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D. Riche

Researcher at Centre national de la recherche scientifique

Publications -  33
Citations -  1545

D. Riche is an academic researcher from Centre national de la recherche scientifique. The author has contributed to research in topics: Lesion & Dopaminergic. The author has an hindex of 19, co-authored 33 publications receiving 1516 citations.

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Long-term effects of intrahippocampal kainic acid injection in rats: A method for inducing spontaneous recurrent seizures☆

TL;DR: Serial events offer a new method to induce spontaneous recurrent seizures with brain damage in Wistar rats and Neuropathological examination revealed dose-dependent alterations.
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A primate model of Huntington's disease: Behavioral and anatomical studies of unilateral excitotoxic lesions of the caudate-putamen in the baboon

TL;DR: A hypothesis is presented for the observed abnormal movements suggesting that the CP lesions reduce movement thresholds while the activation of dopaminoceptive regions induces dyskinesias.
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Chronic MPTP treatment reproduces in baboons the differential vulnerability of mesencephalic dopaminergic neurons observed in Parkinson's disease.

TL;DR: It is confirmed that chronic mitochondrial complex I inhibition using MPTP in primates is sufficient to reproduce the typical dopaminergic cell loss and striatal fibre depletion observed in Parkinson's disease.
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Stable Parkinsonian syndrome and uneven loss of striatal dopamine fibres following chronic MPTP administration in baboons

TL;DR: Observations and behavioural data show that chronic rather than acute MPTP injection regimens can replicate most of the neuropathological and the clinical features typical of idiopathic Parkinson's disease, possibly by increasing the ability of this neurotoxin to target specific subpopulations of mesencephalic dopaminergic neurons.
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Intrastriatal transplantation of cross-species fetal striatal cells reduces abnormal movements in a primate model of Huntington disease

TL;DR: The implantation of cross-species striatal neural precursor cells into the lesioned striatum of nonhuman primates (baboons) reduced the abnormal movements seen in the disease model and encouraged the use of cell sources other than human fetal cells in a potential clinical application to Huntington disease.