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Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis. [1] In the context of Parkinson's disease (PD), dyskinesia is often the result of long-term dopamine therapy.
Therefore, when levodopa is introduced, excessive proteins are discouraged, while in advanced stages, additional intake of low-protein products such as bread or pasta is recommended for similar reasons. [20] To minimize interaction with proteins, levodopa is recommended to be taken 30 minutes before meals. [20]
[170] [171] [note 1] Symptoms may become unresponsive to levodopa, with sudden changes between a state of mobility ("ON time") and immobility ("OFF time"). [173] Long-term levodopa use may also induce dyskinesia and motor fluctuations. Although this often causes levodopa use to be delayed to later stages, earlier administration leads to ...
Carbidopa/levodopa, also known as levocarb and co-careldopa, is the combination of the two medications carbidopa and levodopa. [6] It is primarily used to manage the symptoms of Parkinson's disease, but it does not slow down the disease or stop it from getting worse. [6] It is taken by mouth. [6]
The long term use of levodopa increases oxidative stress through monoamine oxidase led enzymatic degradation of synthesized dopamine causing neuronal damage and cytotoxicity. The oxidative stress is caused by the formation of reactive oxygen species (H 2 O 2 ) during the monoamine oxidase led metabolism of dopamine.
The 2001 Nobel Prize in Chemistry was also related to l-DOPA: the Nobel Committee awarded one-quarter of the prize to William S. Knowles for his work on chirally catalysed hydrogenation reactions, the most noted example of which was used for the synthesis of l-DOPA. [14] [15] [16] Synthesis of l-DOPA via hydrogenation with C 2-symmetric ...
Peripheral inhibitors of DOPA decarboxylase (AADC) block one of two ways levodopa can be inactivated before it reaches the central nervous system and is activated to dopamine. (Dopamine in the periphery only causes side effects, no antiparkinson effect.) COMT inhibitors block the second way. [1]
Entacapone together with levodopa and carbidopa allows levodopa to have a longer effect in the brain and reduces Parkinson's disease signs and symptoms for a greater length of time than levodopa and carbidopa therapy alone. [2] Entacapone is a selective and reversible inhibitor of the enzyme catechol-O-methyltransferase (COMT). [2]
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