In research involving both mice and humans, a genetically-engineered medication was found to replenish the levels of a critical protein, thereby preserving the function of motor neurons. This breakthrough, specifically relevant to amyotrophic lateral sclerosis where this function is typically compro
In nearly all cases of amyotrophic lateral sclerosis and in as many as half of alldisease and frontotemporal dementia incidents, a protein known as TDP-43 is misplaced from its usual position in the cell’s nucleus. This displacement results in the loss of stathmin-2, a protein that is vital for the regeneration of neurons and the preservation of their links to muscle fibers, both of which are essential for muscle contraction and movement., a group of researchers, led by Don Cleveland, Ph.D.
Cleveland is broadly credited with developing the concept of designer DNA drugs, which act to either turn on or turn off genes associated with many degenerative diseases of the aging human nervous system, including ALS, AD, Huntington’s disease, and cancer. The new study builds upon ongoing research by Cleveland and others regarding the role and loss of TDP-43, a protein associated with ALS, AD, and other neurodegenerative disorders. In ALS, TDP-43 loss impacts the motor neurons that innervate and trigger the contraction of skeletal muscles, causing them to degenerate, eventually resulting in paralysis.
“Without stathmin-2, motor neurons disconnect from muscle, driving paralysis that is characteristic of ALS. What we have now found is that we can mimic TDP-43 function with a designer DNA drug, thereby restoring correct stathmin-2 RNA and protein level in the mammalian nervous system.”
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