Cognition, improvement

Some of the cognitive improvements with tacrine, which is chemically related to amidopyridine, may be due to blockage of K+ channels. 

The evidence cited here is only a very small sample of the vast quantity of research into putative cognitive enhancers. However, many of these compounds that have demonstrated positive effects are believed to influence cerebral metabolism, whether through increased blood flow, glucose metabolism or other indirect routes, as outlined above. Furthermore, these metabolic effects are hypothesised to be at least partly responsible for the cognitive improvements documented. Indeed, many of the putative cognitive enhancers currently available claim modes of influence (Table 14.1) that would fall in line with a metabolic model of cognitive enhancement. 

L-Deprenyl selectively inhibits MAO-B and increases activity in the catecholaminergic system. In an initial placebo-controlled study, no cognitive improvement was found, but studies have shown an improvement in the performance in neuropsychiatric batteries in patients taking deprenyl. More... 

The only clinically available cholinergic therapy to date is an anticholinesterase (tacrine). Studies have shown short-term improvement in some aspects of memory and a delay in decline in some patients. It has been generally assumed that these effects are solely the result of enhancement of muscarinic mechanisms however, this assumption may be unwarranted. Direct muscarinic augmentation produces little measurable cognitive improvement and does not generally reproduce the memory-enhancing effects of anticholinesterases (Bruno et al. 1986 Tariot et al. 1988). 

Carbamazepine small risk of cognitive impairment on chrome doses some reports on cognitive improvement iLoiseau. 2002). 

Veroff AE, Bodick NC, Offen WW, Sramek JJ, Cutler NR. 1998. Efficacy of xanomeline in alzheimer disease Cognitive improvement measured using the computerized neuropsychological test battery (CNTB). Alzheimer Dis Assoc Disord 12 304-312. 

Wagner M, Quednow BB, Westheide J, Schlaepfer TE, Maier W, Kuhn KU. Cognitive improvement in schizophrenic patients does not require a serotonergic mechanism randomized controlled trial of olanzapine vs amisulpride. Neuropsychopharmacology 2005 30 381-90. 

Evans M, Ellis A, Watson D, Chowdhury T. Sustained cognitive improvement following treatment of Alzheimer s disease with donepezil. Int J Geriatr Psychiatry 2000 15(l) 50-3. 

Tang, X. C. Xiong, Z. Q. Qian, B. C. Zhou, Z. R Zhang, C. C. Cognitive improvement by oral huperzine A a novel acetylcholinesterase inhibitor, hr Giacobini, E. Becker, R., editors. Alzheimer Therapy Therapeutic Strategies. Boston, MA Birkhauser, 1994, 113-119. 

In fact, new effects, earlier masked by the simultaneous action of the nonsubtype-specific drug can also be discovered this way and GABA 5 receptor antagonists are now in trials for cognitive improvement. Thus this approach may uncover new targets. 

Cognitive improvement may be linked to substantial (>65%) inhibition of acetylcholinesterase... 

Woodward ND, Jayathilake K, Meltzer HY (2007) COMT vaill08/158met genotype, cognitive function, and cognitive improvement with clozapine in schizophrenia. Schizophr Res 90 86-96... 

The length of hthium treatment, the munber of subjects and the level of GSK-3 inhibition achievable with lithiiun might be borderline to measure a cognitive improvement in these studies. However, these findings indicate that GSK-3 inhibition may slow down the cognitive dechne of Alzheimer s disease patients and warrants further studies using more potent GSK-3 inhibitors. 

Donepezil is approved for treatment of cognitive impairment in mild to moderately severe AD (MMSE score 10 to 26) at doses of 5 mg and 10 mg daily. Preliminary evidence suggests that it may also be beneficial in patients with moderate to severe AD. Cognitive improvement is generally modest with a sustained cognitive benefit of 6 to 9 months, followed by a gradual decline thereafter. ... 

Rivastigmine is efficacious at doses of 6 to 12 mg/day. Cognitive improvement was modest and sustained for 6 to 12 months in the treatment groups. Improvement in activities of daily living have also been demonstrated in this dosing range." Rivastigmine has not been evaluated in patients with severe dementia or for treatment of behavioral symptoms. 

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