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APOE and AßPP gene variation in cortical and cerebrovascular amyloid-ß pathology and Alzheimer's disease: a population-based analysis.

https://arctichealth.org/en/permalink/ahliterature133862
Source
J Alzheimers Dis. 2011;26(2):377-85
Publication Type
Article
Date
2011
Author
Terhi Peuralinna
Maarit Tanskanen
Mira Mäkelä
Tuomo Polvikoski
Anders Paetau
Hannu Kalimo
Raimo Sulkava
John Hardy
Shiao-Lin Lai
Sampath Arepalli
Dena Hernandez
Bryan J Traynor
Andrew Singleton
Pentti J Tienari
Liisa Myllykangas
Author Affiliation
University of Helsinki, Research Program of Molecular Neurology, Biomedicum-Helsinki, Helsinki, Finland.
Source
J Alzheimers Dis. 2011;26(2):377-85
Date
2011
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alleles
Alzheimer Disease - genetics - metabolism - pathology
Amyloid beta-Peptides - genetics - metabolism
Amyloid beta-Protein Precursor - genetics - metabolism
Apolipoproteins E - genetics - metabolism
Cerebral Amyloid Angiopathy - genetics - metabolism - pathology
Cerebral Cortex - metabolism - pathology
Female
Finland
Genetic Association Studies
Genetic Variation
Humans
Male
Middle Aged
Phenotype
Promoter Regions, Genetic
Abstract
Cortical and cerebrovascular amyloid-? (A?) deposition is a hallmark of Alzheimer's disease (AD), but also occurs in elderly people not affected by dementia. The apolipoprotein E (APOE) e4 is a major genetic modulator of A? deposition and AD risk. Variants of the amyloid-? protein precursor (A?PP) gene have been reported to contribute to AD and cerebral amyloid angiopathy (CAA). We analyzed the role of APOE and A?PP variants in cortical and cerebrovascular A? deposition, and neuropathologically verified AD (based on modified NIA-RI criteria) in a population-based autopsy sample of Finns aged = 85 years (Vantaa85 + Study; n = 282). Our updated analysis of APOE showed strong associations of the e4 allele with cortical (p = 4.91 ? 10-17) and cerebrovascular (p = 9.87 ? 10-11) A? deposition as well as with NIA-RI AD (p = 1.62 ? 10-8). We also analyzed 60 single nucleotide polymorphisms (SNPs) at the A?PP locus. In single SNP or haplotype analyses there were no statistically significant A?PP locus associations with cortical or cerebrovascular A? deposition or with NIA-RI AD. We sequenced the promoter of the A?PP gene in 40 subjects with very high A? deposition, but none of these subjects had any of the previously reported or novel AD-associated mutations. These results suggest that cortical and cerebrovascular A? depositions are useful quantitative traits for genetic studies, as highlighted by the strong associations with the APOE e4 variant. Promoter mutations or common allelic variation in the A?PP gene do not have a major contribution to cortical or cerebrovascular A? deposition, or very late-onset AD in this Finnish population based study.
Notes
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PubMed ID
21654062 View in PubMed
Less detail

Chromosome 9 ALS and FTD locus is probably derived from a single founder.

https://arctichealth.org/en/permalink/ahliterature131202
Source
Neurobiol Aging. 2012 Jan;33(1):209.e3-8
Publication Type
Article
Date
Jan-2012
Author
Kin Mok
Bryan J Traynor
Jennifer Schymick
Pentti J Tienari
Hannu Laaksovirta
Terhi Peuralinna
Liisa Myllykangas
Adriano Chiò
Aleksey Shatunov
Bradley F Boeve
Adam L Boxer
Mariely DeJesus-Hernandez
Ian R Mackenzie
Adrian Waite
Nigel Williams
Huw R Morris
Javier Simón-Sánchez
John C van Swieten
Peter Heutink
Gabriella Restagno
Gabriele Mora
Karen E Morrison
Pamela J Shaw
Pamela Sara Rollinson
Ammar Al-Chalabi
Rosa Rademakers
Stuart Pickering-Brown
Richard W Orrell
Michael A Nalls
John Hardy
Author Affiliation
Reta Lila Weston Research Laboratories, Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK.
Source
Neurobiol Aging. 2012 Jan;33(1):209.e3-8
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Amyotrophic Lateral Sclerosis - genetics
Chromosomes, Human, Pair 9 - genetics
Finland
Frontotemporal Dementia - genetics
Genetic Linkage
Genome-Wide Association Study
Haplotypes
Humans
Polymorphism, Single Nucleotide
Abstract
We and others have recently reported an association between amyotrophic lateral sclerosis (ALS) and single nucleotide polymorphisms on chromosome 9p21 in several populations. Here we show that the associated haplotype is the same in all populations and that several families previously shown to have genetic linkage to this region also share this haplotype. The most parsimonious explanation of these data are that there is a single founder for this form of disease.
Notes
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PubMed ID
21925771 View in PubMed
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Familial Lund frontotemporal dementia caused by C9ORF72 hexanucleotide expansion.

https://arctichealth.org/en/permalink/ahliterature125411
Source
Neurobiol Aging. 2012 Aug;33(8):1850.e13-6
Publication Type
Article
Date
Aug-2012
Author
Elisabet Englund
Lars Gustafson
Ulla Passant
Elisa Majounie
Alan E Renton
Bryan J Traynor
Jonathan D Rohrer
Kin Mok
John Hardy
Author Affiliation
Department of Pathology, Lund University, Regional Laboratories Region Skåne, Lund, Sweden.
Source
Neurobiol Aging. 2012 Aug;33(8):1850.e13-6
Date
Aug-2012
Language
English
Publication Type
Article
Keywords
Frontotemporal Lobar Degeneration - epidemiology - genetics
Genetic Markers - genetics
Genetic Predisposition to Disease - epidemiology - genetics
Genetic Variation - genetics
Humans
Pedigree
Polymorphism, Single Nucleotide - genetics
Prevalence
Proteins - genetics
Repetitive Sequences, Nucleic Acid - genetics
Risk factors
Sweden - epidemiology
Abstract
Frontotemporal dementia (FTD) as an important clinical entity was rediscovered in Lund and Manchester in the early 1990s. Here we show that the large Lund pedigree with behavioral variant of frontotemporal dementia previously described with this disorder has an expansion in the recently described C9ORF72 locus on chromosome 9.
PubMed ID
22483864 View in PubMed
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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD.

https://arctichealth.org/en/permalink/ahliterature131029
Source
Neuron. 2011 Oct 20;72(2):257-68
Publication Type
Article
Date
Oct-20-2011
Author
Alan E Renton
Elisa Majounie
Adrian Waite
Javier Simón-Sánchez
Sara Rollinson
J Raphael Gibbs
Jennifer C Schymick
Hannu Laaksovirta
John C van Swieten
Liisa Myllykangas
Hannu Kalimo
Anders Paetau
Yevgeniya Abramzon
Anne M Remes
Alice Kaganovich
Sonja W Scholz
Jamie Duckworth
Jinhui Ding
Daniel W Harmer
Dena G Hernandez
Janel O Johnson
Kin Mok
Mina Ryten
Danyah Trabzuni
Rita J Guerreiro
Richard W Orrell
James Neal
Alex Murray
Justin Pearson
Iris E Jansen
David Sondervan
Harro Seelaar
Derek Blake
Kate Young
Nicola Halliwell
Janis Bennion Callister
Greg Toulson
Anna Richardson
Alex Gerhard
Julie Snowden
David Mann
David Neary
Michael A Nalls
Terhi Peuralinna
Lilja Jansson
Veli-Matti Isoviita
Anna-Lotta Kaivorinne
Maarit Hölttä-Vuori
Elina Ikonen
Raimo Sulkava
Michael Benatar
Joanne Wuu
Adriano Chiò
Gabriella Restagno
Giuseppe Borghero
Mario Sabatelli
David Heckerman
Ekaterina Rogaeva
Lorne Zinman
Jeffrey D Rothstein
Michael Sendtner
Carsten Drepper
Evan E Eichler
Can Alkan
Ziedulla Abdullaev
Svetlana D Pack
Amalia Dutra
Evgenia Pak
John Hardy
Andrew Singleton
Nigel M Williams
Peter Heutink
Stuart Pickering-Brown
Huw R Morris
Pentti J Tienari
Bryan J Traynor
Author Affiliation
Neuromuscular Diseases Research Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
Source
Neuron. 2011 Oct 20;72(2):257-68
Date
Oct-20-2011
Language
English
Publication Type
Article
Keywords
Alleles
Amyotrophic Lateral Sclerosis - genetics
Chromosomes, Human, Pair 9
Female
Finland
Frontotemporal Dementia - genetics
Genetic Predisposition to Disease
Genotype
Haplotypes
Humans
Male
Microsatellite Repeats
Pedigree
Polymorphism, Single Nucleotide
Abstract
The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. We have previously shown that a founder haplotype, covering the MOBKL2b, IFNK, and C9ORF72 genes, is present in the majority of cases linked to this region. Here we show that there is a large hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72 on the affected haplotype. This repeat expansion segregates perfectly with disease in the Finnish population, underlying 46.0% of familial ALS and 21.1% of sporadic ALS in that population. Taken together with the D90A SOD1 mutation, 87% of familial ALS in Finland is now explained by a simple monogenic cause. The repeat expansion is also present in one-third of familial ALS cases of outbred European descent, making it the most common genetic cause of these fatal neurodegenerative diseases identified to date.
Notes
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PubMed ID
21944779 View in PubMed
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Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease.

https://arctichealth.org/en/permalink/ahliterature100428
Source
PLoS Genet. 2010;6(9)
Publication Type
Article
Date
2010
Author
Oyinkan Sofola
Fiona Kerr
Iain Rogers
Richard Killick
Hrvoje Augustin
Carina Gandy
Marcus J Allen
John Hardy
Simon Lovestone
Linda Partridge
Author Affiliation
Department of Genetics, Evolution, and Environment, Institute of Healthy Ageing and Research, University College London, London, United Kingdom.
Source
PLoS Genet. 2010;6(9)
Date
2010
Language
English
Publication Type
Article
Keywords
Aging - drug effects - pathology
Alzheimer Disease - enzymology - mortality - pathology - physiopathology
Amyloid beta-Protein Precursor - metabolism - toxicity
Animals
Disease Models, Animal
Drosophila Proteins - antagonists & inhibitors - metabolism
Drosophila melanogaster - drug effects - enzymology
Genes, Dominant - genetics
Glycogen Synthase Kinase 3 - antagonists & inhibitors - metabolism
Humans
Lithium - pharmacology
Mutant Proteins - toxicity
Nervous System - drug effects - metabolism - pathology
Neurons - drug effects - enzymology - pathology
Peptides - toxicity
Phosphorylation - drug effects
Phosphoserine - metabolism
tau Proteins - metabolism
Abstract
Abeta peptide accumulation is thought to be the primary event in the pathogenesis of Alzheimer's disease (AD), with downstream neurotoxic effects including the hyperphosphorylation of tau protein. Glycogen synthase kinase-3 (GSK-3) is increasingly implicated as playing a pivotal role in this amyloid cascade. We have developed an adult-onset Drosophila model of AD, using an inducible gene expression system to express Arctic mutant Abeta42 specifically in adult neurons, to avoid developmental effects. Abeta42 accumulated with age in these flies and they displayed increased mortality together with progressive neuronal dysfunction, but in the apparent absence of neuronal loss. This fly model can thus be used to examine the role of events during adulthood and early AD aetiology. Expression of Abeta42 in adult neurons increased GSK-3 activity, and inhibition of GSK-3 (either genetically or pharmacologically by lithium treatment) rescued Abeta42 toxicity. Abeta42 pathogenesis was also reduced by removal of endogenous fly tau; but, within the limits of detection of available methods, tau phosphorylation did not appear to be altered in flies expressing Abeta42. The GSK-3-mediated effects on Abeta42 toxicity appear to be at least in part mediated by tau-independent mechanisms, because the protective effect of lithium alone was greater than that of the removal of tau alone. Finally, Abeta42 levels were reduced upon GSK-3 inhibition, pointing to a direct role of GSK-3 in the regulation of Abeta42 peptide level, in the absence of APP processing. Our study points to the need both to identify the mechanisms by which GSK-3 modulates Abeta42 levels in the fly and to determine if similar mechanisms are present in mammals, and it supports the potential therapeutic use of GSK-3 inhibitors in AD.
PubMed ID
20824130 View in PubMed
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Senile systemic amyloidosis affects 25% of the very aged and associates with genetic variation in alpha2-macroglobulin and tau: a population-based autopsy study.

https://arctichealth.org/en/permalink/ahliterature157937
Source
Ann Med. 2008;40(3):232-9
Publication Type
Article
Date
2008
Author
Maarit Tanskanen
Terhi Peuralinna
Tuomo Polvikoski
Irma-Leena Notkola
Raimo Sulkava
John Hardy
Andrew Singleton
Sari Kiuru-Enari
Anders Paetau
Pentti J Tienari
Liisa Myllykangas
Author Affiliation
Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland. maarit.tanskanen@helsinki.fi
Source
Ann Med. 2008;40(3):232-9
Date
2008
Language
English
Publication Type
Article
Keywords
Age Factors
Aged, 80 and over
Amyloidosis - epidemiology - genetics
Autopsy
Congo Red
Exons
Female
Finland - epidemiology
Gene Frequency
Haplotypes
Humans
Immunohistochemistry
Male
Myocardial Infarction - complications
Myocardium - pathology
Polymorphism, Genetic
Prealbumin - metabolism
Prevalence
Risk factors
alpha-Macroglobulins - genetics
tau Proteins - genetics
Abstract
Senile systemic amyloidosis (SSA) is characterized by deposition of wild-type transthyretin (TTR)-based amyloid in parenchymal organs in elderly individuals. Previously, no population-based studies have been performed on SSA.
Here we have studied the prevalence and risk factors for SSA in a Finnish autopsied population aged 85 or over, as part of the population-based Vantaa 85+ Autopsy Study (n = 256). The diagnosis of SSA was based on histological examination of myocardial samples stained with Congo red and anti-TTR immunohistochemistry. The genotype frequencies of 20 polymorphisms in 9 genes in subjects with and without SSA were compared.
The prevalence of SSA was 25%. SSA was associated with age, myocardial infarctions, the G/G (Val/Val) genotype of the exon 24 polymorphism in the alpha2-macroglobulin (alpha2M), and the H2 haplotype of the tau gene (P-values 0.002, 0.004, 0.042, and 0.016).
This population-based study shows that SSA is very common in old individuals, affecting one-quarter of people aged over 85 years. Myocardial infarctions and variation in the genes for alpha2M and tau may be associated with SSA.
PubMed ID
18382889 View in PubMed
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The tau H1 haplotype is associated with Parkinson's disease in the Norwegian population.

https://arctichealth.org/en/permalink/ahliterature190560
Source
Neurosci Lett. 2002 Apr 5;322(2):83-6
Publication Type
Article
Date
Apr-5-2002
Author
Matt Farrer
Lisa Skipper
Marianne Berg
Gina Bisceglio
Melissa Hanson
John Hardy
Amanda Adam
Katrina Gwinn-Hardy
Jan Aasly
Author Affiliation
Laboratory of Familial Movement Disorders, Mayo Clinic, Jacksonville, FL, USA.
Source
Neurosci Lett. 2002 Apr 5;322(2):83-6
Date
Apr-5-2002
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Confidence Intervals
Female
Genotype
Haplotypes - genetics
Humans
Male
Middle Aged
Norway - epidemiology
Odds Ratio
Parkinson Disease - epidemiology - genetics
tau Proteins - genetics
Abstract
We investigated the association of Parkinson's disease (PD) with tau gene H1 haplotypes in the Norwegian population. In a sample of 96 unrelated PD cases and 68 control subjects, we observed an increased risk of PD for persons with the tau H1 haplotype (odds ratio=5.52; 95% confidence interval: 2.64-11.10; P=2.17x10(-6)). Findings provide evidence that tau participates in the PD pathogenic process and demonstrate the value of isolated populations in mapping complex traits.
PubMed ID
11958849 View in PubMed
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7 records – page 1 of 1.