Abstract
These results suggest that neither the loss of entorhinal efferents nor cholinergic deficit explains all the metabolic features seen in very early AD. Given recent immunohistological evidence of massive glutamatergic synaptic alteration in early AD cortex and insights into neuronal and glial mechanisms of glucose metabolism, very early metabolic changes in AD probably reflect a significant impairment of glycolytic activities in the cortico-cortical glutamatergic systems in a preclinical stage of the disease. However, the exact mechanisms of such impairment in these neurons are yet to be determined.
MeSH terms
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Acetylcholinesterase / metabolism
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology*
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Alzheimer Disease / physiopathology
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Atrophy
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Brain / diagnostic imaging
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Brain / metabolism*
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Brain / pathology*
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Cerebellum / metabolism
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Cerebellum / pathology
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Cerebral Cortex / metabolism
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Cerebral Cortex / pathology
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Energy Metabolism*
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Fluorodeoxyglucose F18 / pharmacokinetics
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Glucose / metabolism
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Humans
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Longitudinal Studies
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Neurofibrillary Tangles / pathology*
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Neuroglia / metabolism
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Neurons / metabolism
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Radiopharmaceuticals / pharmacokinetics
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Retrospective Studies
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Tomography, Emission-Computed
Substances
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Radiopharmaceuticals
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Fluorodeoxyglucose F18
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Acetylcholinesterase
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Glucose