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Levodopa crosses the protective blood–brain barrier, whereas dopamine itself cannot. [3] [4] Thus, levodopa is used to increase dopamine concentrations in the treatment of Parkinson's disease, Parkinsonism, dopamine-responsive dystonia and Parkinson-plus syndrome. The therapeutic efficacy is different for different kinds of symptoms.
L-DOPA is used medically under the name levodopa in the treatment of Parkinson's disease and certain other medical conditions. It is usually used in combination with a peripherally selective aromatic L-amino acid decarboxylase (AAAD) inhibitor such as carbidopa or benserazide. These agents increase the strength and duration of levodopa.
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 ]
Levodopa is a precursor to the neurotransmitter dopamine, which is administered to increase its levels in the central nervous system.However, most levodopa is decarboxylated to dopamine before it reaches the brain, and since dopamine is unable to cross the blood–brain barrier, this translates to little therapeutic gain with strong peripheral side effects.
Its metabolic precursor L-DOPA can be manufactured; Levodopa, a pure form of L-DOPA, is the most widely used treatment for Parkinson's. There is evidence that schizophrenia involves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists which reduce dopamine activity. [10]
Levodopa and proteins use the same transportation system in the intestine and the blood–brain barrier, competing between them for access. [20] When taken together, the consequences of such competition is a reduced effectiveness of the drug. [ 20 ]
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