Regular and moderate exercise initiated in middle age prevents age-related amyloidogenesis and preserves synaptic and neuroprotective signalling in mouse brain cortex. (Articolo in rivista)

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Label
  • Regular and moderate exercise initiated in middle age prevents age-related amyloidogenesis and preserves synaptic and neuroprotective signalling in mouse brain cortex. (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.exger.2014.05.006 (literal)
Alternative label
  • Di Loreto S, Falone S, D'Alessandro A, Santini S Jr, Sebastiani P, Cacchio M, Amicarelli F (2014)
    Regular and moderate exercise initiated in middle age prevents age-related amyloidogenesis and preserves synaptic and neuroprotective signalling in mouse brain cortex.
    in Experimental gerontology; Elsevier, New York (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Di Loreto S, Falone S, D'Alessandro A, Santini S Jr, Sebastiani P, Cacchio M, Amicarelli F (literal)
Pagina inizio
  • 57 (literal)
Pagina fine
  • 65 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 57 (literal)
Rivista
Note
  • Scopus (literal)
  • ISI Web of Science (WOS) (literal)
  • Google Scholar (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Istituto Farmacologia Traslazionale UOS L'Aquila Dipart. MESVA Università L'Aquila (literal)
Titolo
  • Regular and moderate exercise initiated in middle age prevents age-related amyloidogenesis and preserves synaptic and neuroprotective signalling in mouse brain cortex. (literal)
Abstract
  • Although the beneficial responses induced in the central nervous system by early-initiated exercise have been broadly investigated, the effects of a chronic and moderate lately-initiated exercise on biochemical hallmarks of very early brain senescence have not been extensively studied. We previously reported that a midlife-initiated regimen of moderate running was able not only to prevent the age-related decay of antioxidative and detoxification functions in mouse brain cortex, but also to preserve neurotrophic support and molecular integrity. On this basis, this work investigated whether and how a 2-mo or 4-mo midlife-initiated running protocol could affect the activity of those systems involved in maintaining neuronal function and in preventing the onset of neurodegeneration within the brain cortex of middle-aged CD-1 mice. In particular, we analyzed the production of the peptide amyloid-? and the expression of synapsin Ia, which is known to play a key role in neurotransmission and synaptic plasticity. In addition, we studied the expression of sirtuin 3, as a protein marker of neuroprotection against age-dependent mitochondrial dysfunction, as well as the pro-death pathway induced by proBDNF through the interaction with p75NTR and the co-receptor sortilin. The midlife-initiated 4-mo running program triggered multiple responses within the mouse brain cortex, through the activation of anti-amyloidogenic, pro-survival, synaptogenic and neuroprotective pathways. However, most of the beneficial actions of the exercise regimen appeared only after 4 months, since 2-mo-exercised mice showed marked impairments of the endpoints we considered. This could imply that a midlife-initiated regimen of moderate treadmill running may require an adequate time lag to activate beneficial compensative mechanisms within the mouse brain cortex. (literal)
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