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Brain Glucose Transporters: Role in Pathogenesis and Potential Targets for the Treatment of Alzheimer's Disease

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MDPI
DOI: 10.3390/ijms22158142

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Alzheimer's disease; glucose transporters; hypometabolism; therapy of Alzheimer's disease

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Alzheimer's disease is the most common cause of dementia in elderly people, with aging being a main risk factor. Impairment of brain energy and glucose hypometabolism are hallmarks of the disease. There are several hypotheses on the role of glucose hypometabolism in AD, but further investigations are needed on this subject.
The most common cause of dementia, especially in elderly people, is Alzheimer's disease (AD), with aging as its main risk factor. AD is a multifactorial neurodegenerative disease. There are several factors increasing the risk of AD development. One of the main features of Alzheimer's disease is impairment of brain energy. Hypometabolism caused by decreased glucose uptake is observed in specific areas of the AD-affected brain. Therefore, glucose hypometabolism and energy deficit are hallmarks of AD. There are several hypotheses that explain the role of glucose hypometabolism in AD, but data available on this subject are poor. Reduced transport of glucose into neurons may be related to decreased expression of glucose transporters in neurons and glia. On the other hand, glucose transporters may play a role as potential targets for the treatment of AD. Compounds such as antidiabetic drugs, agonists of SGLT1, insulin, siRNA and liposomes are suggested as therapeutics. Nevertheless, the suggested targets of therapy need further investigations.

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