Abstract
Administration of triacetyluridine (TAU) is a means of delivering exogenous pyrimidines to the brain, which may help to compensate for bioenergetic defects. TAU has previously been shown to be neuroprotective in animal models of Huntington's and Alzheimer's diseases. We examined whether oral administration of TAU in the diet could exert significant neuroprotective effects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity model of Parkinson's disease. Administration of TAU significantly attenuated MPTP-induced depletion of striatal dopamine and loss of tyrosine-hydroxylase-positive neurons in the substantia nigra. These findings suggest that administration of TAU may be a novel approach for treating neurodegenerative diseases associated with impaired mitochondrial function.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
-
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / antagonists & inhibitors
-
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / pharmacokinetics*
-
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / pharmacology*
-
3,4-Dihydroxyphenylacetic Acid / metabolism
-
Acetates
-
Animals
-
Dietary Supplements
-
Disease Models, Animal
-
Dopamine / metabolism
-
Homovanillic Acid / metabolism
-
MPTP Poisoning / prevention & control
-
Mice
-
Neuroprotective Agents / pharmacology*
-
Neurotoxins / antagonists & inhibitors
-
Neurotoxins / toxicity*
-
Uridine / administration & dosage
-
Uridine / analogs & derivatives*
-
Uridine / pharmacology
Substances
-
Acetates
-
Neuroprotective Agents
-
Neurotoxins
-
3,4-Dihydroxyphenylacetic Acid
-
uridine triacetate
-
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
-
Dopamine
-
Uridine
-
Homovanillic Acid