properly and hopefully forget about it soon. With that being said…
You might’ve already heard that Covid-19 doesn’t just cause respiratory symptoms, but a whole range of other fun stuff, including neurological symptoms, such as stroke or encephalopathy. Encephalopathy, in particular, is an interesting one, because it’s not a single disease, but a syndrome of overall brain dysfunction, with symptoms such as confusion, memory loss, or delirium.
But it’s still unclear exactly how the virus leads to these relatively non-specific symptoms. One hypothesis is that the extended hypoxia (lack of oxygen due to poor lung function) and inflammation associated with this disease end up damaging both neurons and glial cells. If that’s true, then blood biomarkers which indicate this neural damage should be much higher in Covid-19 patients compared to healthy controls.
And according to a study published in the Alzheimer’s & Dementia journal, that’s true. Researchers compared a set of biomarkers generally associated with neuronal and glial damage, as well as a more specific one for Alzheimer’s disease. In addition to the healthy controls and the Covid-19 patients, they also included older adults with either mild cognitive impairment or Alzheimer’s disease (AD), but who had not contracted Covid-19.
The results were striking. Not only did Covid-19 patients have higher levels of neurodegenerative markers compared to healthy controls, but also compared to AD patients. Plus, the more neurodegenerative markers they had, the worse their outcome from Covid-19 was.
So what does this mean? Well, for one, it means that severe Covid-19 infections seem to significantly increase the level of neurodegenerative markers in the blood. But it also means that we need more studies to help us better understand the evolution of these effects.
In particular, researchers need to look not only at blood biomarkers, but also at the brain scans of these patients. Additionally, we need to understand how these change over time. It could be that the body needs more time, but the damage is, to a certain extent, reversible. Or it could be that it’s the kick needed to jumpstart the development of AD. The point is that we don’t know yet and only time and more research can answer that.
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Bjornevik K, Cortese M, Healy BC, Kuhle J, Mina MJ, Leng Y, Elledge SJ, Niebuhr DW, Scher AI, Munger KL, Ascherio A. Longitudinal analysis reveals high prevalence of Epstein-Barr virus associated with multiple sclerosis. Science. 2022 Jan 21.
Frontera, J. A., Boutajangout, A., Masurkar, A. V., Betensky, R. A., Ge, Y., Vedvyas, A., … & Wisniewski, T. (2022). Comparison of serum neurodegenerative biomarkers among hospitalized COVID‐19 patients versus non‐COVID subjects with normal cognition, mild cognitive impairment, or Alzheimer’s dementia. Alzheimer’s & Dementia.
Kaise, T., Fukui, M., Sueda, R., Piao, W., Yamada, M., Kobayashi, T., … & Kageyama, R. (2022). Functional rejuvenation of aged neural stem cells by Plagl2 and anti-Dyrk1a activity. Genes & Development, 36(1-2), 23-37.
Musall, S., Kaufman, M. T., Juavinett, A. L., Gluf, S., & Churchland, A. K. (2019). Single-trial neural dynamics are dominated by richly varied movements. Nature neuroscience, 22(10), 1677-1686.