PMID- 26553058
OWN - NLM
STAT- MEDLINE
DCOM- 20161228
LR  - 20211203
IS  - 1559-1174 (Electronic)
IS  - 1535-1084 (Linking)
VI  - 18
IP  - 1
DP  - 2016 Mar
TI  - Genetic Factors Affecting Late-Onset Alzheimer's Disease Susceptibility.
PG  - 37-49
LID - 10.1007/s12017-015-8376-4 [doi]
AB  - Alzheimer's disease is considered a progressive brain disease in the older 
      population. Late-onset Alzheimer's disease (LOAD) as a multifactorial dementia 
      has a polygenic inheritance. Age, environment, and lifestyle along with a growing 
      number of genetic factors have been reported as risk factors for LOAD. Our aim 
      was to present results of LOAD association studies that have been done in 
      northwestern Iran, and we also explored possible interactions with apolipoprotein 
      E (APOE) status. We re-evaluated the association of these markers in dominant, 
      recessive, and additive models. In all, 160 LOAD and 163 healthy control subjects 
      of Azeri Turkish ethnicity were studied. The Chi-square test with Yates' 
      correction and Fisher's exact test were used for statistical analysis. A 
      Bonferroni-corrected p value, based on the number of statistical tests, was 
      considered significant. Our results confirmed that chemokine receptor type 2 
      (CCR2), estrogen receptor 1 (ESR1), toll-like receptor 2 (TLR2), tumor necrosis 
      factor alpha (TNF alpha), APOE, bridging integrator 1 (BIN1), and 
      phosphatidylinositol-binding clathrin assembly protein (PICALM) are LOAD 
      susceptibility loci in Azeri Turk ancestry populations. Among them, variants of 
      CCR2, ESR1, TNF alpha, and APOE revealed associations in three different genetic 
      models. After adjusting for APOE, the association (both allelic and genotypic) 
      with CCR2, BIN1, and ESRalpha (PvuII) was evident only among subjects without the 
      APOE epsilon4, whereas the association with CCR5, without Bonferroni correction, was 
      significant only among subjects carrying the APOE epsilon4 allele. This result is an 
      evidence of a synergistic and antagonistic effect of APOE on variant associations 
      with LOAD.
FAU - Rezazadeh, Maryam
AU  - Rezazadeh M
AD  - Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical 
      Sciences, Tabriz, Iran.
FAU - Khorrami, Aziz
AU  - Khorrami A
AD  - Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical 
      Sciences, Tabriz, Iran.
FAU - Yeghaneh, Tarlan
AU  - Yeghaneh T
AD  - Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical 
      Sciences, Tabriz, Iran.
FAU - Talebi, Mahnaz
AU  - Talebi M
AD  - Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, 
      Iran.
FAU - Kiani, Seyed Jalal
AU  - Kiani SJ
AD  - Virology Department, School of Public Health, Tehran University of Medical 
      Sciences, Tehran, Iran.
FAU - Heshmati, Yaser
AU  - Heshmati Y
AD  - Department of Medicine, Huddinge, H7, Karolinska Institutet, Stockholm, Sweden.
FAU - Gharesouran, Jalal
AU  - Gharesouran J
AD  - Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical 
      Sciences, Tabriz, Iran. Gharesouranj@tbzmed.ac.ir.
LA  - eng
PT  - Journal Article
DEP - 20151109
PL  - United States
TA  - Neuromolecular Med
JT  - Neuromolecular medicine
JID - 101135365
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (ApoE protein, human)
RN  - 0 (Apolipoprotein E4)
RN  - 0 (Apolipoproteins E)
RN  - 0 (BIN1 protein, human)
RN  - 0 (CCR2 protein, human)
RN  - 0 (ESR1 protein, human)
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (Monomeric Clathrin Assembly Proteins)
RN  - 0 (Nuclear Proteins)
RN  - 0 (PICALM protein, human)
RN  - 0 (Receptors, CCR2)
RN  - 0 (TLR2 protein, human)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Tumor Suppressor Proteins)
RN  - Alzheimer disease type 2
SB  - IM
MH  - Adaptor Proteins, Signal Transducing/genetics
MH  - Aged
MH  - Aged, 80 and over
MH  - Alzheimer Disease/epidemiology/*genetics
MH  - Apolipoprotein E4/genetics
MH  - Apolipoproteins E/genetics
MH  - Estrogen Receptor alpha/genetics
MH  - Ethnicity/genetics
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - Genotype
MH  - Humans
MH  - Iran/epidemiology
MH  - Late Onset Disorders/epidemiology/*genetics
MH  - Male
MH  - Models, Genetic
MH  - Monomeric Clathrin Assembly Proteins/genetics
MH  - Multifactorial Inheritance
MH  - Nuclear Proteins/genetics
MH  - *Polymorphism, Single Nucleotide
MH  - Receptors, CCR2/genetics
MH  - Toll-Like Receptor 2/genetics
MH  - Tumor Necrosis Factor-alpha/genetics
MH  - Tumor Suppressor Proteins/genetics
OTO - NOTNLM
OT  - APOE
OT  - Alzheimer's disease
OT  - Association
OT  - Azeri Turkish
OT  - Neurodegenerative diseases
OT  - Polymorphism
EDAT- 2015/11/11 06:00
MHDA- 2016/12/29 06:00
CRDT- 2015/11/11 06:00
PHST- 2015/04/22 00:00 [received]
PHST- 2015/10/19 00:00 [accepted]
PHST- 2015/11/11 06:00 [entrez]
PHST- 2015/11/11 06:00 [pubmed]
PHST- 2016/12/29 06:00 [medline]
AID - 10.1007/s12017-015-8376-4 [pii]
AID - 10.1007/s12017-015-8376-4 [doi]
PST - ppublish
SO  - Neuromolecular Med. 2016 Mar;18(1):37-49. doi: 10.1007/s12017-015-8376-4. Epub 
      2015 Nov 9.