JH Growdon

Massachusetts General Hospital

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i-10 index

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Co-Authors

Lindsay A. Farrer

Boston University

L. Adrienne Cupples

Boston University

Christine Van Broeckhoven

VIB-UAntwerp Center for Molecular Neurology

TD Bird

University of Washington

Ignacio Mateo

Universidad de Cantabria

Nicholas Bass

University College London

Antony Bayer

University of Pennsylvania

Iwona Kłoszewska

Medical University of Lodz

Kevin Morgan

University of Nottingham

Qiong Yang

Boston University

Cooperative Institutions

Boston University

149

Erasmus MC

102

Framingham Heart Study

Institute for Neurodegenerative Disorders

The University of Texas Health Science Center at San Antonio

Alzheimer’s Disease Neuroimaging Initiative

University College London

Inserm

Molecular Biology Consortium

University of Washington

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Automatically segmenting midbrain structures using new multispectral MRI tools: Method and application to Parkinson's disease

NeuroImage (2009)

DA Ziegler JS Wonderlick AJ Murphy Bruce Fischl JH Growdon

10.1016/s1053-8119(09)71064-x

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Citations (0)

Meta-analysis of genetic association with diagnosed Alzheimer’s disease identifies novel risk loci and implicates Abeta, Tau, immunity and lipid processing

bioRxiv (Cold Spring Harbor Laboratory) (2018)

B K Kunkle Benjamin Grenier‐Boley Rebecca Sims JC Bis A.C. Naj

Introduction Late-onset Alzheimer’s disease (LOAD, onset age > 60 years) is the most prevalent dementia in the elderly 1 , and risk is partially driven by genetics 2 . Many of the loci responsible for this genetic risk were identified by genome-wide association studies (GWAS) 3–8 . To identify additional LOAD risk loci, the we performed the largest GWAS to date (89,769 individuals), analyzing both common and rare variants. We confirm 20 previous LOAD risk loci and identify four new genome-wide loci ( IQCK , ACE , ADAM10 , and ADAMTS1 ). Pathway analysis of these data implicates the immune system and lipid metabolism, and for the first time tau binding proteins and APP metabolism. These findings show that genetic variants affecting APP and Aβ processing are not only associated with early-onset autosomal dominant AD but also with LOAD. Analysis of AD risk genes and pathways show enrichment for rare variants ( P = 1.32 × 10 −7 ) indicating that additional rare variants remain to be identified.

Genome-wide Association Study

Genetic Association

10.1101/294629

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Citations (39)

Paralysis and movement disorders

JH Growdon

Movement Disorders

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Citations (16)

Transmission and age-at-onset patterns in familial Alzheimer??s disease: evidence for heterogeneity

Alzheimer Disease & Associated Disorders (1991)

Lindsay A. Farrer R E Myers L. Adrienne Cupples Ph St George-Hyslop TD Bird

Farrer, LA; Myers, RH; Cupples, LA; St. George-Hyslop, PH; Bird, TD; Rossor, MN; Mullan, MJ; Polinsky, R; Nee, L; Heston, L; Van Broeckhoven, C; Martin, JJ; Crapper-McLachlan, D; Growdon, JH

10.1097/00002093-199100510-00015

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Citations (4)

Herbicide exposure modifies GSTP1 haplotype association to Parkinson onset age

Neurology (2006)

J. B. Wilk J. E. Tobin Oksana Suchowersky H. A. Shill Christine Klein

Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides.Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses.Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group.Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.

GSTP1

10.1212/01.wnl.0000249149.22407.d1

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Citations (42)