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GWAS Study

Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias.

Beecham GW, Hamilton K, Naj AC et al.

25188341 PubMed ID
GWAS Study Type
4914 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

BG
Beecham GW
HK
Hamilton K
NA
Naj AC
ME
Martin ER
HM
Huentelman M
MA
Myers AJ
CJ
Corneveaux JJ
HJ
Hardy J
VJ
Vonsattel JP
YS
Younkin SG
BD
Bennett DA
DJ
De Jager PL
LE
Larson EB
CP
Crane PK
KM
Kamboh MI
KJ
Kofler JK
MD
Mash DC
DL
Duque L
GJ
Gilbert JR
GH
Gwirtsman H
BJ
Buxbaum JD
KP
Kramer P
DD
Dickson DW
FL
Farrer LA
FM
Frosch MP
GB
Ghetti B
HJ
Haines JL
HB
Hyman BT
KW
Kukull WA
MR
Mayeux RP
PM
Pericak-Vance MA
SJ
Schneider JA
TJ
Trojanowski JQ
RE
Reiman EM
SG
Schellenberg GD
MT
Montine TJ
Chapter II

Abstract

Summary of the research findings

Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. We performed a genome-wide association study and analysis of known genetic risk loci for AD dementia using neuropathologic data from 4,914 brain autopsies. Neuropathologic data were used to define clinico-pathologic AD dementia or controls, assess core neuropathologic features of AD (neuritic plaques, NPs; neurofibrillary tangles, NFTs), and evaluate commonly co-morbid neuropathologic changes: cerebral amyloid angiopathy (CAA), Lewy body disease (LBD), hippocampal sclerosis of the elderly (HS), and vascular brain injury (VBI). Genome-wide significance was observed for clinico-pathologic AD dementia, NPs, NFTs, CAA, and LBD with a number of variants in and around the apolipoprotein E gene (APOE). GalNAc transferase 7 (GALNT7), ATP-Binding Cassette, Sub-Family G (WHITE), Member 1 (ABCG1), and an intergenic region on chromosome 9 were associated with NP score; and Potassium Large Conductance Calcium-Activated Channel, Subfamily M, Beta Member 2 (KCNMB2) was strongly associated with HS. Twelve of the 21 non-APOE genetic risk loci for clinically-defined AD dementia were confirmed in our clinico-pathologic sample: CR1, BIN1, CLU, MS4A6A, PICALM, ABCA7, CD33, PTK2B, SORL1, MEF2C, ZCWPW1, and CASS4 with 9 of these 12 loci showing larger odds ratio in the clinico-pathologic sample. Correlation of effect sizes for risk of AD dementia with effect size for NFTs or NPs showed positive correlation, while those for risk of VBI showed a moderate negative correlation. The other co-morbid neuropathologic features showed only nominal association with the known AD loci. Our results discovered new genetic associations with specific neuropathologic features and aligned known genetic risk for AD dementia with specific neuropathologic changes in the largest brain autopsy study of AD and related dementias.

up to 3,887 cases, up to 1,027 controls

Chapter III

Study Statistics

Key metrics and study information

4914
Total Participants
GWAS
Study Type
No
Replicated
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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