Mouse Gene Set: LEE_CALORIE_RESTRICTION_NEOCORTEX_UP

For the Human gene set with the same name, see LEE_CALORIE_RESTRICTION_NEOCORTEX_UP

Standard name LEE_CALORIE_RESTRICTION_NEOCORTEX_UP
Systematic name MM652
Brief description Up-regulated in the neocortex of aged (30-month) mice subjected to caloric restriction since young adulthood.
Full description or abstract Ageing of the brain leads to impairments in cognitive and motor skills, and is the major risk factor for several common neurological disorders such as Alzheimer disease (AD) and Parkinson disease (PD). Recent studies suggest that normal brain ageing is associated with subtle morphological and functional alterations in specific neuronal circuits, as opposed to large-scale neuronal loss. In fact, ageing of the central nervous system in diverse mammalian species shares many features, such as atrophy of pyramidal neurons, synaptic atrophy, decrease of striatal dopamine receptors, accumulation of fluorescent pigments, cytoskeletal abnormalities, and reactive astrocytes and microglia. To provide the first global analysis of brain ageing at the molecular level, we used oligonucleotide arrays representing 6,347 genes to determine the gene-expression profile of the ageing neocortex and cerebellum in mice. Ageing resulted in a gene-expression profile indicative of an inflammatory response, oxidative stress and reduced neurotrophic support in both brain regions. At the transcriptional level, brain ageing in mice displays parallels with human neurodegenerative disorders. Caloric restriction, which retards the ageing process in mammals, selectively attenuated the age-associated induction of genes encoding inflammatory and stress responses.
Collection M2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 10888876   Authors: Lee CK,Weindruch R,Prolla TA
Exact source Table 3S
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Source species Mus musculus
Contributed by John Newman (University of Washington)
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identifier namespace
MOUSE_SEQ_ACCESSION
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Version history 2022.1.Mm: First Introduced.

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