Scientists find a new piece of the puzzle to understand how the brains of Alzheimer’s patients work

Why does it become more difficult to concentrate when you have Alzheimer’s disease? The explanation may be that the signals transmitted from the glial cells to the nerve cells are disturbed.

When you contract Alzheimer’s disease, the brain receives “senile plaques”. Nerve cells are destroyed and brain functions fail. There is still a lot we don’t know about the disease. Why is it getting harder to remember? Why are you no longer able to maintain your level of attention and concentration?

A group of scientists from the Institute for Basic Medical Sciences at the University of Oslo have discovered an important new piece of the puzzle for understanding how the brains of patients with Alzheimer’s disease work. The hope is that the results can lay the groundwork for the development of new ways to treat Alzheimer’s disease in the future.

“We use advanced laser microscopes worth millions of crowns that now allow us to examine the brains of awake mice with Alzheimer’s. In previous studies, scientists have studied anesthetized mice,” says Rune Enger . He is an associate professor at the Letten Center, part of the Institute of Basic Medical Sciences at the University of Oslo.

Scientists studied pupils’ responses, behavior and activity in the brain

In a new study, Enger and his colleagues studied types of brain cells called astrocytes. They are important handymen in the brain that are located around nerve cells and act as support cells. Cells allow nerve cells to function normally.

Astrocytes use calcium signals inside the cell to communicate. These signals are thought to help coordinate nerve cell activity over a large area.”

Enger rune. Associate Professor, Letten Center, Institute of Basic Medical Sciences, University of Oslo

Scientists studied several things: what happened to the pupils of mice with Alzheimer’s when they moved, what the mice were doing at the same time, and what was going on inside the brain. Using genetically coded nanosensors that light up where there is activity in the brain, they were able to study the calcium signals produced by astrocytes. They could then compare what happened in the Alzheimer’s mice with healthy mice.

“Among other things, the mice got a sudden puff of air to their face so we could see what happened when they got spooked,” Enger said.

Calcium signals in astrocytes were reduced in Alzheimer’s mice

Because the scientists were able to study mice that weren’t anesthetized but were free to move around, a slightly different picture of what’s going on in the brain emerged compared to previous studies.

“Scientists who studied anesthetized Alzheimer’s mice saw that the activity of these cells increased. At the same time, we know that anesthesia influences astrocytes. In the new study, we found that this was not a given that activity increased signals in astrocytes were weaker when mice were running and when frightened compared to healthy mice Astrocytes from diseased mice were also significantly different from healthy mice in that ‘they were bigger and had altered shape and expression of specific proteins linked to inflammation,’ says Enger.

It is very likely that the connections between the astrocytes and the centers of concentration are damaged

“We can imagine that the role of astrocytes is a bit like the volume button of a radio which can affect several nerve cells at the same time. In Alzheimer’s mice, this mechanism seems to be disturbed. The drop in activity of astrocytes can be due to the damaged connection between these cells and one of the brain systems related to stress and concentration,” explains the associate professor.

He envisions a possible future drug that could help people with Alzheimer’s disease.

“Perhaps in the future we can use drugs that affect calcium activity in astrocytes to affect brain function in those with this diagnosis?” Enger asks.

Source:

University of Oslo, Faculty of Medicine

Journal reference:

Åbjørsbråten, KS, et al. (2022) Altered astrocytic Ca2+ signaling in awake transgenic mice with Alzheimer’s disease. eLife. doi.org/10.7554/eLife.75055.

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