Autoradiographic study on dopamine uptake sites and their correlation with dopamine levels and their striata from patients with Parkinson disease, Alzheimer disease, and neurologically normal controls

Mizukawa, Kiminao; McGeer, Edith G.; McGeer, Patrick L.

doi:10.1007/bf03160027

Cited by 22 publications

(11 citation statements)

References 21 publications

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“…The morphologically-demonstrated loss of neurons in the pars compacta of the SN correlates significantly with the reduction of dopamine in the Mizukawa et al (1993) DOPA 3,4-dihydroxyphenylalanine, DOPAC 3,4-dihydroxyphenylacetic acid, HVA homovanillic acid. *For further reading and original data see references indicated in Table 1 striatum, and the extent of the dopamine deficit correlates with the degree of akinesia (Bernheimer et al, 1973).…”

Section: Changes In Dopaminergic Systemsmentioning

confidence: 98%

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

Gerlach

Riederer

1996

J. Neural Transmission

441

221

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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 nigrostriatal dopaminergic neurons with 6-OHDA, methamphetamine, MPTP, MPP+, tetrahydroisoquinolines, beta-carbolines, and iron) critically reviewed next, and are compared with the characteristic features of the disease in man.

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Section: Changes In Dopaminergic Systemsmentioning

confidence: 98%

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

Gerlach

Riederer

1996

J. Neural Transmission

441

221

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“…In the hypothalamus, the D2 receptor binding potentials were also significantly reduced without a correlation with age and levodopa equivalent dose (Politis et al, 2008). Mizukawa et al reported a significant reduction in the density of dopamine receptors in both the caudate and putamen of advanced PD patients (Mizukawa et al, 1993); while Boileau et al found decreased dopamine D3 receptor binding in the ventral striatum and globus pallidus in drug-naive PD patients (Boileau et al, 2009). …”

Section: Alterations In Neurotransmitter Receptors In Parkinson’s mentioning

confidence: 99%

Neurotransmitter receptors and cognitive dysfunction in Alzheimer's disease and Parkinson's disease

Yan

Zhou

et al. 2012

Progress in Neurobiology

249

139

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Cognitive dysfunction is one of the most typical characteristics in various neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease (advanced stage). Although several mechanisms like neuronal apoptosis and inflammatory responses have been recognized to be involved in the pathogenesis of cognitive dysfunction in these diseases, recent studies on neurodegeneration and cognitive dysfunction have demonstrated a significant impact of receptor modulation on cognitive changes. The pathological alterations in various receptors appear to contribute to cognitive impairment and/or deterioration with correlation to diversified mechanisms. This article recapitulates the present understandings and concepts underlying the modulation of different receptors in human beings and various experimental models of Alzheimer’s disease and Parkinson’s disease as well as a conceptual update on the underlying mechanisms. Specific roles of serotonin, adrenaline, acetylcholine, dopamine receptors, and N-methyl-D-aspartate receptors in Alzheimer’s disease and Parkinson’s disease will be interactively discussed. Complex mechanisms involved in their signaling pathways in the cognitive dysfunction associated with the neurodegenerative diseases will also be addressed. Substantial evidence has suggested that those receptors are crucial neuroregulators contributing to cognitive pathology and complicated correlations exist between those receptors and the expression of cognitive capacities. The pathological alterations in the receptors would, therefore, contribute to cognitive impairments and/or deterioration in Alzheimer’s disease and Parkinson’s disease. Future research may shed light on new clues for the treatment of cognitive dysfunction in neurodegenerative diseases by targeting specific alterations in these receptors and their signal transduction pathways in the frontal-striatal, fronto–striato–thalamic, and mesolimbic circuitries.

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“…[2][3][4] In addition, a reduction of striatal dopamine reuptake sites has been found in postmortem studies using various ligands in AD patients 5 and in patients with AD and parkinsonism, 6 but no significant decrease in the striatal dopamine uptake sites in AD was found in another study. 7 Molecular techniques have revealed the existence of at least five different dopamine receptor subtypes. These receptors are named D1-D5 receptors and are divided in broad terms into "D1-like" (D1 and D5) and "D2-like" (D2, D3, D4) receptors.…”

mentioning

confidence: 99%

PET shows that striatal dopamine D1 and D2 receptors are differentially affected in AD

Kemppainen

Ruottinen²,

Någren³

et al. 2000

Neurology

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Autoradiographic study on dopamine uptake sites and their correlation with dopamine levels and their striata from patients with Parkinson disease, Alzheimer disease, and neurologically normal controls

Cited by 22 publications

References 21 publications

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

Neurotransmitter receptors and cognitive dysfunction in Alzheimer's disease and Parkinson's disease

PET shows that striatal dopamine D1 and D2 receptors are differentially affected in AD

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