Send the link below via email or IMCopy
Present to your audienceStart remote presentation
- Invited audience members will follow you as you navigate and present
- People invited to a presentation do not need a Prezi account
- This link expires 10 minutes after you close the presentation
- A maximum of 30 users can follow your presentation
- Learn more about this feature in our knowledge base article
Do you really want to delete this prezi?
Neither you, nor the coeditors you shared it with will be able to recover it again.
Make your likes visible on Facebook?
You can change this under Settings & Account at any time.
Transcript of ALS
There is no cure for ALS; however, Riluzole is believed to reduce damage to motor neurons by decreasing the release of glutamate, the neurotransmitter in the nerve cells involved in ALS. Clinical trials have shown that Riluzole prolongs life for several months.
ALS affects the nervous system, but it only affects motor neurons which control voluntary muscle movement. Involuntary muscles (like the ones in your organs) are not affected.
Tight and stiff muscles
Muscle weakness affecting an arm or a leg
Slurred and nasal speech
Difficulty chewing or swallowing
The specific cause is unknown; however, the symptoms shown in the diagnosed person are caused by neuro-degeneration.
Neuro-degeneration is when the neurons are broken down because of:
abnormal breakdown of calcium
damage from too much calcium being in the neuron too long
a disruption in the transportation of the message through the axon (transduction)
In ALS, too much calcium enters through the calcium ion channel. Calcium tells the vesicles to let neuro-transmitters into the synaptic cleft. When too much calcium is in the cell, too many neuro-tramsmitters are released and they overload the receptors causing the calcium channels to be open too long. If calcium is in the cell too long, it causes damage and even apoptosis (CELL SUICIDE). This is what causes the degeneration of cells.
Degeneration (More Specific)
Our treatment involves engineering a protein with a large number of negatively charged amino acids. The protein would absorb calcium ions which would shut down the calcium ion channel. This would prevent the release of too many neurotransmitters which causes over-stimulation.