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APOE ε4 carriers may undergo synaptic damage conferring risk of Alzheimer's disease
Author(s) -
Sun Xiaoyan,
Dong Chuanhui,
Levin Bonnie,
Crocco Elizabeth,
Loewenstein David,
Zetterberg Henrik,
Blennow Kaj,
Wright Clinton B.
Publication year - 2016
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.05.003
Subject(s) - neurogranin , apolipoprotein e , medicine , biomarker , alzheimer's disease , psychology , disease , pathogenesis , endocrinology , neuroscience , chemistry , biochemistry , signal transduction , protein kinase c
Pathogenesis of Alzheimer's disease (AD) in apolipoprotein E ε4 ( APOE ε4) carriers remains unclear. We hypothesize that APOE isoforms have differential effects on synaptic function. Methods We compared levels of CSF neurogranin (Ng) between APOE ε4 carriers and noncarriers in 399 subjects with normal cognition, mild cognitive impairment (MCI), and AD. We examined associations between Ng levels and age, education, gender, CSF‐Aβ42, and tau protein. Results Neurogranin levels were significantly higher in APOE ε4 carriers compared to APOE ε4 noncarriers with MCI. Levels of Ng between the APOE ε4 carriers and APOE ε4 noncarriers with AD did not differ. Ng levels were correlated with MMSE and levels of tau and Aβ42. Discussion Significantly higher CSF Ng levels in APOE ε4 carriers with MCI may reflect synaptic injury underlying early cognitive impairment. Neurogranin may be an early biomarker of AD and important for disease diagnosis and timing of intervention in APOE ε4 carriers.