Motor system disorders
10 important questions on Motor system disorders
What do all the motor diseases have in common? (9)
- Role of aging => neurons don’t come back
- Glutamate excitotoxicity
- Protein mishandling/misfolding and aggregation, “seeding”
- Ubiquitin/proteasomal dysfunction (normally this would be the way to get rid of the misfolded proteitns)
- Disrupted intracellular transport => size is large; transport is important if you have such a long cell. Neuron from your brain to my spinal cord.
- Neuroinflammation, microglial activation, T-cell. Issue with inflammation is swelling => problem
- Mitochondrial dysfunction, oxidative stress (glucose and oxygen dysfunction)
- Apoptosis, autophagy, (programmed necrosis, “necroptosis”)
- Selective vulnerability => why for example only in the striatum or substantia nigra
Which protein belongs to which disease?
Parkinson: Synucleinopahties
Huntington: Polyglutamine
ALS: TDP43 proteinopathies
Why are misfolded proteins a problem? (3)
- Loss of function
- Gain of function
- Inflammation
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What is pathophysiology of parkinson?
- Gets stimulated by acetylcholine
- Gets inhibited by Dopamine from the sustantia nigra.
- In parkinson the GABA get no inhibiton => more inhibition from GABA. There is an imbalance
- So you have two options. Add dopamine or remove acetylcholine.
How can you increase the amount of dopamine? (4)
- Increase the synthesis of dopamine - L-dopa
- Inhibit degradation - selegiline (MAO B inhibitors)
- Agonist of dopamine for the receptor - Bromocriptine & pramipexole
- Blocking the uptake and enhancing the release of dopamine ? -Amantadine
You dont want that levodopa is transformed in the periphery, because then in will not come into the brain. How can you prevent this? Give names.
Carbidopa
Works in the GI tract and peripheral tissues.
What change in symptoms do you see after giving L-dopa?
- Bradykinesia
- Rigidity
- Tremor
- No effect on the instability and shuffling gait
Side effect
- Symptoms returns between doses
- levodopa-induced dyskinesia (like a huntington patient)
How does tetrabenzaine work?
Inhibits this => monoamines are not protected. Degradated.
What is another target for huntingtin?
Blocking these.
What is one of the drugs against ALS that prolongs your life?
The question on the page originate from the summary of the following study material:
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