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We are analyzing https://link.springer.com/article/10.1007/bf01291788.

Title:
Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man | Journal of Neural Transmission
Description:
Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases. Once the causative mechanism is understood, animal models are also helpful in the development of therapeutic approaches exploiting this understanding. On the basis of experimental and clinical findings. Parkinson
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,643,078 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

google, scholar, disease, brain, parkinsons, dopamine, mptp, riederer, res, pharmacol, neural, neurochem, dopaminergic, rat, transm, effects, neurosci, striatal, methylphenyltetrahydropyridine, neurotoxicity, hydroxydopamine, iron, neurol, rats, mice, parkinsonism, nigrostriatal, methamphetamine, induced, lett, neurons, mpp, substantia, nigra, sci, biochem, suppl, gerlach, eur, york, effect, models, nigral, administration, model, eds, methylphenylpyridinium, sect, mechanisms, neurochemical,

Topics {✒️}

post-mortem-befunde und mptp-modell n-methyl-d-aspartate receptors protect l'étude des anticatatoniques 6-nitro-sulfamoyl-benzo-quinoxaline-dione n-methyl-d-aspartate antagonists 3-carboxy-piperazin-propyl phosphonic acid nmda-antagonist cpp withl-dopa n-methylated β-carbolines n-methyl-β-carbolines nigro-neo-striatal dopamine neurons striosome-matrix dopamine systems month download article/chapter langzeitbehandlung des parkinson-syndroms nmda-dependent superoxide production 4-dihydro-β-carboline analogs parkinsonian-inducing neurotoxin 1-methyl-4-phenyl-1 nmda antagonist mk-801 activity ofl-dopa decarboxylase oxyradical-mediated dna damage spätsyndrome der parkinson-krankheit n-methyl-4-phenylpyridinium cation extra-striatal dopaminergic nuclei catalepsy test arznei-mittelforsch/drug res 43 n-methyl-4-phenylpyridinium ion nigro-striatal dopaminergic neurons primate mptp-induced hemiparkinsonism methamphetamine-induced dopaminergic damage methamphetamine-induced dopamine depletion nigro-striatal dopamine neurons brain-derived neurotrophic factor free radical-generated neurotoxicity methamphetamine-induced neuronal damage long-term methamphetamine induced repeated methamphet-amine administration retards 6-hydroxydopamine-induced degeneration 1-methyl-4-phenyl-pyridinium studied mptp-treated squirrel monkey mptp-induced reversible model l-dopa activity mptp-lesioned c57bl/6 mice electron transport chain ampa-antagonist nbqx 1-methyl-4-phenyl-pyridinium ion important animal models mptp-treated common marmosets neuroleptic-induced catalepsy lipid peroxidation induced long-term behavioural effects 4-tetahydro-β-carboline

Questions {❓}

  • Arendash GW, Olanow CW, Sengstock GJ (1993) Intranigral iron infusion in rats: a progressive model for excess nigral iron levels in Parkinson's disease?
  • Beal MF (1992) Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses?
  • Danysz W, Gossel M, Zajaczkowski W, Dill D, Quack G (1994) Are NMDA antagonistic properties relevant for antiparkinsonian-like activity in rats?
  • German DC, Dubach M, Askaria S, Speciale G, Bowden DM (1988) 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinsonian syndrome in macaca fascicularis: which midbrain dopaminergic neurons are lost?
  • Heikkila RE, Sonsalla P (1991) The MPTP-treated mouse as a model of Parkinsonism: how good is it?
  • Krueger MJ, Tan AK, Ackrell BAC, Singer TP (1993) Is complex II involved in the inhibition of mitochondrial respiration by N-methyl-4-phenylpyridinium cation (MPP+) and N-methyl-β-carbolines?
  • Kupsch A, Loeschmann P, Sauer H, Arnold G, Renner P, Pufal D, Burg M, Wachtel H, ten Bruggencate G, Oertel WH (1992) Do NMDA receptor antagonists protect against MPTP-toxicity?
  • Russ H, Mihatsch W, Gerlach M, Riederer P, Przuntek H (1991) Neurochemical and behavioural features induced by chronic low dose treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the common marmoset: implications for Parkinson's disease?
  • Testa B, Naylor R, Costall B, Jenner P, Marsden CD (1985) Does an endogenous methylpyridinium analogue cause Parkinson's disease?

Schema {🗺️}

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         headline:Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man
         description:Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases. Once the causative mechanism is understood, animal models are also helpful in the development of therapeutic approaches exploiting this understanding. On the basis of experimental and clinical findings. Parkinson's disease (PD) became the first neurological disease to be treated palliatively by neurotransmitter replacement therapy. The pathological hallmark of PD is a specific degeneration of nigral and other pigmented brainstem nuclei, with a characteristic inclusion, the Lewy body, in remaining nerve cells. There is now a lot of evidence that degeneration of the dopaminergic nigral neurones and the resulting striatal dopamine-deficiency syndrome are responsible for its classic motor symptoms akinesia and bradykinesia. PD is one of many human diseases which do not appear to have spontaneously arisen in animals. The characteristic features of the disease can however be more or less faithfully imitated in animals through the administration of various neurotoxic agents and drugs disturbing the dopaminergic neurotransmission. The cause of chronic nigral cell death in PD and the underlying mechanisms remain elusive. The partial elucidation of the processes underlie the selective action of neurotoxic substances such as 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has however revealed possible molecular mechanisms that give rise to neuronal death. Accordingly, hypotheses concerning the mechanisms of these neurotoxines have been related to the pathogenesis of nigral cell death in PD. The present contribution starts out by describing some of the clinical, pathological and neurochemical phenomena of PD. The currently most important animal models (e.g. the reserpine model, neuroleptic-induced catalepsy, tremor models, experimentally-induced degeneration of nigro-striatal dopaminergic neurons with 6-OHDA, methamphetamine, MPTP, MPP+, tetrahydroisoquinolines, β-carbolines, and iron) critically reviewed next, and are compared with the characteristic features of the disease in man.
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