Dementia is a major public health problem. The burden of poor metabolic health is also rising worldwide and is a strong risk factor for dementia. The presence of type 2 diabetes mellitus (DM), in particular, doubles the risk of dementia in older age. Findings from the majority of longitudinal studies suggest that type 2 DM is associated with a greater decline in executive function, processing speed, verbal fluency and memory.
There is great interest in identifying pathways linking DM and cognitive decline. Type 2 DM is associated with lower total brain volume, more infarcts and greater white matter hyperintensity volume. Cross-sectional analyses suggest that lower grey matter (area responsible for muscle control and sensory perceptions) volume may substantially mediate the association between type 2 DM and cognitive function.
But why does this happen?
Although not all the pathological mechanisms involved in the neurological complications of DM are completely elucidated, the secondary neurological manifestations of chronic DM are mainly the result of several serious complications involving medium and large-caliber arteries (macroangiopathies) and in the capillaries of some target organs (microangiopathies).
In addition, metabolic alterations lead to demyelination in Schwann cells, reducing the nerve conduction velocity and hyperactivity of the Insulin Degrading Enzyme, accumulating toxins that can lead to Alzheimer’s Disease.
Physiologically, hyperglycemia can generate a situation of hyperosmolarity, where the patient becomes dehydrated and develops a state of mental confusion, torpor and even coma.
Hypoglycemia is also an important factor to be analysed since the diabetic patient can develop tolerance to low glycemic levels. In this case, hypoglycemia functions in the brain as a hypoxic situation, with initial selective damage to the large pyramidal neurons of the cortex, resulting in cortex necrosis.
Thus, the DM patient has a 5 to 10 times increased risk of arteriosclerosis, compromising the micro and macrocirculation. Vascular lesions are the same as observed in non-diabetic patients, however, in patients with DM, this process is advanced and intensified.
Arteriosclerosis can lead the patient to a stroke with different intensities, from small and multiple lesions to a large lesion, and may even lead to death. It is important to emphasise that vascular diseases are the most frequent causes of deaths involving DM patients. Especially in type II DM, changes occur in elasticity, resistance and vascular impedance, being predictive factors of strokes and cognitive changes.
Several studies show that DM can contribute to the onset of cognitive deficits and the development of Alzheimer’s Disease. In this condition, two pathological changes occur that characterise it: formation of neuritic or senile plaques and neurofibrillary degeneration. Both have a neurotoxic action, impairing the transmission of nerve impulses.
Another important factor for the origin of cognitive deficits and dementia in DM patients is vascular involvement. DM increases the incidence of arteriosclerosis, affecting cerebral irrigation and compromising microcirculation.
Regarding cognition, strokes, demyelination, hippocampal and frontal lobe volumetric reduction and changes in brain metabolism, are factors that affect it, especially in relation to executive and mnesic-attentional dysfunction.
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