SA JOURNAL OF DIABETES & VASCULAR DISEASE
REVIEW
VOLUME 11 NUMBER 2 • JUNE 2014
85
and physical exercise, control of hypertension and dyslipidaemia
and treatment of brain infarcts, cardiovascular diseases and
depression.
70,96,97
With hyperglycaemia, it is important to regularly monitor the
blood glucose levels and keep glycaemic control, with the aim
of an HbA
1c
level of 6.5%, but no lower than that, and possibly
higher.
98
Hypoglycaemia should be treated with a defined dose
of carbohydrates rather than a mixed meal. Insulin-sensitising
drugs are able to slow down, prevent, or perhaps even improve
DM-related cognitive decline.
Neuroprotective strategies must be included, aside from the
treatment of DM, from the beginning, to prevent long-term diabetic
complications. These include: free radical scavengers/antioxidants
[as alpha-lipoic acid (ALPA), evening primrose oil (EPO), vitamin C,
vitamin E and vitamin B complex),
68,99
modifiers of mitochondrial
dysfunction, anti-apoptotics, and neurotrophic factors.
76
Future studies must be directed to better understanding of the
patho-physiological mechanisms underlying cognitive dysfunction in
diabetes. There is also a need for construction of longitudinal studies
that prospectively assess the relationship of the disease process to
cognition over time and randomised clinical trials that compare
cognitive function in DM patients receiving memory enhancers and
antidepressants, versus a control group of DM patients.
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