Linked Life Data

20600435

Source:http://linkedlifedata.com/resource/pubmed/id/20600435

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-9-6
pubmed:abstractText
Oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD) causing neurodegeneration and decreased monoamine neurotransmitters. We investigated the effect of administration of a pro-oxidant diet on the levels of monoamines and metabolites in the brains of wildtype and transgenic mice expressing mutant APP and PS-1 (TASTPM mice). Three-month-old TASTPM and wildtype (C57BL6/J) mice were fed either normal or pro-oxidant diet for 3 months. The neocortex, cerebellum, hippocampus and striatum were assayed for their monoamine and monoamine metabolite content using HPLC with electrochemical detection. Striatal tyrosine hydroxylase (TOH) levels were analysed by Western blotting. In the striatum, female TASTPM mice had higher levels of DOPAC and male TASTPM mice had higher levels of 5-HIAA compared to wildtype mice. Administration of pro-oxidant diet increased striatal MHPG, turnover of NA and 5-HT levels in female TASTPM mice compared to TASTPM mice fed control diet. The pro-oxidant diet also decreased DOPAC levels in female TASTPM mice compared to those fed control diet. Striatal TOH did not depend on diet, gender or genotype. In the neocortex, the TASTPM genotype increased levels of 5-HIAA in male mice fed control diet compared to wildtype mice. In the cerebellum, the TASTPM genotype led to decreased levels of HVA (male mice only) and also decreased turnover of DA (female mice only) compared to wildtype mice. These data suggest a sparing of monoaminergic neurones in the cortex, striatum and hippocampus of TASTPM mice fed pro-oxidant diet and could be indicative of increased activity in corticostriatal circuits. The decreased cerebellar levels of HVA and turnover of DA in TASTPM mice hint at possible axonal degeneration within this subregion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1872-9754
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
504-11
pubmed:meshHeading
pubmed-meshheading:20600435-Alzheimer Disease, pubmed-meshheading:20600435-Amyloid beta-Protein Precursor, pubmed-meshheading:20600435-Animals, pubmed-meshheading:20600435-Biogenic Monoamines, pubmed-meshheading:20600435-Blotting, Western, pubmed-meshheading:20600435-Brain Chemistry, pubmed-meshheading:20600435-Chromatography, High Pressure Liquid, pubmed-meshheading:20600435-Diet, pubmed-meshheading:20600435-Female, pubmed-meshheading:20600435-Humans, pubmed-meshheading:20600435-Male, pubmed-meshheading:20600435-Mice, pubmed-meshheading:20600435-Mice, Inbred C57BL, pubmed-meshheading:20600435-Mice, Transgenic, pubmed-meshheading:20600435-Neurotransmitter Agents, pubmed-meshheading:20600435-Oxidants, pubmed-meshheading:20600435-Oxidative Stress, pubmed-meshheading:20600435-Presenilins, pubmed-meshheading:20600435-Reference Standards, pubmed-meshheading:20600435-Transgenes, pubmed-meshheading:20600435-Tyrosine 3-Monooxygenase
pubmed:year
2010
pubmed:articleTitle
Neurochemical changes in a double transgenic mouse model of Alzheimer's disease fed a pro-oxidant diet.
pubmed:affiliation
Pharmidex Pharmaceutical Services Ltd., London, UK. E.Ash@Pharmidex.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't