Linked Life Data

17183144

Source:http://linkedlifedata.com/resource/pubmed/id/17183144

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-12-21
pubmed:abstractText
Gain-of-function mutations in the presenilin-1 (PS-1) promote Alzheimer's disease (AD) by increasing reactive oxygen species, at least part of which is derived by an accompanying increase in generation of amyloid-beta (Abeta). Additional studies indicate that impaired Apolipoprotein E function, which also increases oxidative stress and is also associated with AD, potentiates the deleterious activity of PS-1. Folate deficiency is also associated with AD and potentiates the impact of both ApoE deficiency and beta exposure. More recently, folate deficiency has been shown to increase PS-1 expression. Since dietary supplementation with apple juice provides neuroprotection against ApoE deficiency, Abeta exposure and folate deficiency, we examined the impact of apple juice on PS-1 overexpression. Herein, we demonstrate that dietary deficiency in folate and vitamin E increased PS-1 expression in juvenile and adult normal C57B1/6J and ApoE-/- mice and in aged normal mice. Supplementation with apple juice concentrate (AJC) attenuated or prevent these increases. Prior studies demonstrate that impaired DNA methylation resulting from a deficiency in S-adenosylmethionine (SAM, which is rapidly depleted following folate deprivation) leads to PS-1 overexpression, and that direct supplementation with SAM attenuates PS-1 overexpression. We determined that AJC contained levels of SAM comparable to those capable of suppressing PS-1 overexpression, suggesting that the SAM content of AJC represents a potential mechanism for preventing PS-1 overexpression, and further highlighting the possibility that AJC provides neuroprotection by mechanisms in addition to its antioxidant potential.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1387-2877
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
353-8
pubmed:meshHeading
pubmed-meshheading:17183144-Acetylcholine, pubmed-meshheading:17183144-Age Factors, pubmed-meshheading:17183144-Alzheimer Disease, pubmed-meshheading:17183144-Animals, pubmed-meshheading:17183144-Antioxidants, pubmed-meshheading:17183144-Apolipoproteins E, pubmed-meshheading:17183144-Beverages, pubmed-meshheading:17183144-Brain, pubmed-meshheading:17183144-DNA Methylation, pubmed-meshheading:17183144-Disease Models, Animal, pubmed-meshheading:17183144-Folic Acid Deficiency, pubmed-meshheading:17183144-Gene Expression Regulation, pubmed-meshheading:17183144-Humans, pubmed-meshheading:17183144-Malus, pubmed-meshheading:17183144-Mice, pubmed-meshheading:17183144-Mutation, pubmed-meshheading:17183144-Neuroprotective Agents, pubmed-meshheading:17183144-Oxidative Stress, pubmed-meshheading:17183144-Presenilin-1, pubmed-meshheading:17183144-Reactive Oxygen Species, pubmed-meshheading:17183144-S-Adenosylmethionine, pubmed-meshheading:17183144-Vitamin E Deficiency
pubmed:year
2006
pubmed:articleTitle
Supplementation with apple juice attenuates presenilin-1 overexpression during dietary and genetically-induced oxidative stress.
pubmed:affiliation
Department of Biological Sciences, Center for Cellular Neurobiology and Neurodegeneration Research, University of Massachusetts, Lowell, MA 01854, USA.
pubmed:publicationType
Journal Article