Saturday, May 27, 2023

Study Reveals How Botox Breaches Brain Cells

Is your doctor familiar with this? And why is your doctor prescribing botox? It doesn't directly help recovery.  It makes your doctor look like something is being done but that's all it does, 'looks'.

And why use botox for stroke anyway, it provides no functional improvement.

 My botox shots did nothing to improve my arm use, because botox does nothing directly to fix the brain problem that causes spasticity.

Does Spasticity Reduction by Botulinum Toxin Type A Improve Upper Limb Functionality in Adult Post-Stroke Patients? A Systematic Review of Relevant Studies December 2022 

In this study from December 2022 is this line: No improvement in global functionality of activity daily living was observed.

Study Reveals How Botox Breaches Brain Cells

Summary: Researchers have cracked the mystery behind how the Botulinum neurotoxin type-A, also known as Botox, infiltrates neurons. The toxin utilizes a small complex formed by a receptor called Synaptotagmin 1, along with two other clostridial neurotoxin receptors, to enter synaptic vesicles in neurons.

This infiltration interrupts nerve-to-muscle communication, leading to paralysis. The findings, which provide a complete picture of Botox’s method of operation, will aid in identifying new therapeutic targets for botulism treatment.

Key Facts:

  1. Researchers discovered that a receptor called Synaptotagmin 1, in collaboration with two other receptors, helps Botox enter neurons.
  2. Once inside the neurons, Botox disrupts communication between nerves and muscle cells, causing paralysis.
  3. The study’s insights could lead to the identification of new therapeutic targets to treat botulism.

Source: University of Queensland

Researchers from The University of Queensland have determined how Botox—a drug made from a deadly biological substance—enters brain cells.

Professor Frederic Meunier and Dr. Merja Joensuu at UQ’s Queensland Brain Institute have discovered the specific molecular mechanism by which the highly deadly Botulinum neurotoxin type-A, more widely known as Botox, enters neurons.

The research is published in The EMBO Journal.

“We used super-resolution microscopy to show that a receptor called Synaptotagmin 1 binds to two other previously known clostridial neurotoxin receptors to form a tiny complex that sits on the plasma membrane of neurons,” Professor Meunier said.

This shows a woman's head.
The discovery means new therapeutic targets can be identified to develop effective treatments for botulism—a rare but potentially fatal bacterial infection. Credit: Neuroscience News

“The toxin hijacks this complex and enters the synaptic vesicles which store neurotransmitters critical to communication between neurons.

“Botox then interrupts the communication between nerves and muscle cells, causing paralysis.”

The discovery means new therapeutic targets can be identified to develop effective treatments for botulism—a rare but potentially fatal bacterial infection.

“Now we know how this complex allows the toxin internalization, we can block interactions between any two of the three receptors to stop the deadly toxins from getting into neurons,” Professor Meunier said.

The injectable drug Botox was originally developed to treat people with the eye condition strabismus, but was quickly found to alleviate(NOT CURE!) migraine, chronic pain, and spasticity disorders.

Now, it’s regularly used in plastic surgeries and is commonly known as a cosmetic treatment to smooth wrinkles.

Dr. Joensuu said just how the neurotoxin worked to relax muscles has previously been difficult to track.

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