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Literature DB >> 6388779

Parkinson's disease in 1984: an update.

Abstract

This update reviews several important topics in the field of Parkinson's disease, including etiologic studies, the types and mechanisms of drug complications and their treatment, when and how to begin treatment, the association of dementia with Parkinson's disease, and the development of the newer research tools. The recent discovery of a highly selective neurotoxin (MPTP) that causes parkinsonism in humans and other primates and the use of positron emission tomography in living patients should improve our understanding of the cause of cell death in Parkinson's disease and assist in the development of more definitive treatment for this common, disabling neurologic condition.

Entities: Chemical Disease Species

Mesh：

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Year: 1984 PMID： 6388779 PMCID： PMC1483814

Source DB: PubMed Journal: Can Med Assoc J ISSN： 0008-4409 Impact factor: 8.262

57 in total

1. Evidence for abnormal long-loop reflexes in rigid Parkinsonian patients.

Authors: W G Tatton; R G Lee
Journal: Brain Res Date: 1975-12-26 Impact factor: 3.252

2. Stimulant properties of bromocriptine on central dopamine receptors in comparison to apomorphine, (+)-amphetamine and L-DOPA.

Authors: A M Johnson; D M Loew; J M Vigouret
Journal: Br J Pharmacol Date: 1976-01 Impact factor: 8.739

3. "On-off" phenomenon with levodopa therapy in Parkinsonism. Clinical and pharmacologic correlations and the effect of intramuscular pyridoxine.

Authors: S Fahn
Journal: Neurology Date: 1974-05 Impact factor: 9.910

4. Monoamine oxidase inhibitors and L-dopa.

Authors: K R Hunter; A J Boakes; D R Laurence; G M Stern
Journal: Br Med J Date: 1970-08-15

5. L-dopa therapy of Parkinson's disease: plasma L-dopa concentration, therapeutic response, and side effects.

Authors: M D Muenter; G M Tyce
Journal: Mayo Clin Proc Date: 1971-04 Impact factor: 7.616

6. Letter: Diphasic dyskinesia during levodopa therapy.

Authors: A Barbeau
Journal: Lancet Date: 1975-03-29 Impact factor: 79.321

7. Bilateral projections from precentral motor cortex to the putamen and other parts of the basal ganglia. An autoradiographic study in Macaca fascicularis.

Authors: H Künzle
Journal: Brain Res Date: 1975-05-02 Impact factor: 3.252

5. Conditional deletion of Ndufs4 in dopaminergic neurons promotes Parkinson's disease-like non-motor symptoms without loss of dopamine neurons.

Authors: Won-Seok Choi; Hyung-Wook Kim; François Tronche; Richard D Palmiter; Daniel R Storm; Zhengui Xia
Journal: Sci Rep Date: 2017-03-22 Impact factor: 4.379

5 in total

Parkinson's disease in 1984: an update.

1. Evidence for abnormal long-loop reflexes in rigid Parkinsonian patients.

2. Stimulant properties of bromocriptine on central dopamine receptors in comparison to apomorphine, (+)-amphetamine and L-DOPA.

3. "On-off" phenomenon with levodopa therapy in Parkinsonism. Clinical and pharmacologic correlations and the effect of intramuscular pyridoxine.

4. Monoamine oxidase inhibitors and L-dopa.

5. L-dopa therapy of Parkinson's disease: plasma L-dopa concentration, therapeutic response, and side effects.

6. Letter: Diphasic dyskinesia during levodopa therapy.

7. Bilateral projections from precentral motor cortex to the putamen and other parts of the basal ganglia. An autoradiographic study in Macaca fascicularis.

8. Parkinsonism: onset, progression and mortality.

9. Patterns of dystonia ("I-D-I" and "D-I-D-") in response to l-dopa therapy for Parkinson's disease.

10. Success and problems of long-term levodopa therapy in Parkinson's disease.

1. Genetic reduction of mitochondrial complex I function does not lead to loss of dopamine neurons in vivo.

2. Essential tremor as a harbinger: What is the cognitive fallout of having essential tremor?

3. Dopamine Agonists and their risk to induce psychotic episodes in Parkinson's disease: a case-control study.

4. Differential effects of Parkinson's disease and dopamine replacement on memory encoding and retrieval.

5. Conditional deletion of Ndufs4 in dopaminergic neurons promotes Parkinson's disease-like non-motor symptoms without loss of dopamine neurons.