Amyotrophic lateral sclerosis (ALS) is a widespread neurodegenerative disease caused by the loss of neurons that control movement. Although abnormal accumulation of proteins called TDP-43 accompanies ALS, its role in disease progression is not well understood. Recently, using novel mouse models of ALS, researchers have identified the neurological spreading patterns through which TDP-43 perpetuates the degeneration of the movement-related neural circuitry.
Our movements are controlled by multiple neural pathways that connect the brain and spinal cord. In particular, neurons in the cerebral cortex send commands to the motor neurons in the spinal cord and then to the muscles, thus eliciting the required movement. However, this flow of neural information is compromised in amyotrophic lateral sclerosis -- a widespread progressive neurodegenerative disease in which the muscles gradually atrophy, making movement and breathing difficult.
To address this question, the researchers developed ALS mouse models that primarily accumulate TDP-43 in the cortical motor neurons, spinal motor neurons, or skeletal muscles. They then examined how the TDP-43 in specific motor neurons initiates disease progression to other motor-related neurons. Their study was published in Acta Neuropathologica on Aug 9, 2023.
The researchers found that TDP-43 induced in the cortical neurons of the mouse ALS models caused mild degeneration. They further found that TDP-43 was transported along the axons and transferred to the oligodendrocytes -- non-neuronal cells that support neurons by enwrapping axons with a protective layer called myelin to facilitate neuronal signal transmission.
Regarding their findings, co-senior author Dr. Masaki Ueno, a professor in the same institute, says,"Our findings suggest that pathogenic TDP-43 has multiple properties to propagate degeneration in the motor pathways in ALS, probably by spreading itself and inducing other toxic events such as degeneration and inflammation."
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