Metabolism/cognition

In addition to this known aspect of metabolism, there is another one, albeit less frequent, that refers to the interaction of novel compounds. This is important, as it gives die possibility of permanent changes, and is associated with adaptation and evolution. In odier words, one should consider two aspects of metabolism/cognition the normal homeostatic metabolism, which corresponds to die normal life and self-maintenance of the cell from within and a metabolism of novel elements diat may operate changes in die structure. 

Of course, it is apparent that this conclusion is based on a particular dehnition of metabolism/cognition, albeit quite general and simple. However, I believe that this discrimination is useful and in fact it can help to clarify the difference between the feeding bacterium and the feeding vesicle. 

Vigilance for drug-drug interactions is required because of the greater number of medications prescribed to elderly patients and enhanced sensitivity to adverse effects. Pharmacokinetic interactions include metabolic enzyme induction or inhibition and protein binding displacement interactions (e.g., divalproex and warfarin). Pharmacodynamic interactions include additive sedation and cognitive toxicity, which increases risk of falls and other impairments. 

These types of antidepressant were introduced around 10 years after the SSRIs. They include the serotonin noradrenaline reuptake inhibitor venlafaxine and the selective noradrenaline reuptake inhibitor reboxetine. Although there are fewer data about these drugs, clinical experience has shown they are well tolerated and, unlike the SSRIs, they are only weak inhibitors of drug metabolism (Kent, 2000). Depression is a common psychiatric disorder seen in the elderly and often remains untreated or inadequately treated (Forsell and Fastbom, 2000). Venlafaxine was shown to improve the mood in a group of 36 older patients without any effect on cognitive function, an important consideration where there is the possibility of the coexistence of mild or undiagnosed dementia (Tsolaki et al., 2000). 

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. 

Figure 14.2. A metabolic resource model of cognitive enhancement. ANS = autonomic nervous system.

---