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Expression of C9orf72-related dipeptides impairs motor function in a vertebrate model

Human molecular genetics, 2018-05, Vol.27 (10), p.1754-1762

2018

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Identification of biological pathways regulated by PGRN and GRN peptide treatments using transcriptome analysis

The European journal of neuroscience, 2016-09, Vol.44 (5), p.2214-2225

2016

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The cellular expression and proteolytic processing of the amyloid precursor protein is independent of TDP-43

Bioscience reports, 2020-04, Vol.40 (4)

2020

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TDP-43 protein in plasma may index TDP-43 brain pathology in Alzheimer’s disease and frontotemporal lobar degeneration

Acta neuropathologica, 2008-08, Vol.116 (2), p.141-146

2008

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Pathogenesis/genetics of frontotemporal dementia and how it relates to ALS

Experimental neurology, 2014-12, Vol.262, p.84-90

2014

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Analysis of the hexanucleotide repeat in C9ORF72 in Alzheimer's disease

Neurobiology of aging, 2012-08, Vol.33 (8), p.1846.e5-1846.e6

2012

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Distinct clinical and pathological characteristics of frontotemporal dementia associated with C9ORF72 mutations

Brain (London, England : 1878), 2012-03, Vol.135 (Pt 3), p.693-708

2012

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Progranulin and frontotemporal lobar degeneration

Acta neuropathologica, 2007-07, Vol.114 (1), p.39-47

Pickering-Brown, Stuart M

2007

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CRISPR/Cas9 does not facilitate stable expression of long C9orf72 dipeptides in mice

Neurobiology of aging, 2019-12, Vol.84, p.235.e1-235.e8

2019

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Modelling C9orf72 dipeptide repeat proteins of a physiologically relevant size

Human molecular genetics, 2016-12, Vol.25 (23), p.5069-5082

2016

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Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

Nature, 2006-08, Vol.442 (7105), p.916-919

2006

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An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies

Acta neuropathologica, 2006-04, Vol.111 (4), p.329-340

2006

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Extracellular Vesicles Isolated from Human Induced Pluripotent Stem Cell-Derived Neurons Contain a Transcriptional Network

Neurochemical research, 2020-07, Vol.45 (7), p.1711-1728

2020

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Ubiquitin associated protein 1 is a risk factor for frontotemporal lobar degeneration

Neurobiology of aging, 2009-04, Vol.30 (4), p.656-665

2009

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Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration

Human molecular genetics, 2006-10, Vol.15 (20), p.2988-3001

2006

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TDP-43 pathological changes in early onset familial and sporadic Alzheimer’s disease, late onset Alzheimer’s disease and Down’s Syndrome: association with age, hippocampal sclerosis and clinical phenotype

Acta neuropathologica, 2011-12, Vol.122 (6), p.703-713

2011

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FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

Acta neuropathologica, 2010-07, Vol.120 (1), p.33-41

2010

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Frequency and clinical characteristics of progranulin mutation carriers in the Manchester frontotemporal lobar degeneration cohort: comparison with patients with MAPT and no known mutations

Brain (London, England : 1878), 2008-03, Vol.131 (3), p.721-731

2008

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The most common type of FTLD-FUS (aFTLD-U) is associated with a distinct clinical form of frontotemporal dementia but is not related to mutations in the FUS gene

Acta neuropathologica, 2011-07, Vol.122 (1), p.99-110

2011

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Plasma levels of progranulin and interleukin-6 in frontotemporal lobar degeneration

Neurobiology of aging, 2015-03, Vol.36 (3), p.1603.e1-1603.e4

2015

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p62/SQSTM1 analysis in frontotemporal lobar degeneration

Neurobiology of aging, 2015-03, Vol.36 (3), p.1603.e5-1603.e9

2015

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A small deletion in C9orf72 hides a proportion of expansion carriers in FTLD

Neurobiology of aging, 2015-03, Vol.36 (3), p.1601.e1-1601.e5

2015

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No association of PGRN 3′UTR rs5848 in frontotemporal lobar degeneration

Neurobiology of aging, 2011-04, Vol.32 (4), p.754-755

2011

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The complex aetiology of frontotemporal lobar degeneration

Experimental neurology, 2007-07, Vol.206 (1), p.1-10

Pickering-Brown, Stuart M.

2007

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Frontotemporal dementia and parkinsonism associated with the IVS1+1G→A mutation in progranulin: a clinicopathologic study

Brain (London, England : 1878), 2006-11, Vol.129 (11), p.3103-3114

2006

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Expression of C9orf72-related dipeptides impairs motor function in a vertebrate model

Identification of biological pathways regulated by PGRN and GRN peptide treatments using transcriptome analysis

The cellular expression and proteolytic processing of the amyloid precursor protein is independent of TDP-43

TDP-43 protein in plasma may index TDP-43 brain pathology in Alzheimer’s disease and frontotemporal lobar degeneration

Pathogenesis/genetics of frontotemporal dementia and how it relates to ALS

Analysis of the hexanucleotide repeat in C9ORF72 in Alzheimer's disease

Distinct clinical and pathological characteristics of frontotemporal dementia associated with C9ORF72 mutations

Progranulin and frontotemporal lobar degeneration

CRISPR/Cas9 does not facilitate stable expression of long C9orf72 dipeptides in mice

Modelling C9orf72 dipeptide repeat proteins of a physiologically relevant size

Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17

An immunohistochemical study of cases of sporadic and inherited frontotemporal lobar degeneration using 3R- and 4R-specific tau monoclonal antibodies

Extracellular Vesicles Isolated from Human Induced Pluripotent Stem Cell-Derived Neurons Contain a Transcriptional Network

Ubiquitin associated protein 1 is a risk factor for frontotemporal lobar degeneration

Mutations in progranulin are a major cause of ubiquitin-positive frontotemporal lobar degeneration

TDP-43 pathological changes in early onset familial and sporadic Alzheimer’s disease, late onset Alzheimer’s disease and Down’s Syndrome: association with age, hippocampal sclerosis and clinical phenotype

FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

Frequency and clinical characteristics of progranulin mutation carriers in the Manchester frontotemporal lobar degeneration cohort: comparison with patients with MAPT and no known mutations

The most common type of FTLD-FUS (aFTLD-U) is associated with a distinct clinical form of frontotemporal dementia but is not related to mutations in the FUS gene

Plasma levels of progranulin and interleukin-6 in frontotemporal lobar degeneration

p62/SQSTM1 analysis in frontotemporal lobar degeneration

A small deletion in C9orf72 hides a proportion of expansion carriers in FTLD

No association of PGRN 3′UTR rs5848 in frontotemporal lobar degeneration

The complex aetiology of frontotemporal lobar degeneration

Frontotemporal dementia and parkinsonism associated with the IVS1+1G→A mutation in progranulin: a clinicopathologic study

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