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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: Myelin in Alzheimer’s disease: culprit or bystander?

Fig. 2

Dysregulation in multiple biochemical pathways underlie the pathogenesis of AD. Metabolomic approaches conducted from the blood or CSF of AD patients compared to controls highlighted abnormalities in the energy metabolism of patients. A diabetic-type pathology is often evoked with a decrease in insulin sensitivity. In addition to disorders in glycolysis and the respiratory chain, abnormalities involving accumulations of ketone bodies resulting from the metabolism of acetyl-CoA residues, a product of the accelerated degradation of fatty acids by β-oxidation, have been described. The bioavailability and metabolism of several amino acids could also be affected, especially concerning tryptophan degraded in the kynurenine cycle and resulting in the formation of neuroprotective (kynurenic acid) or neurotoxic (quinolinic acid) compounds. Abbreviations: AD, Alzheimer’s disease; CSF, cerebrospinal fluid; NADH, nicotinamide-adenine-dinucleotide; ROS, reactive oxygen species; TCA, tricarboxylic acid; βOHD, beta-hydroxybutyrate

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