US researchers find “undead” neurons causing Parkinson’s troubles
A new lead has opened up in the study of Parkinson’s disease (PD) – its seemingly “dead” neurons have not only stopped working but can induce surrounding healthy neurons to stop working as well. Uncommon to the nerve cells of the brain, the affected dopamine neurons, which regulate motivation, memory and movement, can become “undead” or senescent, according to researchers from The Rockefeller University(Rockefeller) and Memorial Sloan Kettering Cancer Center (MSK), in New York.
In a process called senescence, cells may shut down after significant DNA damage during division, which prevents damaged cells from growing uncontrollably and causing problems like cancer.
Surprisingly, the researchers found that only dopamine-producing neurons lacked a protein called SATB1, which eventually caused senescence in its neighbor neurons, aside from inflammation, damaged mitochondria and enlarged nuclei. It was also discovered that SATB1 protects dopamine neurons from going into senescence – when the researchers reduced SATB1 in the midbrains of mice, they noted high levels of a protein that promotes senescence. Brain tissue from people with PD also showed similar high levels of the protein.
Senior Research Associate Markus Riessland, of Rockefeller, likens the senescent cells to zombie cells because “they’re undead, basically, and because their dead-like appearance is spreading.” The novel findings might explain why dopamine levels in Parkinson’s patients go down well before the dopamine neurons themselves die; and as for possible therapies, senolytic drugs may help patients remove senescent cells while new drugs could be developed to specifically target SATB1.
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