Clinical and metabolic features of diabetic encephalopathy

BACKGROUND: Actual mindset, concerning the pathogenesis of type 2 diabetes mellitus and its complications, is described in the glucocentric, lipocentric and lipokine theories. At the same time, it is known, that acute cerebrovascular disorder in type 2 diabetes mellitus can also develop with normoglycemia. The mechanism of association between obesity and type 2 diabetes mellitus in metabolic syndrome has not yet been studied, and 40% of diabetic patients are not obese. In the physiological state hyperglycemia is prevented by pancreatic regulatory oligopeptides rather than insulin, and protein glycation occurs before the development of diabetes symptoms. That facts indicate the need to continue investigation of the pathogenesis in general and diabetic encephalopathy in particular from the standpoint of metabology in order to substantiate the peptidergic theory of the diabetes mellitus and dyscirculatory encephalopathy pathogenesis.

AIM: To consider little-known clinical, morphological and metabolic manifestations of diabetic encephalopathy from the standpoint of improving the disease diagnosis.

MATHERIALS AND METHODS: Among 162 elderly and senile patients in the pre-stroke and stroke stages of diabetic encephalopathy, modern methods of radiological, laboratory, histological, psychometric and clinical analysis have been used: the relationship between low total cholesterol and disease progression has been determined according to Schulte and MMSE psychometric tests with the same hyperglycemia in different age groups sick; cases of amyloid angioencephalopathy on magnetic resonance imaging in the ultrasensitive weighted imaging mode and amyloidosis have been identified.

Staining post-mortem ultrathin tissue biopsy sections with Congo red allowed to find amyloid deposition in 12% of autopsy cases in the absence of diagnosing amyloidosis during life; preparations, in which Congo red staining was positive for the presence of amyloid, were taken for inspection in polarizing light and typing of amyloid. Staining of histological preparations with hematoxylin-eosin and Van Gieson revealed a morphological characteristic of diabetic encephalopathy different from that of atherogenic and hypertensive dyscirculatory encephalopathy; using immunological studies, a statistically significant increased content of induced interleukin-1β production, a trigger for the serum amyloid analogue in the liver synthesis, was determined, and an experimental method for beta-amyloid peptide adhesion by monocytes and the density of amyloid expression on the surface of monocytes in patients with diabetic encephalopathy at senile age at 2–3 times higher than the density of the peptide in the elderly and in the patients with dyscirculatory encephalopathy of the same old age.

RESULTS: It has been established that a fairly frequent and early manifestation of metabolic disorders in diabetic encephalopathy is a violation of protein metabolism with its final conformation into toxic amyloid tissue components. These observations indicate the multifactorial nature of diabetic encephalopathy. Literature data on the parametabolism of the serotonin mediator and tryptophan in the pathogenesis of diabetic encephalopathy are presented.

CONCLUSIONS: Modern immunological, morphological, and histochemical capabilities make it possible to diagnose the conformation of the protein matrix and develop a protein-centric hypothesis of diabetic encephalopathy.