TY - JOUR
T1 - Cerebrospinal fluid levels of amyloid β-peptide1-42, but not tau have positive correlation with brain glucose metabolism in humans
AU - Okamura, Nobuyuki
AU - Arai, Hiroyuki
AU - Higuchi, Makoto
AU - Tashiro, Manabu
AU - Matsui, Toshifumi
AU - Itoh, Masatoshi
AU - Iwatsubo, Takeshi
AU - Tomita, Taisuke
AU - Sasaki, Hidetada
PY - 1999/10/8
Y1 - 1999/10/8
N2 - To address the question of whether assay for cerebrospinal fluid (CSF) levels of amyloid β-peptide 1-42 (Aβ1-42) and tau allow us to monitor the neurodegenerative processes that lead to a progressive and massive death of neurons in Alzheimer's disease (AD) and non-AD patients, cerebral glucose metabolism using 2-[18F] fluoro-2-deoxy-glucose was quantified by positron emission tomography in fifteen AD patients and nine non-AD patients with defined levels of CSF-Aβ1-42 and CSF-tau. The CSF-Aβ1-42 levels, but not the CSF-tau levels, in both AD and non-AD patients consistently and significantly correlated with global and, in particular, temporal lobe glucose metabolism. Results from our study suggest that the CSF-Aβ1-42 levels may reflect residual brain function and help monitoring progression of dementing disorders. Copyright (C) 1999 Elsevier Science Ireland Ltd.
AB - To address the question of whether assay for cerebrospinal fluid (CSF) levels of amyloid β-peptide 1-42 (Aβ1-42) and tau allow us to monitor the neurodegenerative processes that lead to a progressive and massive death of neurons in Alzheimer's disease (AD) and non-AD patients, cerebral glucose metabolism using 2-[18F] fluoro-2-deoxy-glucose was quantified by positron emission tomography in fifteen AD patients and nine non-AD patients with defined levels of CSF-Aβ1-42 and CSF-tau. The CSF-Aβ1-42 levels, but not the CSF-tau levels, in both AD and non-AD patients consistently and significantly correlated with global and, in particular, temporal lobe glucose metabolism. Results from our study suggest that the CSF-Aβ1-42 levels may reflect residual brain function and help monitoring progression of dementing disorders. Copyright (C) 1999 Elsevier Science Ireland Ltd.
KW - Alzheimer's disease
KW - Amyloid β-peptide 1-42
KW - Cerebral glucose metabolism
KW - Cerebrospinal fluid
KW - Positron emission tomography
KW - Tau
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U2 - 10.1016/S0304-3940(99)00644-8
DO - 10.1016/S0304-3940(99)00644-8
M3 - Article
C2 - 10515194
AN - SCOPUS:0032860564
SN - 0304-3940
VL - 273
SP - 203
EP - 207
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -