Memory cognitive enhancers

Cognitive effects Human nonsmokers Administration of nicotine to tobacco nonusers produces small cognitive enhancements. Studies in tobacco nonusers have primarily measured attention, information processing speed, and memory. Nicotine improves perceptual speed, choice reaction time, and digit recall (Stough et al. 1995 Le Houezec et al. 1994 Foulds et al. 1996). Improvements also occur in digit symbol substitution and continuous performance tests without reducing accuracy (Petrie and Deary 1989 Levin et al. 1998). 

To reveal the cognition-enhancing potential of the S-HTj antagonists, studies in age-related memory impairment have been carried out with psy-chiatrically healthy subjects impaired with scopolamine and patients with dementia. In a randomized double-blind, double-dummy, four-way crossover study in a small number of subjects, each psychiatrically healthy male subject received placebo, scopolamine [0.4 mg im], scopolamine plus alosetron [10 J,g iv], or alosetron [250 Jg] [Preston 1994 Preston et al. 1991). Assessments of verbal and spatial memory, sedation, and sustained attention were performed before and after treatment. The main results from the study were that scopolamine induced robust deficits on all primary variables measured, the reduction in verbal and spatial memories being attenuated by 10- Jg and 250- Jg doses of alosetron, respectively. No effects on the sedation or on changes in attention were noted. 

It improves the functioning of the brain involved in cognitive processes e.g. memory, thought, learning in normal and in subnormal conditions. It is categorized as nootropic agent (cognition enhancers). 

In this chapter, we have looked at two topics in cognitive enhancement attention and memory. We have first reviewed the role of dopamine and norepinephrine/ noradrenaline in the neuropharmacology of attention, and then the syndrome of attention deficit disorder as a common problem associated with a disorder of attention. We then discussed the use of stimulants for improving attention, primarily in attention deficit disorder, and reviewed the pharmacological mechanisms of action of methylphenidate, d and 1 amphetamine, pemoline, and secondary therapies such as clonidine and guanfacine. 

To discuss future cognitive enhancers, including enhancement of attention and memory. 

The role in learning and memory processes of neuronal versus mast cell-derived HA has also been investigated. Histamine, administered icv immediately post-training have been shown to increase memory in a step-down inhibitory avoidance task.3 However, 48/80, a mast cell HA releaser, was ineffective in producing cognition enhancement when administered icv.4 These findings indicate that neuronally derived HA is responsible for the improvements in learning and memory tasks. 

Franowicz JS, Kessler LE, Borja CM, Kobilka BK, Limbird LE, Arnsten AF. Mutation of the a -adrenoceptor impairs working memory performance and annuls cognitive enhancement by guanfacine. J Neurosci 2002 22 8771-8777. 

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