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At least 1,297 records · Page 72Linked to original sources
PubMed2000

Toward a primate model of L-dopa-unresponsive parkinsonism mimicking striatonigral degeneration.

We developed a primate model of striatonigral degeneration (SND), the neuropathology underlying levodopa-unresponsive parkinsonism associated with multiple systemic atrophy (MSA-P), by sequential systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 3-nitropropionic acid (3NP) in a Macaca fascicularis monkey. L-Dopa-responsive parkinsonian features emerged after MPTP injections. Subsequent chronic 3NP administration aggravated the motor symptoms and abolished the L-dopa response. In vivo magnetic resonance imaging revealed bilateral striatal lesions. Histopathologically, there was severe dopaminergic cell loss in the substantia nigra pars compacta compared with the control monkey. Furthermore, we observed circumscribed areas of severe neuronal degeneration in the motor striatum. These changes were absent in the control monkey, and they were associated with diffuse metabolic failure as demonstrated by cytochrome oxidase histochemistry. The striatal pathology predominantly involved output pre-pro-enkephalin A- and substance P-containing cells, whereas somatostatin (NADPH-diaphorase)-containing interneurons were relatively spared. Our model therefore reproduced levodopa-unresponsive parkinsonism and SND-like pathologic changes characteristic of MSA-P. The double-lesion primate model of SND may serve as a preclinical test-bed for the evaluation of novel therapeutic strategies in MSA-P.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2003

Type I glutaric aciduria, part 2: a model of acute striatal necrosis.

Type I glutaric aciduria (GA1) is an inborn error of organic acid metabolism that is associated with acute neurological crises, typically precipitated by an infectious illness. The neurological crisis coincides with swelling, metabolic depression, and necrosis of basal ganglia gray matter, especially the putamina and can be visualized as focal, stroke-like, signal hyperintensity on MRI. Here we focus on the stroke-like nature of striatal necrosis and its similarity to brain injury that occurs in infants after hypoxia-ischemia or systemic intoxication with 3-nitropropionic acid (NPA). These conditions share several features including abrupt onset, preferential effect in the striatum and age-specific susceptibility. The pathophysiology of the conditions is reviewed and a model proposed herein. We encourage investigators to test this model in an appropriate experimental system.

Brain Diseases, Metabolic, Inborn↗
PubMed2005

Protective effects of ginseng components in a rodent model of neurodegeneration.

To test the proposed neuroprotective activity of whole ginseng extract and its components, we used 3-nitropropionic acid (3-NP), an inhibitor of succinate dehydrogenase, to produce neurodegeneration. Treatment with 3-nitropropionic acid (90 mg/kg) over a 5-day period resulted in severe impairment of movement and loss of neurons in the striatum. Pretreatment with a preparation from the whole root of American ginseng had no protective effects. Pretreatment with a preparation of ground leaves and stems, which contains greater levels of ginsenosides than ground root, improved the behavioral score and reduced the volume of the striatal lesion. A partial purification of American ginseng was performed to concentrate the putative protective components: Rb1, Rb3, and Rd (termed Rb extract). Pretreatment with the Rb extract significantly reduced the 3-nitropropionic acid-induced motor impairment and cell loss in the striatum, and it completely prevented any mortality. Significant effects on motor function, mortality, and the striatal lesion volume also were measured in animals pretreated with the individual ginsenosides, Rb1, Rb3, or Rd. The results demonstrate that some of the ginsenosides have neuroprotective activity, and that a partial purification of whole ginseng to concentrate the neuroprotective components may have utility as a neuroprotective agent.

Animals↗