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Neural subtype specification of fertilization and nuclear transfer embryonic stem cells and application in parkinsonian mice
A set of coculture conditions is provided that allows rapid and efficient derivation of most central nervous system phenotypes and transplantation of ES and ntES cell–derived dopaminergic neurons corrected the phenotype of a mouse model of Parkinson disease, demonstrating an in vivo application of therapeutic cloning in neural disease.
Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis
It was found that oral administration of creatine produced a dose-dependent improvement in motor performance and extended survival in G93A transgenic mice, and it protected mice from loss of both motor neurons and substantia nigra neurons at 120 days of age.
Neuroprotective Effects of Phenylbutyrate in the N171-82Q Transgenic Mouse Model of Huntington's Disease*
Results show that administration of phenylbutyrate, at doses that are well tolerated in man, exerts significant neuroprotective effects in a transgenic mouse model of HD, and therefore represents a very promising therapeutic approach for HD.
Creatine and Cyclocreatine Attenuate MPTP Neurotoxicity
Oral supplementation with either creatine or cyclocreatine produced significant protection against MPTP-induced dopamine depletions in mice, and this results further implicate metabolic dysfunction in MPTP neurotoxicity and suggest a novel therapeutic approach, which may have applicability for Parkinson's disease.
Mice Deficient in Cellular Glutathione Peroxidase Show Increased Vulnerability to Malonate, 3-Nitropropionic Acid, and 1-Methyl-4-Phenyl-1,2,5,6-Tetrahydropyridine
The present results indicate that a knock-out of GSHPx may be adequately compensated under nonstressed conditions, but that after administration of mitochondrial toxins GSHpx plays an important role in detoxifying increases in oxygen radicals.
Nonlinear Decrease over Time in N‐Acetyl Aspartate Levels in the Absence of Neuronal Loss and Increases in Glutamine and Glucose in Transgenic Huntington's Disease Mice
NAA is reflective of the health of neurons and thus is a noninvasive marker, with a temporal progression similar to nuclear inclusion bodies and symptoms, of neuronal dysfunction in transgenic mice, and the presence of elevated glutamine is evidence of a profound metabolic defect.
Additive neuroprotective effects of creatine and cyclooxygenase 2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis
- P. Klivényi, M. Kiaei, G. Gárdián, N. Calingasan, M. Beal
- BiologyJournal of neurochemistry
- 23 December 2003
The results suggest that combinations of therapies targeting different disease mechanisms may be a useful strategy in the treatment of ALS.
The Alzheimer’s Association external quality control program for cerebrospinal fluid biomarkers
Increased glucose metabolism and ATP level in brain tissue of Huntington’s disease transgenic mice
The results suggest that the neuronal damage in HD tissue may be associated with increased energy metabolism at the tissue level leading to modified levels of various intermediary metabolites with pathological consequences.