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2. TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions.

Author

Gallagher, Michael D, Suh, Eunran, Grossman, Murray, Elman, Lauren, McCluskey, Leo, Van Swieten, John C, Al-Sarraj, Safa, Neumann, Manuela, Gelpi, Ellen, Ghetti, Bernardino, Rohrer, Jonathan D, Halliday, Glenda, Van Broeckhoven, Christine, Seilhean, Danielle, Shaw, Pamela J, Frosch, Matthew P, Alafuzoff, Irina, Antonell, Anna, Bogdanovic, Nenad, Brooks, William, Cairns, Nigel J, Cooper-Knock, Johnathan, Cotman, Carl, Cras, Patrick, Cruts, Marc, De Deyn, Peter P, DeCarli, Charles, Dobson-Stone, Carol, Engelborghs, Sebastiaan, Fox, Nick, Galasko, Douglas, Gearing, Marla, Gijselinck, Ilse, Grafman, Jordan, Hartikainen, Päivi, Hatanpaa, Kimmo J, Highley, J Robin, Hodges, John, Hulette, Christine, Ince, Paul G, Jin, Lee-Way, Kirby, Janine, Kofler, Julia, Kril, Jillian, Kwok, John BJ, Levey, Allan, Lieberman, Andrew, Llado, Albert, Martin, Jean-Jacques, Masliah, Eliezer, McDermott, Christopher J, McKee, Ann, McLean, Catriona, Mead, Simon, Miller, Carol A, Miller, Josh, Munoz, David G, Murrell, Jill, Paulson, Henry, Piguet, Olivier, Rossor, Martin, Sanchez-Valle, Raquel, Sano, Mary, Schneider, Julie, Silbert, Lisa C, Spina, Salvatore, van der Zee, Julie, Van Langenhove, Tim, Warren, Jason, Wharton, Stephen B, White, Charles L, Woltjer, Randall L, Trojanowski, John Q, Lee, Virginia MY, Van Deerlin, Vivianna, and Chen-Plotkin, Alice S

Subjects
Humans, Amyotrophic Lateral Sclerosis, Genetic Predisposition to Disease, Intercellular Signaling Peptides and Proteins, Proteins, Membrane Proteins, Nerve Tissue Proteins, Cohort Studies, Age Factors, Age of Onset, DNA Repeat Expansion, Genotype, Heterozygote, Polymorphism, Single Nucleotide, Alleles, Adult, Aged, Aged, 80 and over, Middle Aged, Female, Male, Frontotemporal Lobar Degeneration, C9orf72 Protein, Progranulins, Rare Diseases, Aging, Neurosciences, Alzheimer's Disease Related Dementias (ADRD), Brain Disorders, Neurodegenerative, Prevention, Genetics, Dementia, Frontotemporal Dementia (FTD), Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Acquired Cognitive Impairment, Aetiology, 2.1 Biological and endogenous factors, Neurological, TMEM106B, C9orf72, Frontotemporal dementia, Frontotemporal lobar degeneration, Amyotrophic lateral sclerosis, Genetic modifier, Clinical Sciences, Neurology & Neurosurgery
Abstract

Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9orf72) have recently been linked to frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis, and may be the most common genetic cause of both neurodegenerative diseases. Genetic variants at TMEM106B influence risk for the most common neuropathological subtype of FTLD, characterized by inclusions of TAR DNA-binding protein of 43 kDa (FTLD-TDP). Previous reports have shown that TMEM106B is a genetic modifier of FTLD-TDP caused by progranulin (GRN) mutations, with the major (risk) allele of rs1990622 associating with earlier age at onset of disease. Here, we report that rs1990622 genotype affects age at death in a single-site discovery cohort of FTLD patients with C9orf72 expansions (n = 14), with the major allele correlated with later age at death (p = 0.024). We replicate this modifier effect in a 30-site international neuropathological cohort of FTLD-TDP patients with C9orf72 expansions (n = 75), again finding that the major allele associates with later age at death (p = 0.016), as well as later age at onset (p = 0.019). In contrast, TMEM106B genotype does not affect age at onset or death in 241 FTLD-TDP cases negative for GRN mutations or C9orf72 expansions. Thus, TMEM106B is a genetic modifier of FTLD with C9orf72 expansions. Intriguingly, the genotype that confers increased risk for developing FTLD-TDP (major, or T, allele of rs1990622) is associated with later age at onset and death in C9orf72 expansion carriers, providing an example of sign epistasis in human neurodegenerative disease.

Published
2014

4. Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions

Author

Van Deerlin, Vivianna M, Sleiman, Patrick MA, Martinez-Lage, Maria, Chen-Plotkin, Alice, Wang, Li-San, Graff-Radford, Neill R, Dickson, Dennis W, Rademakers, Rosa, Boeve, Bradley F, Grossman, Murray, Arnold, Steven E, Mann, David MA, Pickering-Brown, Stuart M, Seelaar, Harro, Heutink, Peter, van Swieten, John C, Murrell, Jill R, Ghetti, Bernardino, Spina, Salvatore, Grafman, Jordan, Hodges, John, Spillantini, Maria Grazia, Gilman, Sid, Lieberman, Andrew P, Kaye, Jeffrey A, Woltjer, Randall L, Bigio, Eileen H, Mesulam, Marsel, al-Sarraj, Safa, Troakes, Claire, Rosenberg, Roger N, White, Charles L, Ferrer, Isidro, Lladó, Albert, Neumann, Manuela, Kretzschmar, Hans A, Hulette, Christine Marie, Welsh-Bohmer, Kathleen A, Miller, Bruce L, Alzualde, Ainhoa, de Munain, Adolfo Lopez, McKee, Ann C, Gearing, Marla, Levey, Allan I, Lah, James J, Hardy, John, Rohrer, Jonathan D, Lashley, Tammaryn, Mackenzie, Ian RA, Feldman, Howard H, Hamilton, Ronald L, Dekosky, Steven T, van der Zee, Julie, Kumar-Singh, Samir, Van Broeckhoven, Christine, Mayeux, Richard, Vonsattel, Jean Paul G, Troncoso, Juan C, Kril, Jillian J, Kwok, John BJ, Halliday, Glenda M, Bird, Thomas D, Ince, Paul G, Shaw, Pamela J, Cairns, Nigel J, Morris, John C, McLean, Catriona Ann, DeCarli, Charles, Ellis, William G, Freeman, Stefanie H, Frosch, Matthew P, Growdon, John H, Perl, Daniel P, Sano, Mary, Bennett, David A, Schneider, Julie A, Beach, Thomas G, Reiman, Eric M, Woodruff, Bryan K, Cummings, Jeffrey, Vinters, Harry V, Miller, Carol A, Chui, Helena C, Alafuzoff, Irina, Hartikainen, Päivi, Seilhean, Danielle, Galasko, Douglas, Masliah, Eliezer, Cotman, Carl W, Tuñón, M Teresa, Martínez, M Cristina Caballero, Munoz, David G, Carroll, Steven L, Marson, Daniel, Riederer, Peter F, Bogdanovic, Nenad, Schellenberg, Gerard D, Hakonarson, Hakon, Trojanowski, John Q, and Lee, Virginia M-Y

Subjects
Biological Sciences, Genetics, Frontotemporal Dementia (FTD), Neurodegenerative, Dementia, Rare Diseases, Brain Disorders, Neurosciences, Acquired Cognitive Impairment, Aetiology, 2.1 Biological and endogenous factors, Case-Control Studies, Chromosomes, Human, Pair 7, DNA-Binding Proteins, Frontotemporal Lobar Degeneration, Gene Frequency, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Inclusion Bodies, Intercellular Signaling Peptides and Proteins, Linkage Disequilibrium, Membrane Proteins, Polymorphism, Single Nucleotide, Progranulins, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP). FTLD-TDP is frequently familial, resulting from mutations in GRN (which encodes progranulin). We assembled an international collaboration to identify susceptibility loci for FTLD-TDP through a genome-wide association study of 515 individuals with FTLD-TDP. We found that FTLD-TDP associates with multiple SNPs mapping to a single linkage disequilibrium block on 7p21 that contains TMEM106B. Three SNPs retained genome-wide significance following Bonferroni correction (top SNP rs1990622, P = 1.08 x 10(-11); odds ratio, minor allele (C) 0.61, 95% CI 0.53-0.71). The association replicated in 89 FTLD-TDP cases (rs1990622; P = 2 x 10(-4)). TMEM106B variants may confer risk of FTLD-TDP by increasing TMEM106B expression. TMEM106B variants also contribute to genetic risk for FTLD-TDP in individuals with mutations in GRN. Our data implicate variants in TMEM106B as a strong risk factor for FTLD-TDP, suggesting an underlying pathogenic mechanism.

Published
2010

6. Assessment of Alzheimer-related pathologies of dementia using machine learning feature selection

Author

Rajab, Mohammed D, Jammeh, Emmanuel, Taketa, Teruka, Brayne, Carol, Matthews, Fiona E, Su, Li, Ince, Paul G, Wharton, Stephen B, Wang, Dennis, Cognitive Function and Ageing Neuropathology Study Group, and Apollo - University of Cambridge Repository

Subjects
Machine Learning, Cerebral Amyloid Angiopathy, Amyloid beta-Peptides, Alzheimer Disease, Feature selection, Humans, Brain, Dementia, Neurofibrillary Tangles, Beta-amyloid, Alzheimer’s, Neuropathology
Abstract

Although a variety of brain lesions may contribute to the pathological assessment of dementia, the relationship of these lesions to dementia, how they interact and how to quantify them remains uncertain. Systematically assessing neuropathological measures by their degree of association with dementia may lead to better diagnostic systems and treatment targets. This study aims to apply machine learning approaches to feature selection in order to identify critical features of Alzheimer-related pathologies associated with dementia. We applied machine learning techniques for feature ranking and classification to objectively compare neuropathological features and their relationship to dementia status during life using a cohort (n=186) from the Cognitive Function and Ageing Study (CFAS). We first tested Alzheimer's Disease and tau markers and then other neuropathologies associated with dementia. Seven feature ranking methods using different information criteria consistently ranked 22 out of the 34 neuropathology features for importance to dementia classification. Although highly correlated, Braak neurofibrillary tangle stage, beta-amyloid and cerebral amyloid angiopathy features were ranked the highest. The best-performing dementia classifier using the top eight neuropathological features achieved 79% sensitivity, 69% specificity and 75% precision. However, when assessing all seven classifiers and the 22 ranked features, a substantial proportion (40.4%) of dementia cases was consistently misclassified. These results highlight the benefits of using machine learning to identify critical indices of plaque, tangle and cerebral amyloid angiopathy burdens that may be useful for classifying dementia.

Published
2023
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7. Insights into the pathological basis of dementia from population‐based neuropathology studies.

Author

Wharton, Stephen B., Simpson, Julie E., Ince, Paul G., Richardson, Connor D., Merrick, Richard, Matthews, Fiona E., and Brayne, Carol

Subjects
ALZHEIMER'S disease, NEUROLOGICAL disorders, DEMENTIA, LEWY body dementia, NEUROFIBRILLARY tangles
Abstract

The epidemiological neuropathology perspective of population and community‐based studies allows unbiased assessment of the prevalence of various pathologies and their relationships to late‐life dementia. In addition, this approach provides complementary insights to conventional case–control studies, which tend to be more representative of a younger clinical cohort. The Cognitive Function and Ageing Study (CFAS) is a longitudinal study of cognitive impairment and frailty in the general United Kingdom population. In this review, we provide an overview of the major findings from CFAS, alongside other studies, which have demonstrated a high prevalence of pathology in the ageing brain, particularly Alzheimer's disease neuropathological change and vascular pathology. Increasing burdens of these pathologies are the major correlates of dementia, especially neurofibrillary tangles, but there is substantial overlap in pathology between those with and without dementia, particularly at intermediate burdens of pathology and also at the oldest ages. Furthermore, additional pathologies such as limbic‐predominant age‐related TDP‐43 encephalopathy, ageing‐related tau astrogliopathy and primary age‐related tauopathies contribute to late‐life dementia. Findings from ageing population‐representative studies have implications for the understanding of dementia pathology in the community. The high prevalence of pathology and variable relationship to dementia status has implications for disease definition and indicate a role for modulating factors on cognitive outcome. The complexity of late‐life dementia, with mixed pathologies, indicates a need for a better understanding of these processes across the life‐course to direct the best research for reducing risk in later life of avoidable clinical dementia syndromes. [ABSTRACT FROM AUTHOR]

Published
2023
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10. Education, the Brain and Dementia: Neuroprotection or Compensation?

Author

Brayne, Carol, Ince, Paul G., and Keage, Hannah A. D.

Abstract

The potential protective role of education for dementia is an area of major interest. Almost all older people have some pathology in their brain at death but have not necessarily died with dementia. We have explored these two observations in large population-based cohort studies (Epidemiological Clinicopathological Studies in Europe; EClipSE) in an investigation of the relationships of brain pathology at death, clinical dementia and time in education, testing the hypothesis that greater exposure to education reduces the risk of dementia. EClipSE has harmonized longitudinal clinical data and neuropathology from three longstanding population-based studies that included post-mortem brain donation. These three studies started between 1985 and 1991. Number of years of education during earlier life was recorded at baseline. Incident dementia was detected through follow-up interviews, complemented by retrospective informant interviews, death certificate data and linked health/social records (dependent on study) after death. Dementia-related neuropathologies were assessed in each study in a comparable manner based on the Consortium to Establish a Registry for Alzheimer's Disease protocol. Eight hundred and seventy-two brain donors were included, of whom 56% were demented at death. Longer years in education were associated with decreased dementia risk and greater brain weight but had no relationship to neurodegenerative or vascular pathologies. The associations between neuropathological variables and clinical dementia differed according to the "dose" of education such that more education reduced dementia risk largely independently of severity of pathology. More education did not protect individuals from developing neurodegenerative and vascular neuropathology by the time they died but it did appear to mitigate the impact of pathology on the clinical expression of dementia before death. The findings suggest that an understanding of the mechanisms leading to functional protection in the presence of pathology may be of considerable value to society.

Published
2010
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11. Controversies and priorities in amyotrophic lateral sclerosis

Author

Turner, Martin R, Hardiman, Orla, Benatar, Michael, Brooks, Benjamin R, Chio, Adriano, de Carvalho, Mamede, Ince, Paul G, Lin, Cindy, Miller, Robert G, Mitsumoto, Hiroshi, Nicholson, Garth, Ravits, John, Shaw, Pamela J, Swash, Michael, Talbot, Kevin, Traynor, Bryan J, Van den Berg, Leonard H, Veldink, Jan H, Vucic, Steve, and Kiernan, Matthew C

Published
2013
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14. Neuropathological assessments of the pathology in frontotemporal lobar degeneration with TDP43-positive inclusions: an inter-laboratory study by the BrainNet Europe consortium

Author

Alafuzoff, Irina, Pikkarainen, Maria, Neumann, Manuela, Arzberger, Thomas, Al-Sarraj, Safa, Bodi, Istvan, Bogdanovic, Nenad, Bugiani, Orso, Ferrer, Isidro, Gelpi, Ellen, Gentleman, Stephen, Giaccone, Giorgio, Graeber, Manuel B., Hortobagyi, Tibor, Ince, Paul G., Ironside, James W., Kavantzas, Nikolaos, King, Andrew, Korkolopoulou, Penelope, Kovács, Gábor G., Meyronet, David, Monoranu, Camelia, Nilsson, Tatjana, Parchi, Piero, Patsouris, Efstratios, Revesz, Tamas, Roggendorf, Wolfgang, Rozemuller, Annemieke, Seilhean, Danielle, Streichenberger, Nathalie, Thal, Dietmar R., Wharton, Stephen B., and Kretzschmar, Hans

Published
2015
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16. Dementia in the older population is associated with neocortex content of serum amyloid P component

Author

Ellmerich, Stephan, Taylor, Graham W, Richardson, Connor D, Minett, Thais, Schmidt, Amand Floriaan, Brayne, Carol, Matthews, Fiona E, Ince, Paul G, Wharton, Stephen B, Pepys, Mark B, Cognitive Function And Ageing Study, Brayne, Carol [0000-0001-5307-663X], Matthews, Fiona E [0000-0002-1728-2388], Pepys, Mark B [0000-0003-2614-3248], and Apollo - University of Cambridge Repository

Subjects
serum amyloid P component, mental disorders, neocortex, dementia
Abstract

Despite many reported associations, the direct cause of neurodegeneration responsible for cognitive loss in Alzheimer's disease and some other common dementias is not known. The normal human plasma protein, serum amyloid P component, a constituent of all human fibrillar amyloid deposits and present on most neurofibrillary tangles, is cytotoxic for cerebral neurones in vitro and in experimental animals in vivo. The neocortical content of serum amyloid P component was immunoassayed in 157 subjects aged 65 or more with known dementia status at death, in the large scale, population-representative, brain donor cohort of the Cognitive Function and Ageing Study, which avoids the biases inherent in studies of predefined clinico-pathological groups. The serum amyloid P component values were significantly higher in individuals with dementia, independent of serum albumin content measured as a control for plasma in the cortex samples. The odds ratio for dementia at death in the high serum amyloid P component tertile was 5.24 (95% confidence interval 1.79-15.29) and was independent of Braak tangle stages and Thal amyloid-β phases of neuropathological severity. The strong and specific association of higher brain content of serum amyloid P component with dementia, independent of neuropathology, is consistent with a pathogenetic role in dementia.

Published
2021
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21. Heterogeneity of cellular inflammatory responses in ageing white matter and relationship to Alzheimer’s and small vessel disease pathologies

Author

Waller, Rachel, Narramore, Ruth, Simpson, Julie E, Heath, Paul R, Verma, Nikita, Tinsley, Megan, Barnes, Jordan R, Haris, Hanna T, Henderson, Frances E, Matthews, Fiona E, Richardson, Connor D, Brayne, Carol, Ince, Paul G, Kalaria, Raj N, Wharton, Stephen B, CFAS, Waller, Rachel [0000-0001-5815-8829], Matthews, Fiona E. [0000-0002-1728-2388], Kalaria, Raj N. [0000-0001-7907-4923], and Apollo - University of Cambridge Repository

Subjects
Male, Aging, small vessel disease, white matter lesions, Brain, Middle Aged, White Matter, RESEARCH ARTICLES, neuroinflammation, RESEARCH ARTICLE, Alzheimer Disease, Astrocytes, Cerebral Small Vessel Diseases, Neuroinflammatory Diseases, Humans, Microglia, Neuroglia, epidemiological neuropathology, Aged, dementia
Abstract

White matter lesions (WML) are common in the ageing brain, often arising in a field effect of diffuse white matter abnormality. Although WML are associated with cerebral small vessel disease (SVD) and Alzheimer’s disease (AD), their cause and pathogenesis remain unclear. The current study tested the hypothesis that different patterns of neuroinflammation are associated with SVD compared to AD neuropathology by assessing the immunoreactive profile of the microglial (CD68, IBA1 and MHC‐II) and astrocyte (GFAP) markers in ageing parietal white matter (PARWM) obtained from the Cognitive Function and Ageing Study (CFAS), an ageing population‐representative neuropathology cohort. Glial responses varied extensively across the PARWM with microglial markers significantly higher in the subventricular region compared to either the middle‐zone (CD68 p = 0.028, IBA1 p < 0.001, MHC‐II p < 0.001) or subcortical region (CD68 p = 0.002, IBA1 p < 0.001, MHC‐II p < 0.001). Clasmatodendritic (CD) GFAP+ astrocytes significantly increased from the subcortical to the subventricular region (p < 0.001), whilst GFAP+ stellate astrocytes significantly decreased (p < 0.001). Cellular reactions could be grouped into two distinct patterns: an immune response associated with MHC‐II/IBA1 expression and CD astrocytes; and a more innate response characterised by CD68 expression associated with WML. White matter neuroinflammation showed weak relationships to the measures of SVD, but not to the measures of AD neuropathology. In conclusion, glial responses vary extensively across the PARWM with diverse patterns of white matter neuroinflammation. Although these findings support a role for vascular factors in the pathogenesis of age‐related white matter neuroinflammation, additional factors other than SVD and AD pathology may drive this. Understanding the heterogeneity in white matter neuroinflammation will be important for the therapeutic targeting of age‐associated white matter damage.

Published
2021
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25. Type 2 diabetes mellitus-associated transcriptome alterations in cortical neurones and associated neurovascular unit cells in the ageing brain

Author

Bury, Joanna J, Chambers, Annabelle, Heath, Paul R, Ince, Paul G, Shaw, Pamela J, Matthews, Fiona E, Brayne, Carol, Simpson, Julie E, Wharton, Stephen B, Cognitive Function And Ageing Study, Wharton, Stephen B [0000-0003-2785-333X], Apollo - University of Cambridge Repository, and Wharton, Stephen B. [0000-0003-2785-333X]

Subjects
Male, Candidate gene, Aging, medicine.medical_treatment, Laser Capture Microdissection, Biology, lcsh:RC346-429, Pathology and Forensic Medicine, Respiratory electron transport chain, Transcriptome, Cellular and Molecular Neuroscience, Cortical neurone, Differential expression, Type 2 diabetes mellitus, medicine, Humans, RNA, Messenger, lcsh:Neurology. Diseases of the nervous system, Aged, Temporal cortex, Aged, 80 and over, Neurons, Microarray analysis techniques, Research, Insulin, Brain, Endothelial Cells, Temporal Lobe, Cell biology, Ageing, medicine.anatomical_structure, Diabetes Mellitus, Type 2, Astrocytes, Neurovascular unit, Dementia, Female, Neurology (clinical), Astrocyte
Abstract

Type 2 diabetes mellitus (T2D), characterised by peripheral insulin resistance, is a risk factor for dementia. In addition to its contribution to small and large vessel disease, T2D may directly damage cells of the brain neurovascular unit. In this study, we investigated the transcriptomic changes in cortical neurones, and associated astrocytes and endothelial cells of the neurovascular unit, in the ageing brain. Neurone, astrocyte, and endothelial cell-enriched mRNA, obtained by immuno-laser capture microdissection of temporal cortex (Brodmann area 21/22) from 6 cases with self-reported T2D in the Cognitive Function and Ageing Study neuropathology cohort, and an equal number of age and sex-matched controls, was assessed by microarray analysis. Integrated Molecular Pathway Level Analysis was performed using the Kyoto Encyclopaedia of Genes and Genomes database on significantly differentially expressed genes, defined as P

Published
2021
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26. Additional file 1 of Type 2 diabetes mellitus-associated transcriptome alterations in cortical neurones and associated neurovascular unit cells in the ageing brain

Author

Bury, Joanna J., Chambers, Annabelle, Heath, Paul R., Ince, Paul G., Shaw, Pamela J., Matthews, Fiona E., Brayne, Carol, Simpson, Julie E., and Wharton, Stephen B.

Abstract

Additional file 1 Fig. S1 Diabetes and Dementia Network. WGCNA of IMPaLA-generated lists of DEGs enriched in insulin signalling, AGE-RAGE signalling in diabetic complications, and Alzheimer disease pathways in the KEGG database. Hub genes included in the NanoString panel are highlighted in yellow. Targets which were validated by immunohistochemistry are indicated by the asterisks. Two gene products are linked in red, if they participated in the same reaction within a pathway. The strengths of relationships are represented by the intensity of the colour and the thickness of the interconnecting lines. Created using the GeneMANIA plugin for Cytoscape version 3.7.2

Published
2021
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27. Additional file 3 of Type 2 diabetes mellitus-associated transcriptome alterations in cortical neurones and associated neurovascular unit cells in the ageing brain

Author

Bury, Joanna J., Chambers, Annabelle, Heath, Paul R., Ince, Paul G., Shaw, Pamela J., Matthews, Fiona E., Brayne, Carol, Simpson, Julie E., and Wharton, Stephen B.

Abstract

Additional file 3 Fig. S3 (A) DNA Damage Response and (B) Autophagy Networks. WGCNA of IMPaLA-generated lists of DEGs enriched in (A) cell cycle, cellular senescence, p53 signalling, apoptosis, and necroptosis and (B) autophagy pathways in the KEGG database. Hub genes included in the NanoString panel are highlighted in yellow. Targets which were validated by immunohistochemistry are indicated by the asterisks. Two gene products are linked in red, if they participated in the same reaction within a pathway. The strengths of relationships are represented by the intensity of the colour and the thickness of the interconnecting lines. Created using the GeneMANIA plugin for Cytoscape version 3.7.2

Published
2021
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28. Additional file 2 of Type 2 diabetes mellitus-associated transcriptome alterations in cortical neurones and associated neurovascular unit cells in the ageing brain

Author

Bury, Joanna J., Chambers, Annabelle, Heath, Paul R., Ince, Paul G., Shaw, Pamela J., Matthews, Fiona E., Brayne, Carol, Simpson, Julie E., and Wharton, Stephen B.

Abstract

Additional file 2 Fig. S2 Diabetic Complications Network. WGCNA of IMPaLA-generated lists of DEGs enriched in AGE-RAGE signalling in diabetic complications, chemokine signalling, HIF-1 signalling, fluid shear stress and atherosclerosis, and NAFLD pathways in the KEGG database. Hub genes included in the NanoString panel are highlighted in yellow. Targets which were validated by immunohistochemistry are indicated by the asterisks. Two gene products are linked in red, if they participated in the same reaction within a pathway. The strengths of relationships are represented by the intensity of the colour and the thickness of the interconnecting lines. Created using the GeneMANIA plugin for Cytoscape version 3.7.2

Published
2021
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29. DNA damage response and senescence in endothelial cells of human cerebral cortex and relation to Alzheimerʼs neuropathology progression: a population-based study in the Medical Research Council Cognitive Function and Ageing Study (MRC-CFAS) cohort

Author

Garwood, Claire J., Simpson, Julie E., Al Mashhadi, Sufana, Axe, Claire, Wilson, Suzanna, Heath, Pamela R., Shaw, Pamela J., Matthews, Fiona E., Brayne, Carol, Ince, Paul G., and Wharton, Stephen B.

Published
2014
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30. Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones

Author

Highley, Robin J., Kirby, Janine, Jansweijer, Joeri A., Webb, Philip S., Hewamadduma, Channa A., Heath, Paul R., Higginbottom, Adrian, Raman, Rohini, Ferraiuolo, Laura, Cooper-Knock, Johnathan, McDermott, Christopher J., Wharton, Stephen B., Shaw, Pamela J., and Ince, Paul G.

Published
2014
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38. Nomenclature and nosology for neuropathologic subtypes of frontotemporal lobar degeneration: an update

Author

Mackenzie, Ian R. A., Neumann, Manuela, Bigio, Eileen H., Cairns, Nigel J., Alafuzoff, Irina, Kril, Jillian, Kovacs, Gabor G., Ghetti, Bernardino, Halliday, Glenda, Holm, Ida E., Ince, Paul G., Kamphorst, Wouter, Revesz, Tamas, Rozemuller, Annemieke J. M., Kumar-Singh, Samir, Akiyama, Haruhiko, Baborie, Atik, Spina, Salvatore, Dickson, Dennis W., Trojanowski, John Q., and Mann, David M. A.

Published
2010
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40. Staging/typing of Lewy body related α-synuclein pathology: a study of the BrainNet Europe Consortium

Author

Alafuzoff, Irina, Ince, Paul G., Arzberger, Thomas, Al-Sarraj, Safa, Bell, Jeanne, Bodi, Istvan, Bogdanovic, Nenad, Bugiani, Orso, Ferrer, Isidro, Gelpi, Ellen, Gentleman, Stephen, Giaccone, Giorgio, Ironside, James W., Kavantzas, Nikolaos, King, Andrew, Korkolopoulou, Penelope, Kovács, Gábor G., Meyronet, David, Monoranu, Camelia, Parchi, Piero, Parkkinen, Laura, Patsouris, Efstratios, Roggendorf, Wolfgang, Rozemuller, Annemieke, Stadelmann-Nessler, Christine, Streichenberger, Nathalie, Thal, Dietmar R., and Kretzschmar, Hans

Published
2009
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41. Nomenclature for neuropathologic subtypes of frontotemporal lobar degeneration: consensus recommendations

Author

Mackenzie, Ian R. A., Neumann, Manuela, Bigio, Eileen H., Cairns, Nigel J., Alafuzoff, Irina, Kril, Jillian, Kovacs, Gabor G., Ghetti, Bernardino, Halliday, Glenda, Holm, Ida E., Ince, Paul G., Kamphorst, Wouter, Revesz, Tamas, Rozemuller, Annemieke J. M., Kumar-Singh, Samir, Akiyama, Haruhiko, Baborie, Atik, Spina, Salvatore, Dickson, Dennis W., Trojanowski, John Q., and Mann, David M. A.

Published
2009
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42. Age, neuropathology, and dementia

Author

Savva, George M., Wharton, Stephen B., Path, F.R.C., Ince, Paul G., Forster, Gillian, Matthews, Fiona E., and Brayne, Carol

Subjects
Alzheimer's disease -- Research, Alzheimer's disease -- Psychological aspects, Dementia -- Causes of, Logistic regression -- Usage
Abstract

A study was conducted to ascertain the relations between age, neurological problems and dementia. Results revealed that the relation between pathological signs of AlzheimerEs disease and dementia is more likely in younger old persons than in older old persons and age should be one of the factors during assessment of cases.

Published
2009

43. Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration

Author

Cairns, Nigel J., Bigio, Eileen H., Mackenzie, Ian R. A., Neumann, Manuela, Lee, Virginia M.-Y., Hatanpaa, Kimmo J., White, III, Charles L., Schneider, Julie A., Grinberg, Lea Tenenholz, Halliday, Glenda, Duyckaerts, Charles, Lowe, James S., Holm, Ida E., Tolnay, Markus, Okamoto, Koichi, Yokoo, Hideaki, Murayama, Shigeo, Woulfe, John, Munoz, David G., Dickson, Dennis W., Ince, Paul G., Trojanowski, John Q., and Mann, David M. A.

Published
2007
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45. Dementia with Lewy bodies: a comparison of clinical diagnosis, FP-CIT single photon emission computed tomography imaging and autopsy

Author

Walker, Zuzana, Jaros, Evelyn, Walker, Rodney W.H., Lee, Lean, Costa, Durval C., Livingston, Gill, Ince, Paul G., Perry, Robert, McKeith, Ian, and Katona, Cornelius L.E.

Subjects
SPECT imaging -- Methods, SPECT imaging -- Comparative analysis, Lewy body disease -- Diagnosis, Dementia -- Diagnosis, Autopsy -- Comparative analysis, Health, Psychology and mental health
Published
2007

49. Clinico-pathological features in amyotrophic lateral sclerosis with expansions in C9ORF72

Author

Cooper-Knock, Johnathan, Hewitt, Christopher, Highley, J. Robin, Brockington, Alice, Milano, Antonio, Man, Somai, Martindale, Joanne, Hartley, Judith, Walsh, Theresa, Gelsthorpe, Catherine, Baxter, Lynne, Forster, Gillian, Fox, Melanie, Bury, Joanna, Mok, Kin, McDermott, Christopher J., Traynor, Bryan J., Kirby, Janine, Wharton, Stephen B., Ince, Paul G., Hardy, John, and Shaw, Pamela J.

Published
2012
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