[Nicotinic Receptor, XXXX and @entity195 ].

@entity1 @entity73 @entity16 @entity2445 @entity11545 @entity11544 @entity195 @entity8124 @entity934
Population aging has increased and will drastically increase the prevalence of @entity195 . The disease develops inexorably towards a syndrome of marked @entity73 , accompanied of emotional alterations and profound changes of personality. The @entity1 loses its autonomy, and requires special attention of caregivers; this leads to a decrease of the quality of life, not only of the @entity1 but also of its caregivers and family. The reduction of the number of functional nicotinic receptors in brain keeps pace with @entity16 and the severity of the disease (cholinergic theory of @entity195 ). There is a pleyade of data and observations reinforcing the idea that improving cholinergic neurotransmission is an investment in memory. Up to now, although with limited success, this improvement has been achieved only with the reversible inhibitors of acetylcholinesterase @entity2445 , @entity11544 and @entity8124 , available in the clinic since a few years. The last approved has been @entity11545 that in spite of being a modest inhibitor of acetylcholinesterase, improves memory (ADAS cog test) and @entity73 of @entity195 @entity1 . To explain this therapeutic effect, a second mechanism of action for @entity11545 has been suggested, the positive allosteric modulation of presynaptic nicotinic receptors, that will favour the release of @entity934 and other neurotransmitters involved in memory formation. Furthermore, @entity11545 possesses neuroprotectant antiapoptotic effects, according to recent data from our laboratory. These effects provide new ideas and therapeutic targets that might help to find novel and efficacious treatments for @entity1 suffering @entity195 .
