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Decreased cerebrospinal fluid NDRG2 is associated with non-Alzheimer's disease derived mild cognitive impairment
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Abstract
En 中文
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<jats:title>Background</jats:title>
<jats:p>Mild cognitive impairment (MCI) lacks clear clinical biomarkers. N-Myc downstream-regulated gene 2 (NDRG2) is predominantly localized in astrocytes and is implicated in cognitive function.</jats:p>
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<jats:title>Objective</jats:title>
<jats:p>This study aims to explore whether cerebrospinal fluid (CSF) NDRG2 could predict MCI and investigate its underlying mechanisms of cognitive decline.</jats:p>
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<jats:title>Methods</jats:title>
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A total of 650 CSF samples were collected from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, comprising 157 normal individuals, 366 MCI patients, and 127 Alzheimer's disease (AD) patients. One-way analysis of covariance (ANCOVA) was employed to assess differences in CSF NDRG2 levels among groups. Linear regression was used to analyze the correlation between NDRG2 and amyloid-β (Aβ), phosphorylated tau (p-tau),
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F-fluorodeoxyglucose positron emission tomography (FDG-PET), albumin quotient (Qalb), and growth-associated protein 43 (GAP43). Receiver operating characteristic (ROC) curves were used to examine the diagnostic performance of NDRG2 for MCI.
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<jats:title>Results</jats:title>
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CSF NDRG2 levels were significantly reduced in MCI, most prominently in non-Aβ and non-tau subgroups. NDRG2 discriminated Aβ-negative MCI with an area under the curve (AUC) of 0.719, but showed limited discriminatory capacity in Aβ+, tau+, and apolipoprotein E ε4 (
<jats:italic toggle="yes">APOE</jats:italic>
ε4) carrier groups. Furthermore, CSF NDRG2 levels were positively correlated with GAP-43, a marker of synaptic plasticity.
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<jats:title>Conclusions</jats:title>
<jats:p>The present study demonstrates that NDRG2 is a potential biomarker for non-AD derived MCI and suggests its involvement in synaptic plasticity impairment.</jats:p>
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Journal
J
IF:
3.1
Papers:
372
Citations:
0

