Brain glucose metabolism: Role of Wnt signaling in the metabolic impairment in Alzheimer’s disease
•The energy metabolism of glucose is critical for neuronal functions.•The deregulation of brain glucose metabolism has been related with several brain disorders.•The Wnt signaling could represent a new therapeutic tool against Alzheimeŕs disease. The brain is an organ that has a high demand for gluc...
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Published in | Neuroscience and biobehavioral reviews Vol. 80; pp. 316 - 328 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Ltd
01.09.2017
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Subjects | |
Online Access | Get full text |
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Summary: | •The energy metabolism of glucose is critical for neuronal functions.•The deregulation of brain glucose metabolism has been related with several brain disorders.•The Wnt signaling could represent a new therapeutic tool against Alzheimeŕs disease.
The brain is an organ that has a high demand for glucose. In the brain, glucose is predominantly used in energy production, with almost 70% of the energy used by neurons. The importance of the energy requirement in neurons is clearly demonstrated by the fact that all neurodegenerative disorders exhibit a critical metabolic impairment that includes decreased glucose uptake/utilization and decreased mitochondrial activity, with a consequent diminution in ATP production. In fact, in Alzheimer’s disease, the measurement of the general metabolic rate of the brain has been reported to be an accurate tool for diagnosis. Additionally, the administration of metabolic activators such as insulin/glucagon-like peptide 1 can improve memory/learning performance. Despite the importance of energy metabolism in the brain, little is known about the cellular pathways involved in the regulation of this process. Several reports postulate a role for Wnt signaling as a general metabolic regulator. Thus, in the present review, we discuss the antecedents that support the relationship between Wnt signaling and energy metabolism in the Alzheimer’s disease. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0149-7634 1873-7528 |
DOI: | 10.1016/j.neubiorev.2017.06.004 |