TY - JOUR
T1 - Flow-metabolism uncoupling in the cervical spinal cord of ALS patients
AU - Yamashita, Toru
AU - Hatakeyama, Tetsuhiro
AU - Sato, Kota
AU - Fukui, Yusuke
AU - Hishikawa, Nozomi
AU - Ohta, Yasuyuki
AU - Nishiyama, Yoshihiro
AU - Kawai, Nobuyuki
AU - Tamiya, Takashi
AU - Abe, Koji
N1 - Funding Information:
This work was partly supported by a Grant-in-Aid for Scientific Research (B) 25293202, (C) 15K09316 and Challenging Research 15K15527 and Young Research 15K21181, and by Grants-in-Aid from the Research Committees (Mizusawa H, Nakashima K, Nishizawa M, Sasaki H, and Aoki M) from the Ministry of Health, Labour and Welfare of Japan.
Publisher Copyright:
© 2017, Springer-Verlag Italia.
PY - 2017/4/1
Y1 - 2017/4/1
N2 - Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease. In ALS, both glucose consumption and neuronal intensity reportedly decrease in the cerebral motor cortex when measured by positron emission tomography (PET). In this study, we evaluated cervical spinal glucose metabolism, blood flow, and neuronal intensity of 10 ALS patients with upper extremity (U/E) atrophy both with 18F-2-fluoro-2-deoxy-d-glucose (18F-FDG) PET and 11C-flumazenil (11C-FMZ) PET. On the ipsilateral side of C5 and T1 levels, 18F-FDG uptake increased significantly (*p < 0.05), and was correlated with the rate of progression of the ALS FRS-R-U/E score (R = 0.645, *p = 0.041). Despite this hyperglucose metabolism, the 11C-FMZ PET study did not show a coupled increase of spinal blood flow even though neuronal intensity did not decrease. These results indicate a strong correlation between hyperglucose metabolism and ALS progression alongside the uncoupling of flow-metabolism. This mechanism, which could result in subsequent motor neuronal death, may be a potential therapeutic target for ALS.
AB - Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease. In ALS, both glucose consumption and neuronal intensity reportedly decrease in the cerebral motor cortex when measured by positron emission tomography (PET). In this study, we evaluated cervical spinal glucose metabolism, blood flow, and neuronal intensity of 10 ALS patients with upper extremity (U/E) atrophy both with 18F-2-fluoro-2-deoxy-d-glucose (18F-FDG) PET and 11C-flumazenil (11C-FMZ) PET. On the ipsilateral side of C5 and T1 levels, 18F-FDG uptake increased significantly (*p < 0.05), and was correlated with the rate of progression of the ALS FRS-R-U/E score (R = 0.645, *p = 0.041). Despite this hyperglucose metabolism, the 11C-FMZ PET study did not show a coupled increase of spinal blood flow even though neuronal intensity did not decrease. These results indicate a strong correlation between hyperglucose metabolism and ALS progression alongside the uncoupling of flow-metabolism. This mechanism, which could result in subsequent motor neuronal death, may be a potential therapeutic target for ALS.
KW - ALS
KW - C-FMZ
KW - F-FDG
KW - Flow-metabolism uncoupling
KW - Glucose metabolism
KW - PET
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U2 - 10.1007/s10072-017-2823-y
DO - 10.1007/s10072-017-2823-y
M3 - Article
C2 - 28120243
AN - SCOPUS:85010735796
SN - 1590-1874
VL - 38
SP - 659
EP - 665
JO - Italian Journal of Neurological Sciences
JF - Italian Journal of Neurological Sciences
IS - 4
ER -
