Tags

Type your tag names separated by a space and hit enter

APOE ε4 carriers may undergo synaptic damage conferring risk of Alzheimer's disease.
Alzheimers Dement 2016; 12(11):1159-1166AD

Abstract

INTRODUCTION

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.

Authors+Show Affiliations

Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA; Evelyn F. McKnight Brain Institute, University of Miami Miller School of Medicine, Miami, FL, USA. Electronic address: XXS356@med.miami.edu.Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA; Evelyn F. McKnight Brain Institute, University of Miami Miller School of Medicine, Miami, FL, USA.Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA; Evelyn F. McKnight Brain Institute, University of Miami Miller School of Medicine, Miami, FL, USA.Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL, USA.Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University Gothenburg, Molndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK; Clinical Neurochemistry Laboratory Sahlgrenska University Hospital, Mölndal, Sweden.Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University Gothenburg, Molndal, Sweden; Clinical Neurochemistry Laboratory Sahlgrenska University Hospital, Mölndal, Sweden.Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA; Evelyn F. McKnight Brain Institute, University of Miami Miller School of Medicine, Miami, FL, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

27321472

Citation

Sun, Xiaoyan, et al. "APOE Ε4 Carriers May Undergo Synaptic Damage Conferring Risk of Alzheimer's Disease." Alzheimer's & Dementia : the Journal of the Alzheimer's Association, vol. 12, no. 11, 2016, pp. 1159-1166.
Sun X, Dong C, Levin B, et al. APOE ε4 carriers may undergo synaptic damage conferring risk of Alzheimer's disease. Alzheimers Dement. 2016;12(11):1159-1166.
Sun, X., Dong, C., Levin, B., Crocco, E., Loewenstein, D., Zetterberg, H., ... Wright, C. B. (2016). APOE ε4 carriers may undergo synaptic damage conferring risk of Alzheimer's disease. Alzheimer's & Dementia : the Journal of the Alzheimer's Association, 12(11), pp. 1159-1166. doi:10.1016/j.jalz.2016.05.003.
Sun X, et al. APOE Ε4 Carriers May Undergo Synaptic Damage Conferring Risk of Alzheimer's Disease. Alzheimers Dement. 2016;12(11):1159-1166. PubMed PMID: 27321472.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - APOE ε4 carriers may undergo synaptic damage conferring risk of Alzheimer's disease. AU - Sun,Xiaoyan, AU - Dong,Chuanhui, AU - Levin,Bonnie, AU - Crocco,Elizabeth, AU - Loewenstein,David, AU - Zetterberg,Henrik, AU - Blennow,Kaj, AU - Wright,Clinton B, AU - ,, Y1 - 2016/06/16/ PY - 2015/08/28/received PY - 2016/04/15/revised PY - 2016/05/09/accepted PY - 2016/6/21/pubmed PY - 2017/12/2/medline PY - 2016/6/21/entrez KW - APOE KW - APOE ε4 KW - Alzheimer's disease KW - Mild cognitive impairment KW - Neurogranin KW - Synaptic function SP - 1159 EP - 1166 JF - Alzheimer's & dementia : the journal of the Alzheimer's Association JO - Alzheimers Dement VL - 12 IS - 11 N2 - INTRODUCTION: 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. SN - 1552-5279 UR - https://www.unboundmedicine.com/medline/citation/27321472/APOE_ε4_carriers_may_undergo_synaptic_damage_conferring_risk_of_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1552-5260(16)30278-3 DB - PRIME DP - Unbound Medicine ER -