There are many connected and moving biological parts in our brain, which makes the study of brain diseases particularly difficult. New research has shed light on a key brain process potentially involved in Alzheimer’s disease.
The new research focuses on the contactin-4 (CNTN4) protein – believed to play a role in neuronal network formation – and its relationship with amyloid precursor protein (APP) – a protein responsible for the production of beta-amyloid peptides, that collect in clusters called plaques in the brains of people with Alzheimer’s disease.
In tests on mice, the international team of researchers behind the new study found that the interaction of CNTN4 and APP was vital for the process of neuronal elongation, on which neurons depend to grow. and connect correctly.
“It was quite remarkable to discover that CNTN4, a gene linked to developmental processes, also plays a role in modulating factors involved in Alzheimer’s disease,” says neuroscientist Rosemary Bamford, from the University of Exeter in the United Kingdom.
It has already been established that CNTN4 is linked to autism, which first attracted the attention of researchers. They wanted to take a closer look at the protein’s functions in the brain and its possible links to neurodegenerative diseases.
When the gene that produces CNTN4 was knocked out in the motor cortex of the mouse brain – the motor cortex being a key center for planning and instigating voluntary movements – the researchers noticed that neurons in this region did not develop normally because neuronal elongation was disrupted. . What else, CNTN4 appears to work with APP to control neuronal elongation.
Further investigation using lab-grown human cells showed a complex relationship: Disabling CNTN4 production reduced APP levels, but not quite to zero. The idea is that they could compensate each other, to some extent.
“This intersection of developmental and neurodegenerative pathways offers exciting new insights into the broader implications of these proteins,” says Bamford.
Each time scientists are able to understand another biological process linked to Alzheimer’s disease, it offers another way to treat or prevent it.
It’s a bit like trying to piece together a huge puzzle about how Alzheimer’s disease works. The connection between CNTN4 and APP is another piece of this puzzle, although the whole picture is not entirely clear yet.
In future research, the team behind the study wants to delve deeper into this CNTN4-APP relationship, to see exactly how their molecules interact with each other – and how this might affect both disease and Alzheimer and autism.
“Our next steps are to clarify the impact of the CNTN4-APP interaction on neuronal activity,” says neuroscientist Asami Oguro-Ando, from the University of Exeter.
“Understanding this interaction is crucial because it represents a fundamental step towards a comprehensive understanding of neurodevelopmental and neurodegenerative disorders. »
The research was published in Royal Society Open Biology.
News Source : www.sciencealert.com
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