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31 results on '"Mcilroy, Stephen"'

2. Sequence variation in the CHAT locus shows no association with late-onset Alzheimer's disease

Author

Harold, Denise, Peirce, Timothy, Moskvina, Valentina, Myers, Amanda, Jones, Susan, Hollingworth, Paul, Moore, Pamela, Lovestone, Simon, Powell, John, Foy, Catherine, Archer, Nicola, Walter, Sarah, Edmonson, Amanda, McIlroy, Stephen, Craig, David, Passmore, Peter A., Goate, Alison, Hardy, John, O'Donovan, Michael, Williams, Julie, Liddell, Malcolm, Owen, Michael J., and Jones, Lesley

Published
2003
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8. Association between polymorphism in regulatory region of gene encoding tumour necrosis factor a and risk of Alzheimer's disease and vascular dementia: a case-control study

Author

McCusker, Shauna M, Curran, Martin D, Dynan, Kevin B, McCullagh, Catriona D, Urquhart, Duncan D, Middleton, Derek, Patterson, Christopher C, McIlroy, Stephen P, and Passmore, A Peter

Subjects
Alzheimer's disease -- Physiological aspects, Amyloid beta-protein -- Physiological aspects, Tumor necrosis factor -- Genetic aspects, Anti-inflammatory drugs -- Health aspects
Published
2001

11. A single nucleotide polymorphism in CHAT influences response to acetylcholinesterase inhibitors in Alzheimer's disease

Author

Harold, Denise, primary, MacGregor, Stuart, additional, Patterson, Cathryn E., additional, Hollingworth, Paul, additional, Moore, Pamela, additional, Owen, Michael J., additional, Williams, Julie, additional, O'Donovan, Michael, additional, Passmore, Peter, additional, McIlroy, Stephen, additional, and Jones, Lesley, additional

Published
2006
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26. Variation in DCP1, encoding ACE, is associated with susceptibility to Alzheimer disease

Author

Kehoe, Patrick G., primary, Russ, Carsten, additional, McIlroy, Stephen, additional, Williams, Hywel, additional, Holmans, Peter, additional, Holmes, Clive, additional, Liolitsa, Danae, additional, Vahidassr, Djamil, additional, Powell, John, additional, McGleenon, Bronagh, additional, Liddell, Malcolm, additional, Plomin, Robert, additional, Dynan, Kevin, additional, Williams, Nigel, additional, Neal, Jim, additional, Cairns, Nigel J., additional, Wilcock, Gordon, additional, Passmore, Peter, additional, Lovestone, Simon, additional, Williams, Julie, additional, and Owen, Michael J., additional

Published
1999
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27. The interleukin 1β gene promoter polymorphism (−511) acts as a risk factor for psychosis in Alzheimer's dementia

Author

Craig, David, Hart, Dominic J., McCool, Keira, McIlroy, Stephen P., and Passmore, A. Peter

Abstract

The explanation for why some patients develop psychotic change in Alzheimer's disease (AD) is unclear. “Psychosis‐modifier genes” may act in the setting of neurodegeneration to produce AD plus psychosis in a similar way to how genetic modulation during neurodevelopment leads to schizophrenia. Because there is increasing interest in the common disruption of cytokine pathways seen in both AD and schizophrenia, we tested the association between the functional interleukin‐1β −511 promoter polymorphism with delusions and hallucinations in AD. Significant associations between psychotic symptoms and the CC genotype (p= 0.001 ‐ p= 0.043) and C allele (p= 0.014 vs p= 0.048) were found, thus confirming the previously noted increased risk in schizophrenia.

Published
2004
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28. A single nucleotide polymorphism in CHATinfluences response to acetylcholinesterase inhibitors in Alzheimer's disease

Author

Harold, Denise, MacGregor, Stuart, Patterson, Cathryn E., Hollingworth, Paul, Moore, Pamela, Owen, Michael J., Williams, Julie, O'Donovan, Michael, Passmore, Peter, McIlroy, Stephen, and Jones, Lesley

Abstract

Alzheimer's disease (AD) is a devastating neurodegeneration with a characteristic deficit in cholinergic neurotransmission. Treatment with acetylcholinesterase (AChE) inhibitors aims to reverse this deficit and does ameliorate the decline in cognition in some AD patients, although response is variable.

Published
2006
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29. Letters.

Author

Truscott, James, Crompton, Jacob, Warner, Lee, Dunn, George, Egersdorff, Jamie, Cook, Will, Johnson, Mike, McIlroy, Stephen, Correia, Lee, Manby, Alex, Stride, Tommy, and Connor, Steven

Abstract

Several letters to the editor are presented in response to articles in previous issues including one about the FA Cup in the 199th edition, one on the interview with Ryan Giggs in the 200th edition, and the "10 Fictional Supporters," also in the 200th edition.

Published
2011

30. Analysis of alteration of p75NTR processing and signalling by PS2 mutation and γ-secretase inhibition

Author

Ito, Yoshio, Ishii, Azusa, Passmore, A. Peter, and McIlroy, Stephen P.

Subjects
*ALZHEIMER'S disease, *GENES, *PRESENILINS, *GENETIC transduction
Abstract

Abstract: The presenilins (PSs) were identified as causative genes in cases of early-onset familial Alzheimer’s disease (AD) and current evidence indicates that PSs are part of the γ-secretase complex responsible for proteolytic processing of type I membrane proteins. p75NTR, a common neurotrophin receptor, was shown to be subject to γ-secretase processing. However, it is not clear if the p75NTR downstream signal is altered in response to γ-secretase cleavage, and further there is a possibility that AD-related PS mutations may affect this cleavage, resulting in pathogenic alterations in signal transduction. In this study, we confirmed that p75NTR downstream signalling is altered by PS2 mutation or γ-secretase inhibition in SHSY-5Y cells. The activity of the small GTPase RhoA is strongly affected by these treatments. This study demonstrates that γ-secretase and PS2 play an important role in regulating neurotrophin signal transduction and either mutation of PS2 or inhibition of γ-secretase disturbs this function. [Copyright &y& Elsevier]

Published
2007
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31. Analysis of alteration of p75NTR processing and signalling by PS2 mutation and gamma-secretase inhibition.

Author

Ito Y, Ishii A, Passmore AP, and McIlroy SP

Subjects
Cell Line, Tumor, Humans, Immunoblotting, Mutation, TNF Receptor-Associated Factor 4 metabolism, rhoA GTP-Binding Protein metabolism, Amyloid Precursor Protein Secretases antagonists & inhibitors, Presenilin-2 genetics, Receptor, Nerve Growth Factor metabolism, Signal Transduction physiology
Abstract

The presenilins (PSs) were identified as causative genes in cases of early-onset familial Alzheimer's disease (AD) and current evidence indicates that PSs are part of the gamma-secretase complex responsible for proteolytic processing of type I membrane proteins. p75NTR, a common neurotrophin receptor, was shown to be subject to gamma-secretase processing. However, it is not clear if the p75NTR downstream signal is altered in response to gamma-secretase cleavage, and further there is a possibility that AD-related PS mutations may affect this cleavage, resulting in pathogenic alterations in signal transduction. In this study, we confirmed that p75NTR downstream signalling is altered by PS2 mutation or gamma-secretase inhibition in SHSY-5Y cells. The activity of the small GTPase RhoA is strongly affected by these treatments. This study demonstrates that gamma-secretase and PS2 play an important role in regulating neurotrophin signal transduction and either mutation of PS2 or inhibition of gamma-secretase disturbs this function.

Published
2007
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