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KMID : 0381120170390030295
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Genes and Genomics
2017 Volume.39 No. 3 p.295 ~ p.300
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Metabolomics and mitochondrial dysfunction in Alzheimer’s disease
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Kim Dong-Hee
Gim Jeong-An
Yoon Da-Hye
Kim Suhk-Mann
Kim Heui-Soo
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Abstract
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Alzheimer’s disease (AD) is characterized by cognitive impairment, progressive neurodegeneration, and Aβ accumulation. Aβ oligomers can lead to synaptic damage via alterations in glutamate receptors and excitotoxicity, as well as mitochondrial dysfunction. AD is associated with various biological indicators, including (1) predisposing factors such as genetic risk factors, (2) laboratory markers such as Aβ and tau protein, and (3) diagnostic markers such as MRI and PET findings. However, these markers are not confirmed, invasive, or expensive. In the present study, we employed nuclear magnetic resonance (NMR) methods that are inexpensive, time-efficient, and can be performed using samples obtained from various easily accessible sources such as cerebrospinal fluid, plasma, and peripheral tissue, thus highlighting the clinical utility of this approach. NMR analyses of blood metabolites showed that glutamine, glutamate, leucine, oxaloacetate, aspartate, isoleucine, and 3-hydroxyisovalerate are increased in patients with AD compared with control individuals. These metabolites seem to be related to mitochondrial dysfunction. Our data indicated that 3-hydroxyisovalerate, which is linked to known pathologic processes associated with mitochondrial dysfunction and accelerated neurodegeneration, was increased in the blood samples of patients with AD.
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KEYWORD
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Alzheimer’s disease, Biomarker, 3-Hydroxyisovalerate, Metabolite, Neurodegeneration, Nuclear magnetic resonance
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