Open AccessGenetic Interaction of APOE and FGF1 is Associated with Memory Impairment and Hippocampal Atrophy in Alzheimer’s Disease
Author(s) -
YaTing Chang,
Hiroaki Kazui,
Manabu Ikeda,
ChiWei Huang,
Shu-Hua Huang,
ShihWei Hsu,
Wen-Neng Chang,
ChiungChih Chang
Publication year - 2019
Publication title -
aging and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.808
H-Index - 54
ISSN - 2152-5250
DOI - 10.14336/ad.2018.0606
Subject(s) - medicine , disease , atrophy , apolipoprotein e , memory impairment , hippocampal formation , alzheimer's disease , neuroscience , agmatine , bioinformatics , psychiatry , psychology , biology , genetics , cognition , amino acid , arginine
The APOE and fibroblast growth factor 1 ( FGF1 ) have both been associated with amyloid β accumulation and neurodegeneration. Investigation the effect of APOE-FGF1 interactions on episodic memory (EM) deficits and hippocampus atrophy (HA) might elucidate the complex clinical-pathological relationship in Alzheimer's disease (AD). EM performance and hippocampal volume (HV) were characterized in patients with mild AD based on APOE -ε4 carrier status ( APOE -ε4 carriers versus non-carriers) and FGF1 single nucleotide polymorphism ( FGF1- rs34011-GG versus FGF1- rs34011-A-allele carriers). The clinical-pathological relationships within each genotypic group (ε4+/GG-carrier, ε4+/A-allele-carrier, ε4-/GG-carrier and ε4-/A-allele-carrier) were analyzed. There were no significant differences between the FGF1- rs34011-GG and FGF1- rs34011-A-allele carriers for the level of EM performance or HV ( p > 0.05). The bilateral HV was significantly smaller and EM impairment was significantly worse in ε4+/GG-carrier than in ε4-/A-allele-carrier, and an interaction effect of APOE ( APOE -ε4 carriers versus non-carriers) with FGF1 ( FGF1- rs34011-GG versus FGF1- rs34011-A-allele carriers) predicted EM impairment (F4,92= 3.516, p= 0.018) and structural changes in voxel-based morphometry. Our data shows that concurrent consideration of APOE and FGF1 polymorphisms might be required to understand the clinical-pathological relationship in AD.