1. Two main groups of drugs that are important in the treatment of Parkinson’s:

• Drugs that increase dopamine activity
• Drugs that decrease Cholinergic activity

2. In what way does Amantadine act as an antiparkinsonism drug:

Amantadine increases DA neurotransmission by increasing the synthesis or release of dopamine ot the inhibition of DA reuptake. It also blocks muscarinic action.

3. MOA of antiparkinsonism drugs that increases DA concentration indicectly:

• Monoamine Oxidase inhibitors selectively inhibits Monoamine Oxidase type B. This is the form of the enzyme that metabolises dopamine.
• COMT inhibitors inhibits the enzyme in both the CNS and peripheral tissues that coverts levodopa to 3-OMD.
• Amantadine enhances neurotransmission involved in the inhibition of dopamine reuptake

4. Which drugs are ergot derivatives and which are not:

Ergot derivatives:

• Bromocriptine

Non-ergot derivatives:

• Pramipexole
• Ropinirole

5. Dopamine receptors stimulated by each agonist:

• Bromocriptine: D2 receptors
• Pramipexole: D3 receptors
• Ropinirole: D2 receptors

6. Drugs classified as neuron protecting drugs and what that means:

Neuroprotective drugs are those which protects the brain from being damaged. These drugs include all MAO-B inhibitors and Pramipexole.

7. Importance of MAO-B inhibitors in the treatment of Parkinson’s:

It increases the DA concentration in the CNS. It can be given as a combination therapy with L-dopa. Safinamide also increases DA activity by inhibiting DA reuptake and decreases glutamate release.

8. How do COMT inhibitors act in Parkinsonism:

COMT metabolizes L-dopa to 3-OMD. A COMT inhibitor therefore extends the duration of action of L-dopa, it decreases peripheral metabolism and improves the bio availability.

9. How does Istradephyllin work:

It is an Adenosine A_2A antagonist. It can be used as an add-on therapy drug to L-dopa/Carbidopa when experiencing off-episodes.

10. Discuss the MOA of Safinamide:

Safinamide has a novel dual mechanism of action. It increases DA activity by inhibiting MAO-B as well as the inhibition of DA reuptake. The second MOA is that Safinamide decreases glutamate release.