Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Parkinson’s disease, therapy

Rascol O, Payoux P, Ory F, et al. Limitations of current Parkinson s disease therapy. Ann Neurol. 2003 ... [Pg.133]

The sulfuric acid salt of 5 (Parnate Jatrosom ) is used as an antidepressant drug, and best results were achieved in chronic neurotic patients. (+ )-(5) was reported to be also effective as an adjuvant in Parkinson s disease therapy . Differences of activities of the pure enantiomers (for a minireview see Ref. 629 for resolution of racemic 5 see Refs 42, 103, 160, 654, 655 for g.c. separation of racemic 5 as iV-trifluoracetyl-L-prolyl derivative, see Ref. 656) and the trans-cis diastereomers 5/628 have been studied as well as the selectivities of 5 on inhibition of MAO type A and B (e.g. Refs 637, 638, 658-674). (+ )-(5) showed stronger inhibition of platelet (dopamine ... [Pg.1421]

Because of the diminished activity of compounds 34 and 35, compared to 5-OH-DPAT, it is now an interesting challenge to develop new compounds based on the structure of tetrahydrobenzo[/i]thiophenes, which possess the same, improved oral bioavailability as do our compounds 34 and 35, but with a higher affinity and activity at the dopamine D2 and D3 receptor. These compounds will be of great interest for the development of new drugs in Parkinson s disease therapy. [Pg.83]

Pharmaceutical coverage is skewed towards the U.S. and Europe, while the biotechnology and drug discovery publications better represent the Asian and the rest of the world markets. Recent pharmaceutical titles include U.S. Alzheimer s Disease Medications Markets, World Emerging Anti-Obesity Prescription Drug Markets, U.S. Parkinson s Disease Therapies Markets, and R D Portfolio Management. [Pg.156]

Montastruc, J.L. (1991) Recent advances in the clinical pharmacology of Parkinson s disease. Therapie 46 293-303. [Pg.497]

Acetylcholine Precursors. Early efforts to treat dementia using cholinomimetics focused on choline [62-49-7] (12) supplement therapy (Fig. 3). This therapy, analogous to L-dopa [59-92-7] therapy for Parkinson s disease, is based on the hypothesis that increasing the levels of choline in the brain bolsters acetylcholine (ACh) synthesis and thereby reverses deficits in cholinergic function. In addition, because choline is a precursor of phosphatidylcholine as well as ACh, its supplementation may be neuroprotective in conditions of choline deficit (104). [Pg.96]

While advances in the symptomatic drug therapy (summarized below) have certainly improved the lives of many Parkinson patients, the goal of current research is to develop treatments that can prevent, retard or reverse the death of dopaminergic neurons in the substantia nigra pats compacta (and of other neurons involved in the pathogenesis of Parkinson s disease not mentioned in this essay). [Pg.165]

Low affinity use-dependent NMDA recqrtor antagonists meet the criteria for safe administration into patients. Drugs like amantadine and memantine have modest effects on Parkinson s disease and are used as initial therapy or as adjunct to l-DOPA. Their adverse effects include dizziness, lethargy and sleep disturbance. [Pg.166]

The main clinical use of COMT inhibitors is as adjunct (or additional adjunct) in the therapy of Parkinson s disease. The standard therapy of Parkinson s disease is oral L-dopa (as a drug levodopa) given with a dopa decarboxylase (DDC) inhibitor (e.g. carbidopa and benserazide), which does not reach the brain. When the peripheral DDC is inhibited, the concentration of 3-O-methyldopa (3-OMD), a product of COMT, in plasma is many times that of L-dopa. Since the half-life of 3-OMD is about 15 h, compared to about 1 h for L-dopa, the concentration of 3-OMD remains particularly high during chronic therapy, especially if new slow release L-dopa preparations are used. A triple therapy (L-dopa plus DDC inhibitor plus COMT-inhibitor) will... [Pg.336]

Hagan, JJ, Middlemas, DN, Sharpe, PC and Poste, GH (1997) Parkinson s disease prospects for improved therapy. Trends Pharmacol. Sci. 18 156-163. [Pg.323]

Serra, PA, Esposita, G, Enrico, P, Mura, M, Migheli, R, Delogu, MR, Miele, M, Desole, MS, Grella, G and Miele, E (2000) Manganese increases L-dopa auto-oxidation in the striatum of the freely moving rat potential implications to L-dopa long-term therapy of Parkinson s disease. Brit. J. Pharmacol. 130 937-945. [Pg.323]

Develop a monitoring plan to assess effectiveness and adverse effects of nonpharmacologic therapy and pharmacotherapy for Parkinson s disease. [Pg.473]

Jiao, S., Gurevich, V., and Wolff, J. A. (1993). Long-term correction of rat model of Parkinson s disease by gene therapy. Nature 362 450- 153. [Pg.84]

These symptoms are alleviated by administering levodopa (L-dopa), a precursor for dopamine. L-dopa is taken up by the axon terminals of dopaminergic neurons and used to form dopamine. Interestingly, in some patients, a side effect of dopamine replacement therapy is the development of symptoms characteristic of schizophrenia. (Recall that this mental disorder is caused by overactive dopaminergic neurons.) On the other hand, drugs used to treat schizophrenia — dopamine receptor antagonists — may elicit symptoms of Parkinson s disease. [Pg.43]


See other pages where Parkinson’s disease, therapy is mentioned: [Pg.22]    [Pg.1086]    [Pg.26]    [Pg.1985]    [Pg.701]    [Pg.22]    [Pg.1086]    [Pg.26]    [Pg.1985]    [Pg.701]    [Pg.238]    [Pg.359]    [Pg.438]    [Pg.798]    [Pg.845]    [Pg.934]    [Pg.265]    [Pg.266]    [Pg.269]    [Pg.160]    [Pg.256]    [Pg.812]    [Pg.81]    [Pg.43]   
See also in sourсe #XX -- [ Pg.473 ]

See also in sourсe #XX -- [ Pg.55 , Pg.56 , Pg.57 , Pg.58 ]




SEARCH



Disease therapy

Parkinson’s disease

© 2024 chempedia.info