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252 records · Page 14Linked to original sources
PubMed1985

L-threo-3, 4-dihydroxyphenylserine treatment of Parkinson's disease.

L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS) was administered at a maintenance dose of 600-900 mg/day, in 10 patients with Parkinson's disease who exhibited a notable freezing phenomenon under the medication of L-DOPA/DCI (DOPA-decarboxylase inhibitor). Changes in clinical symptoms were examined after 8 weeks of treatment. Frozen gait and dysarthria were markedly alleviated by L-threo-DOPS administration, and the rigidity persisting under conventional medication was also relieved. Marked improvement in frozen gait was observed in 1-2 weeks, and that of dysarthria in 2-3 weeks, after the initiation of L-threo-DOPS administration. Nine of the 10 patients were treated with a combination of DOPA and DCI, and the L-threo-DOPS/benserazide ratio and L-threo-DOPS/carbidopa ratio were 9.2 and 26.3, respectively. The effect of L-threo-DOPS were enhanced in one patient in whom DCI was changed from carbidopa to benserazide, suggesting the necessity of further studies on the type and dose of DCI to be combined with L-threo-DOPS.

Aged↗
PubMed1979

Lack of hypotensive and brain catecholamine depleting effects by erythro- and threo-alpha-methyl DOPS.

An investigation was carried out to ascertain whether erythro- and threo-alpha-methyl-dihydroxy-phenyl-serine were able of depleting cerebral and peripheral norepinephrine (NE) through their metabolization to alpha-mNE. The results show that the alpha-methyl-aminoacids were decarboxylated only at the periphery and that the threo-form caused depletion in cardiac NE. In any case, both isomers were unable to cross the blood-brain barrier leaving the cerebral NE unaffected. Consequently the use of alpha-mDOPS as alternative tool to alpha-mDOPA in the therapy for hypertension seems unlikely to occur. The results also provide evidence for differences in the pharmacokinetics of the two isomers.

Animals↗
PubMed1982

[Ataxia in rolling mouse Nagoya and the norepinephrine system--a psychopharmacological study].

Rolling mouse Nagoya (RMN), an ataxia mutant mouse, is adequate to checking up the efficacy of drugs on the ataxic movement disorders. The effects of some drugs on the ataxia of RMN were investigated by open field study. The drugs administered to RMN were as follows: TRH, FLA-63, DL-threo-DOPS, phenoxybenzamine and propranolol. Ataxic gait of RMN were remarkably improved by TRH, but remained unchanged by other drugs. The pretreatments with FLA-63, DOPS and phenoxybenzamine were not influenced to the antiataxic effects of TRH, while the pretreatment with propranolol increased the antiataxic effect of TRH in RMN. These results suggest that mechanism of the improvement of ataxic gait by TRH may not be sufficiently explained through only changing norepinephrine metabolism.

Animals↗
PubMedDate not supplied

Intranasal L-threo-3,4,-dihydroxyphenylserine in treating diarrhea associated with familial amyloidotic polyneuropathy.

We evaluated the absorption disturbance of the gastrointestinal tract in patients with familial amyloidotic polyneuropathy (FAP). Ursodeoxycholic acid (UDCA) 300 mg was administered orally to 10 patients with FAP and 11 control subjects. Serum levels of total bile acid were determined as an indicator of absorption. The patients had lower serum levels of total bile acid than controls, suggesting an absorption disorder. To attempt to treat the diarrhea commonly associated with FAP, L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), a synthetic precursor of norepinephrine, was administered 100 mg/dose by the oral and 8 mg/0.4 ml by the intranasal route and their effects on the elevation of serum norepinephrine levels were compared. The 3-0-monohemiphthalate salt of glycyrrhizinic acid and sodium ascorbate were used as vehicles for the intranasal preparation to enhance drug absorption and prevent oxidation. Increased serum levels of norepinephrine, the converted metabolite of L-threo-DOPS in serum, was observed 2 hours after intranasal administration, but not after administration of the oral preparation or vehicle alone. Intranasal administration of 8 mg 3 times/day for 1 week resulted in reduction of the daily frequency of diarrhea as well as a decrease in the severe orthostatic hypotension in three patients with FAP. Thus, an intranasal delivery system for L-threo-DOPS, which acts by stimulating adrenergic receptors, may be considered in treating patients with FAP with severe diarrhea.

Administration, Intranasal↗
PubMed1993

Recent advances in pharmacological therapy of Parkinson's disease.

The discovery of a selective striatal dopamine deficiency in Parkinson's disease has led to dopamine replacement therapies including L-DOPA, dopamine full and partial agonists, and MAO-B inhibitors. The development of new compounds and alternative methods of drug delivery may be able to overcome the long-term side effects of the established therapies. Overactivity of central glutamatergic systems appears to be important in the pathophysiology of the disorder and provides the rationale for the use of glutamate antagonists. Recent studies emphasize the significance of oxidative stress and free radical formation in the pathogenesis of Parkinson's disease. Future research will focus on improvements in neuroprotective therapy to prevent or slow the rate of progression of the disease. Possible neuroprotective strategies include selective MAO-B inhibitors, iron chelators, and free radical scavengers.

Antiparkinson Agents↗
PubMed1993

Effects of monoamine precursors on food intake in male rats.

Effects of monoamine precursors on food intake in male rats were studied. Rats were subjected to an artificial circadian pattern of eating, i.e., a five-hour feeding program during daytime and food deprived during the rest of day. Feeding responses after treatment of drugs were examined. Intraperitoneal injection of L-beta-3, 4-dihydroxyphenylalanine (L-DOPA), DL-threo-dihydroxyphenylserine (DOPS), or 5-hydroxy-L-tryptophan (5-HTP) suppressed food intake. The suppression occurred within the first thirty minutes of the test period and their order of potency came out 5-HTP > L-DOPA = DOPS. The suppressive action of 5-HTP was very strong and lasted at least 3 days. The mechanism of this feeding suppressed action by either the central satiety center or the peripheral inhibiting system was discussed in this context.

5-Hydroxytryptophan↗
PubMed1993

[Hyperthermia in a Shy-Drager syndrome patient--pathophysiological effects of body temperature and L-DOPS on orthostatic hypotension].

A 65-year-old man was admitted to our hospital because of syncope, hyperthermia and urinary disturbance. Neurological examination revealed cerebellar ataxia, muscular rigidity, hyperreflexia with Babinski sign in both sides, and various autonomic dysfunctions including anisocoria, orthostatic hypotension and neurogenic bladder. He was diagnosed as having Shy-Drager syndrome (SDS). Oral administration of L-threo-3,4-dihydroxyphenyl-serine (L-DOPS) (300 mg/day) was started for orthostatic hypotension. After discharge he suffered from pneumonia at his house, and he kept himself warm because of a chill. The patient then fell into hyperthermia (44.0 degrees C), resulting in unconsciousness and a state of shock. He was transferred to our hospital again and was treated by body cooling and drip infusion of dopamine after which he recovered completely within one day. Control of body temperature and blood pressure was examined by heat loading and head-up tilt after heat loading, with or without administration of L-DOPS. These examinations showed that his rectal body temperature rose easily during heat loading and that this phenomenon was enhanced by the administration of L-DOPS. Moreover as his body temperature became higher, he more easily developed syncope due to orthostatic hypotension. It is suggested that in SDS patients, L-DOPS facilitates orthostatic hypotension and syncope in high temperature conditions.

Aged↗
PubMed1996

The metabolism of L-DOPA and L-threo-3,4-dihydroxyphenylserine and their effects on monoamines in the human brain: analysis of the intraventricular fluid from parkinsonian patients.

The monoamines and their metabolites were analyzed in the intraventricular fluid of parkinsonian patients treated with L-DOPA alone or together with L-threo-3,4-dihydroxyphenylserine (L-threo-DOPS), the precursor amino acids of dopamine and noradrenaline, respectively. In the intraventricular fluid of the patients administered with L-DOPA, the level of dopamine metabolites were higher than control, suggesting enhanced turnover of dopamine in the brain. However, L-DOPA administration increased free noradrenaline only slightly, and did not affect serotonin and its metabolite. On the other hand, by administration of L-DOPA combined with L-threo-DOPS, the levels of monoamines increased in general, whereas the monoamine metabolites by catechol-O-methyltransferase were reduced compared with those in the patients treated with L-DOPA alone. Only a minor part of L-threo-DOPS was metabolized into noradrenaline by aromatic L-amino acid decarboxylase, and it was metabolized mainly by two other enzymes, catechol-O-methyltransferase and DOPS-aldolase in the brain. An overview of the metabolism of neurotransmitters in the brain proved to be useful to evaluate the therapeutic effects of these precursor amino acids.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

[Pain caused by ephaptic transmission occurring in the recovery phase of diabetic vascular mononeuropathy was effectively suppressed with L-threo-3,4-dihydroxyphenyl-serine].

A 59-year-old man with an 8-years history of diabetes mellitus had an acute onset of sharp pain in the anterior part of right lower leg. One month later, the pain changed to deep dull nature in the deeper site of the peroneal region. The pain increased, when he stood up, walked, and stayed in the cold room and decreased by rest. It was more painful in the evening than in the morning. The first sharp pain was thought to be caused by ischemia due to diabetic vascular neuropathy. The next dull pain was considered to be originated from ephaptic transmission between sympathetic efferent fibers to group IV and afferent ones from the skeletal muscle. The latter dull pain was selectively suppressed by nerve block when it became effective to the branch of deep peroneal nerve to extensor digitorum longus muscle. The hypothesis of ephaptic transmission was supported by meaningful decrease of muscle sympathetic activity detected by microneurography before and after the dosage of L-DOPS, which effectively suppressed the pain as well as other alpha-stimulant, midodrine hydrochloride. We concluded that the ephaptic pain caused by muscle sympathetic activity could be suppressed by the vasoconstrictive drugs through the mechanism of baroreflex control.

Adrenergic alpha-Agonists↗