JERUSALEM, June 18 (Xinhua) -- Israeli researchers have discovered how brain cells defend themselves against the highly toxic botulinum neurotoxin type A, better known as Botox.
In a study published in Genomic Psychiatry, scientists from the Hebrew University and the Israel Institute for Biological Research (IIBR) revealed a natural defense mechanism that neurons activate when exposed to Botox.
Botox, produced by the Clostridium botulinum bacteria, is widely known for its cosmetic application in smoothing wrinkles by temporarily paralyzing muscles. Medically, it is also used to treat muscle spasms, migraines, and excessive sweating. While the toxin effectively paralyzes muscles, it does not kill the neurons it affects -- a phenomenon that has long intrigued researchers.
The study identified a critical group of small transfer RNA (tRNA) fragments that accumulate in neurons exposed to the toxin. These fragments interact with other molecules within the cell to block a specific form of cell death known as ferroptosis, which is triggered by oxidative stress and iron overload. By preventing ferroptosis, these tRNA fragments help neurons survive exposure to the toxin.
Further analysis revealed that these protective tRNA fragments share a common 11-nucleotide sequence. This sequence appears to suppress genes involved in both cell death and neural signaling pathways. The discovery of this sequence in both human and rat neurons suggests that this defense mechanism is ancient, having been conserved throughout evolution.
Essentially, the study demonstrates that neurons are not passive victims of toxins but possess active, built-in strategies to resist damage. This discovery could pave the way for safer, more effective medical applications of Botox, as well as new approaches to protecting the nervous system from neurotoxins. ■
