**8. Conclusion**

These data are very important especially when we consider the increasing prevalence of cognitive disorders. For instance, it is estimated that in 2030 years, the cases of Alzheimer's disease in relation to 2012 will double (35.6 million). No doubts, research in this direction is exceedingly necessary [106]. Previously other authors have also reported that impairment in cerebral glucose metabolism is associated with decline in cognition and memory functions. Schapiro et al (1988) studied the rate of cerebral metabolism for glucose with positron emission tomography and [18F]2-fluoro-2-deoxy-D-glucose in a 47 year-old man with trisomy 21 Down's syndrome and Alzheimer related dementia, and reported poorer general intelligence, visuospatial ability, language, and memory function compared with younger (19-33 years) patients with Down's syndrome [107]. Cerebral metabolism for glucose in the older patient was 28% less than in the younger patients. Besides, hypometabolism was reported in the parietal and temporal lobes of the brain cortices. Importantly, the study of Schapiro et al (1988) was probably one of the most comprehensive investigations to show the association between different diseases involving CNS disorder and their relationship with cerebral glucose metabolism [107]. Approximately a decade after Schapiro et al.'s (1988) work [107], Pietrini et al. (1997) reported another predictor method for Alzheimer's disease risk prior to dementia in patients with Down's syndrome who were above 40 years (mean of 50 years) of age [108]. Pietrini, et al. (1997) confirmed their hypothesis that despite normal cerebral glucose metab‐ olism at rest, an audiovisual stimulation (was used as a stress test) revealed abnormalities in cerebral glucose metabolism before the development of dementia in the parietal and temporal

studied the rate of cerebral metabolism for glucose with positron emission tomography and [18F]2-fluoro-2-deoxy-D-glucose in a 47 year-old man with trisomy 21 Down's syndrome and Alzheimer related dementia, and reported poorer general intelligence, visuospatial ability, language, and memory function compared with younger (19-33 years) patients with Down's syndrome [107]. Cerebral metabolism for glucose in the older patient was 28% less than in the younger patients. Besides, hypometabolism was reported in the parietal and temporal lobes of the brain cortices. Importantly, the study of Schapiro et al (1988) was probably one of the most comprehensive investigations to show the association between different diseases involving CNS disorder and their relationship with cerebral glucose metabolism [107]. Approximately a decade after Schapiro et al.'s (1988) work [107], Pietrini et al. (1997) reported another predictor method for Alzheimer's disease risk prior to dementia in patients with Down's syndrome who were above 40 years (mean of 50 years) of age [108]. Pietrini, et al. (1997) confirmed their hypothesis that despite normal cerebral glucose metabolism at rest, an audiovisual stimulation (was used as a stress test) revealed abnormalities in cerebral glucose metabolism before the development of dementia in the parietal and temporal cortices which represent most vulnerable regions to

cortices which represent most vulnerable regions to Alzheimer's disease [108].

disturbances in glucose metabolism.

disturbances in glucose metabolism.

Neural systems of memory function

Alzheimer's disease [108].

120 Glucose Homeostasis

These CNS pathologies are now believed to be regulated by epigenetic mechanisms [109] and could have pretty good correlations with epigenetic mechanisms of cerebral glucose metabo‐ lism. Other CNS pathologies involving cognitive impairments such as epilepsy [110], schizo‐ phrenia [111, 112], Parkinson's disease [113], multiple sclerosis [114] had been associated with

These CNS pathologies are now believed to be regulated by epigenetic mechanisms [109] and could have pretty good correlations with epigenetic mechanisms of cerebral glucose metabolism. Other CNS pathologies involving cognitive impairments such as epilepsy [110], schizophrenia [111,112], Parkinson's disease [113], multiple sclerosis [114] had been associated with

8

endogenous sources include gluconeogenetic production of glucose molecules, etc.

endogenous sources include gluconeogenetic production of glucose molecules, etc.

**Figure 2.** Interacting system (comprising of memory function, error monitoring and processing system, and modulators) of the reciprocability of neural systems of memory and the error monitoring and processing system. The modulators between the two reciprocals are glucose, other endogenous and exogenous substances/factors. N/B: Glucose can be an endogenous, as well as an exogenous factor; exogenous sources include per os administration of glucose, etc.;

**Figure 2.** Interacting system (comprising of memory function, error monitoring and processing system, and modula‐ tors) of the reciprocability of neural systems of memory and the error monitoring and processing system. The modula‐ tors between the two reciprocals are glucose, other endogenous and exogenous substances/factors. N/B: Glucose can be an endogenous, as well as an exogenous factor; exogenous sources include per os administration of glucose, etc.;

Error monitoring and processing system

Endogenous and exogenous factors (e.g. ethanol)

> Glucose allostasis regulatory systems

Glucose is the foremost energy substrate for neuronal functions (memory). It provides the energy bonds needed for the formation of memory and takes part in information retrieval from neural stores. Both glucose and its metabolites are involved in different stages of memory formation and retrieval. Several factors such as ethanol, some physiological indices, and other competing factors modulate the effect of glucose on memory function.
