Mitochondria, the tiny organelles without which our bodies would be deprived of energy, are gradually revealing their mysteries. In a study published in Nature Neuroscience, researchers from Inserm and the University of Bordeaux at the NeuroCentre Magendie, in collaboration with researchers from the Université de Moncton in Canada, have for the first time succeeded in establishing a causal link between mitochondrial dysfunction and the cognitive symptoms associated with neurodegenerative diseases.

Thanks to the creation of a specific and unprecedented tool, they succeeded in increasing mitochondrial activity in animal models of neurodegenerative diseases, where they observed an improvement in memory deficit symptoms. While these are only initial results, they open the door to considering mitochondria as a new therapeutic target.

The mitochondrion is a small intracellular organelle that provides the energy needed by the cell to function properly. The brain is one of the most energy-demanding organs, and neurons rely on the energy produced by mitochondria to communicate with one another. Indeed, when mitochondrial activity is impaired, neurons do not have the energy required to function correctly.

A research team from the University Hospital Bonn (UKB), the University of Bonn, and the Medical Center—University of Freiburg has gained new insights into the brain processes involved in encoding and retrieving new memory content. The study is based on measurements of individual nerve cells in people with epilepsy and shows how they follow an internal rhythm. The work has now been published in the journal Nature Communications.

“Similar to members of an orchestra who follow a common beat, the activity of nerve cells appears to be linked to electrical oscillations in the brain, occurring one to ten times per second. The cells prefer to fire at specific times within these brain waves, a phenomenon known as theta-phase locking,” says first author and postdoctoral researcher at the University of Bonn, Dr. Tim Guth, who recently joined the Cognitive and Translational Neuroscience group at the UKB from the Medical Center—University of Freiburg.

The research team led by Guth and Lukas Kunz found that the interaction between nerve cells and brain waves is active in both the learning and remembering of new information—specifically in the medial temporal lobe, a central area for human memory. However, in the study on spatial memory, the strength of theta-phase locking of nerve cells during memory formation was independent of whether the test subjects were later able to correctly recall the memory content.

Among the many wonders of the brain is its ability to master learned movements—a dance step, piano sonata, or tying our shoes—acquired through trial-and-error practice. For decades, neuroscientists have known that these tasks require a cluster of brain areas known as the basal ganglia.

According to a new study led by Harvard researchers in Nature Neuroscience, this so-called “learning machine” speaks in two different codes—one for recently-acquired learned movements and another for innate “natural” behaviors. These surprising findings from lab rats may shed light on human movement disorders such as Parkinson’s disease.

“When we compared the codes across these two behavioral domains, we found that they were very different,” said Bence Ölveczky, professor of organismic and evolutionary biology (OEB).

A groundbreaking study reveals that reshaping nuclear speckles — tiny structures inside cell nuclei that regulate protein maintenance — could be a novel way to treat proteinopathies like Alzheimer’s, Parkinson’s, and prion diseases.

Scientists find new compound that could reverse memory loss in mice