Physiological targets for the treatment of diabetic encephalopathy.
Cent Nerv Syst Agents Med Chem
; 2016 Apr 28.
Article
em En
| MEDLINE
| ID: mdl-27121380
BACKGROUND: Diabetes mellitus is a chronic degenerative disease responsible for hyperglycemic episodes through insulin secretion deficiency or cellular resistance. Clinical diagnosis in diabetic patients established that this disease affects the CNS, damaging the brain and impairing cognition, and thus establishing a clinical diabetic condition named diabetic encephalopathy. Despite the physiological mechanisms responsible for the development diabetic encephalopathy are still unclear, an excessive formation of reactive oxygen species, an alteration of acetylcholinesterase activity, and a reduction of growth factor levels, may be related with the pathogenesis of this condition. Pharmacological treatments with natural compounds have been proven useful to treat and cure a wide variety of diseases through their antioxidant actions. METHODS: This study built a compendium of chemical compounds used for the treatment of diabetic encephalopathy demonstrating the most important physiological targets that future drugs should aim for, reviewing them. RESULTS: As previously suspected, antioxidants and acetylcholinesterase inhibitors were useful to prevent memory loss in streptozotocin-induced animals. In addition, growth factors showed an improvement of memory in diabetic rodents. Most studies focused on antioxidant compounds despite cross studies researched both antioxidants and acetylcholinesterase activities. CONCLUSION: Therefore, it could be suggested that future studies regarding treatments for diabetic encephalopathy should focus on the antioxidant profile and acetylcholinesterase, since they seem to play pivotal roles in cognitive impairment in diabetes. No less important, studies with growth factors are also important physiological targets for treating the diabetic encephalopathy.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Cent Nerv Syst Agents Med Chem
Ano de publicação:
2016
Tipo de documento:
Article