12663133

Source:http://linkedlifedata.com/resource/pubmed/id/12663133

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0001811, umls-concept:C0006104, umls-concept:C0027882
pubmed:issue	3
pubmed:dateCreated	2003-3-28
pubmed:abstractText	Molecular and cellular markers of age-related alterations in the brain vary significantly between different brain regions and between different types of neurons. In contrast to what had been thought for years, it has recently become clear that only specific types of neurons show an age-related loss of cells. Based on previous work we hypothesize that there is an interrelationship between two important processes in the aging brain: some types of neurons in the aging brain show an accumulation of unrepaired nuclear (n) nDNA damage since no cells are lost during aging. In contrast, other types of neurons show no accumulation of unrepaired nDNA damage since the cells with the greatest decline in nDNA repair capacity and the highest amount of nDNA damage are lost during aging. Most interestingly, the former types of neurons seem to correlate strongly with those types of neurons afflicted in age-related cognitive decline and in the selective neuronal vulnerability in Alzheimer's disease. Therefore, modulation of the nDNA damage response by stimulation of nDNA repair processes, or by elimination of neurons with a high amount of unrepaired nDNA damage in the aging brain, may lead to a functional improvement in networks of these types of neurons and to a better functioning of the aging brain in general. Ultimately, the implication of this strategy may lead to the prevention of AD.
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/0347227
pubmed:citationSubset	IM
pubmed:status	MEDLINE
pubmed:month	Mar
pubmed:issn	0047-6374
pubmed:author	pubmed-author:KorrHubertH, pubmed-author:RuttenBart P FBP, pubmed-author:SchmitzChristophC, pubmed-author:SteinbuschHarry W MHW
pubmed:issnType	Print
pubmed:volume	124
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	349-55
pubmed:dateRevised	2006-11-15
pubmed:meshHeading	pubmed-meshheading:12663133-Alzheimer Disease, pubmed-meshheading:12663133-Animals, pubmed-meshheading:12663133-Brain, pubmed-meshheading:12663133-DNA Damage, pubmed-meshheading:12663133-DNA Repair, pubmed-meshheading:12663133-Humans, pubmed-meshheading:12663133-Neurons
pubmed:year	2003
pubmed:articleTitle	The aging brain: less neurons could be better.
pubmed:affiliation	Department of Psychiatry and Neuropsychology, Division of Neuroscience, University of Maastricht, P.O. Box 616, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands.
pubmed:publicationType	Journal Article, Review, Research Support, Non-U.S. Gov't