作者: Marco Racchi , Stefano Govoni , S.Bruno Solerte , Corrado L Galli , Emanuela Corsini
DOI: 10.1016/S0165-0173(01)00132-1
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摘要: A progressive decline of cognitive and memory functions, compared to the average young-life performance, characterizes brain aging. The changes in performance may depend upon altered activity neurotransmitters acting on attention trace formation (acetylcholine, catecholamines, glutamate, for example) or failure transduction mechanisms linked receptor activation. One fundamental cellular associated with aging is alteration involving calcium-phospholipid-dependent protein kinase C (PKC). crucial event activation its translocation from cytosol different intracellular sites recent studies have demonstrated key role played by several anchoring proteins this mechanism. defective PKC-dependent pathways during due a mechanism because reduced levels major RACK-1 (receptor activated kinase). Pharmacological strategies aimed at correction age-associated deficits been mostly focused using direct indirect agonists. More recently, has paid enhancing properties some steroid hormones, namely 'neurosteroids'. Among these activities dehydroepiandrosterone (DHEA), pregnenolone (PREG) their sulfates, extensively studied. These neuroactive steroids, can regulate neuronal function through concurrent influence transmitter-gated ion channels gene expression. We addressed possibility that DHEA, among other neurosteroids, could modulate directly impairment PKC signal provide experimental evidence DHEA revert