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2. Multisite Assessment of Aging-Related Tau Astrogliopathy (ARTAG).

Author

Kovacs, Gabor G, Xie, Sharon X, Lee, Edward B, Robinson, John L, Caswell, Carrie, Irwin, David J, Toledo, Jon B, Johnson, Victoria E, Smith, Douglas H, Alafuzoff, Irina, Attems, Johannes, Bencze, Janos, Bieniek, Kevin F, Bigio, Eileen H, Bodi, Istvan, Budka, Herbert, Dickson, Dennis W, Dugger, Brittany N, Duyckaerts, Charles, Ferrer, Isidro, Forrest, Shelley L, Gelpi, Ellen, Gentleman, Stephen M, Giaccone, Giorgio, Grinberg, Lea T, Halliday, Glenda M, Hatanpaa, Kimmo J, Hof, Patrick R, Hofer, Monika, Hortobágyi, Tibor, Ironside, James W, King, Andrew, Kofler, Julia, Kövari, Enikö, Kril, Jillian J, Love, Seth, Mackenzie, Ian R, Mao, Qinwen, Matej, Radoslav, McLean, Catriona, Munoz, David G, Murray, Melissa E, Neltner, Janna, Nelson, Peter T, Ritchie, Diane, Rodriguez, Roberta D, Rohan, Zdenek, Rozemuller, Annemieke, Sakai, Kenji, Schultz, Christian, Seilhean, Danielle, Smith, Vanessa, Tacik, Pawel, Takahashi, Hitoshi, Takao, Masaki, Rudolf Thal, Dietmar, Weis, Serge, Wharton, Stephen B, White, Charles L, Woulfe, John M, Yamada, Masahito, and Trojanowski, John Q

Subjects
Dementia, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Frontotemporal Dementia (FTD), Aging, Neurodegenerative, Acquired Cognitive Impairment, Brain Disorders, Alzheimer's Disease, Aged, Aged, 80 and over, Astrocytes, Female, Humans, Male, Middle Aged, Severity of Illness Index, Tauopathies, tau Proteins, ARTAG, Digital pathology, Interrater agreement, Neuropathology, Tau, Tau-astrogliopathy, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

Aging-related tau astrogliopathy (ARTAG) is a recently introduced terminology. To facilitate the consistent identification of ARTAG and to distinguish it from astroglial tau pathologies observed in the primary frontotemporal lobar degeneration tauopathies we evaluated how consistently neuropathologists recognize (1) different astroglial tau immunoreactivities, including those of ARTAG and those associated with primary tauopathies (Study 1); (2) ARTAG types (Study 2A); and (3) ARTAG severity (Study 2B). Microphotographs and scanned sections immunostained for phosphorylated tau (AT8) were made available for download and preview. Percentage of agreement and kappa values with 95% confidence interval (CI) were calculated for each evaluation. The overall agreement for Study 1 was >60% with a kappa value of 0.55 (95% CI 0.433-0.645). Moderate agreement (>90%, kappa 0.48, 95% CI 0.457-0.900) was reached in Study 2A for the identification of ARTAG pathology for each ARTAG subtype (kappa 0.37-0.72), whereas fair agreement (kappa 0.40, 95% CI 0.341-0.445) was reached for the evaluation of ARTAG severity. The overall assessment of ARTAG showed moderate agreement (kappa 0.60, 95% CI 0.534-0.653) among raters. Our study supports the application of the current harmonized evaluation strategy for ARTAG with a slight modification of the evaluation of its severity.

Published
2017

3. Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy

Author

Kovacs, Gabor G, Ferrer, Isidro, Grinberg, Lea T, Alafuzoff, Irina, Attems, Johannes, Budka, Herbert, Cairns, Nigel J, Crary, John F, Duyckaerts, Charles, Ghetti, Bernardino, Halliday, Glenda M, Ironside, James W, Love, Seth, Mackenzie, Ian R, Munoz, David G, Murray, Melissa E, Nelson, Peter T, Takahashi, Hitoshi, Trojanowski, John Q, Ansorge, Olaf, Arzberger, Thomas, Baborie, Atik, Beach, Thomas G, Bieniek, Kevin F, Bigio, Eileen H, Bodi, Istvan, Dugger, Brittany N, Feany, Mel, Gelpi, Ellen, Gentleman, Stephen M, Giaccone, Giorgio, Hatanpaa, Kimmo J, Heale, Richard, Hof, Patrick R, Hofer, Monika, Hortobágyi, Tibor, Jellinger, Kurt, Jicha, Gregory A, Ince, Paul, Kofler, Julia, Kövari, Enikö, Kril, Jillian J, Mann, David M, Matej, Radoslav, McKee, Ann C, McLean, Catriona, Milenkovic, Ivan, Montine, Thomas J, Murayama, Shigeo, Lee, Edward B, Rahimi, Jasmin, Rodriguez, Roberta D, Rozemüller, Annemieke, Schneider, Julie A, Schultz, Christian, Seeley, William, Seilhean, Danielle, Smith, Colin, Tagliavini, Fabrizio, Takao, Masaki, Thal, Dietmar Rudolf, Toledo, Jon B, Tolnay, Markus, Troncoso, Juan C, Vinters, Harry V, Weis, Serge, Wharton, Stephen B, White, Charles L, Wisniewski, Thomas, Woulfe, John M, Yamada, Masahito, and Dickson, Dennis W

Subjects
Biomedical and Clinical Sciences, Neurosciences, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Rare Diseases, Alzheimer's Disease, Aging, Frontotemporal Dementia (FTD), Brain Disorders, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Neurological, Animals, Astrocytes, Brain, Humans, Neuroglia, Tauopathies, tau Proteins, ARTAG, Tau astrogliopathy, Tau, Clinical Sciences, Neurology & Neurosurgery
Abstract

Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of astroglial tau pathology in the aged brain, facilitating communication among neuropathologists and researchers, and informing interpretation of clinical biomarkers and imaging studies that focus on tau-related indicators.

Published
2016

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

Author

Urwin, Hazel, Josephs, Keith A, Rohrer, Jonathan D, Mackenzie, Ian R, Neumann, Manuela, Authier, Astrid, Seelaar, Harro, Van Swieten, John C, Brown, Jeremy M, Johannsen, Peter, Nielsen, Jorgen E, Holm, Ida E, FReJA Consortium, Dickson, Dennis W, Rademakers, Rosa, Graff-Radford, Neill R, Parisi, Joseph E, Petersen, Ronald C, Hatanpaa, Kimmo J, White, Charles L, Weiner, Myron F, Geser, Felix, Van Deerlin, Vivianna M, Trojanowski, John Q, Miller, Bruce L, Seeley, William W, van der Zee, Julie, Kumar-Singh, Samir, Engelborghs, Sebastiaan, De Deyn, Peter P, Van Broeckhoven, Christine, Bigio, Eileen H, Deng, Han-Xiang, Halliday, Glenda M, Kril, Jillian J, Munoz, David G, Mann, David M, Pickering-Brown, Stuart M, Doodeman, Valerie, Adamson, Gary, Ghazi-Noori, Shabnam, Fisher, Elizabeth MC, Holton, Janice L, Revesz, Tamas, Rossor, Martin N, Collinge, John, Mead, Simon, and Isaacs, Adrian M

Subjects
FReJA Consortium, Hippocampus, Frontal Lobe, Humans, Dyskinesias, RNA-Binding Protein FUS, tau Proteins, DNA-Binding Proteins, Prevalence, Sequence Analysis, DNA, Mental Disorders, Age of Onset, Mutation, Adult, Middle Aged, Female, Male, Frontotemporal Lobar Degeneration, Sequence Analysis, DNA, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS collection specifically focussed on aFTLD-U cases, one of three recently defined subtypes of FTLD-FUS. The aFTLD-U subtype of FTLD-FUS is characterised clinically by behavioural variant frontotemporal dementia (bvFTD) and has a particularly young age of onset with a mean of 41 years. Further, this subtype had a high prevalence of psychotic symptoms (36% of cases) and low prevalence of motor symptoms (3% of cases). We did not find FUS mutations in any aFTLD-U case. To date, the only subtype of cases reported to have ubiquitin-positive but tau-, TDP-43- and FUS-negative pathology, termed FTLD-UPS, is the result of charged multivesicular body protein 2B gene (CHMP2B) mutation. We identified three FTLD-UPS cases, which are negative for CHMP2B mutation, suggesting that the full complement of FTLD pathologies is yet to be elucidated.

Published
2010

9. 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

22. Riluzole is associated with decreasing neuritic plaque severity in amyotrophic lateral sclerosis.

Author

Mazumder, Srestha, McCann, Heather, D'Silva, Susan, Furlong, Sarah, Shepherd, Claire E, Kril, Jillian J, Halliday, Glenda M, Rowe, Dominic B, Kiernan, Matthew C, and Tan, Rachel H

Subjects
AMYLOID plaque, AMYOTROPHIC lateral sclerosis, CEREBRAL amyloid angiopathy, POSTMORTEM changes, RILUZOLE
Abstract

The glutamate modulator, riluzole, extends survival in amyotrophic lateral sclerosis (ALS) and was recently assessed in a clinical trial for Alzheimer's disease (Ad).[1] This trial found that riluzole-treated patients with Ad had a significantly reduced decline of cerebral glucose metabolism in multiple Ad predilection brain regions compared to placebo, which correlated with cognitive performance.[1] Importantly however, assessment of amyloid load was not included in the trial and as such, the effect of riluzole treatment on Ad neuropathological changes in patients remains to be clarified. The severity of neuritic plaques were graded according to the neuritic plaque score of (A) C1: sparse (1-5 neuritic plaques per mm2); (B) C2: moderate (>=6 neuritic plaques per mm2); and (C) C3: frequent (>=20 neuritic plaques per mm2). [Extracted from the article]

Published
2023
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30. CNS cell type–specific gene profiling of P301S tau transgenic mice identifies genes dysregulated by progressive tau accumulation

Author

Ke, Yazi D., primary, Chan, Gabriella, additional, Stefanoska, Kristie, additional, Au, Carol, additional, Bi, Mian, additional, Müller, Julius, additional, Przybyla, Magdalena, additional, Feiten, Astrid, additional, Prikas, Emmanuel, additional, Halliday, Glenda M., additional, Piguet, Olivier, additional, Kiernan, Matthew C., additional, Kassiou, Michael, additional, Hodges, John R., additional, Loy, Clement T., additional, Mattick, John S., additional, Ittner, Arne, additional, Kril, Jillian J., additional, Sutherland, Greg T., additional, and Ittner, Lars M., additional

Published
2019
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33. Retiring the term FTDP-17 as MAPT mutations are genetic forms of sporadic frontotemporal tauopathies

Author

Forrest, Shelley L, primary, Kril, Jillian J, additional, Stevens, Claire H, additional, Kwok, John B, additional, Hallupp, Marianne, additional, Kim, Woojin S, additional, Huang, Yue, additional, McGinley, Ciara V, additional, Werka, Hellen, additional, Kiernan, Matthew C, additional, Götz, Jürgen, additional, Spillantini, Maria Grazia, additional, Hodges, John R, additional, Ittner, Lars M, additional, and Halliday, Glenda M, additional

Published
2017
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34. Multisite Assessment of Aging-Related Tau Astrogliopathy (ARTAG)

Author

Kovacs, Gabor G., Xie, Sharon X., Lee, Edward B., Robinson, John L., Caswell, Carrie, Irwin, David J., Toledo, Jon B., Johnson, Victoria E., Smith, Douglas H., Alafuzoff, Irina, Attems, Johannes, Bencze, Janos, Bieniek, Kevin F., Bigio, Eileen H., Bodi, Istvan, Budka, Herbert, Dickson, Dennis W., Dugger, Brittany N., Duyckaerts, Charles, Ferrer, Isidro, Forrest, Shelley L., Gelpi, Ellen, Gentleman, Stephen M., Giaccone, Giorgio, Grinberg, Lea T., Halliday, Glenda M., Hatanpaa, Kimmo J., Hof, Patrick R., Hofer, Monika, Hortobagyi, Tibor, Ironside, James W., King, Andrew, Kofler, Julia, Kovari, Eniko, Kril, Jillian J., Love, Seth, Mackenzie, Ian R., Mao, Qinwen, Matej, Radoslav, McLean, Catriona, Munoz, David G., Murray, Melissa E., Neltner, Janna, Nelson, Peter T., Ritchie, Diane, Rodriguez, Roberta D., Rohan, Zdenek, Rozemuller, Annemieke, Sakai, Kenji, Schultz, Christian, Seilhean, Danielle, Smith, Vanessa, Tacik, Pawel, Takahashi, Hitoshi, Takao, Masaki, Thal, Dietmar Rudolf, Weis, Serge, Wharton, Stephen B., White, Charles L., III, Woulfe, John M., Yamada, Masahito, Trojanowski, John Q., Kovacs, Gabor G., Xie, Sharon X., Lee, Edward B., Robinson, John L., Caswell, Carrie, Irwin, David J., Toledo, Jon B., Johnson, Victoria E., Smith, Douglas H., Alafuzoff, Irina, Attems, Johannes, Bencze, Janos, Bieniek, Kevin F., Bigio, Eileen H., Bodi, Istvan, Budka, Herbert, Dickson, Dennis W., Dugger, Brittany N., Duyckaerts, Charles, Ferrer, Isidro, Forrest, Shelley L., Gelpi, Ellen, Gentleman, Stephen M., Giaccone, Giorgio, Grinberg, Lea T., Halliday, Glenda M., Hatanpaa, Kimmo J., Hof, Patrick R., Hofer, Monika, Hortobagyi, Tibor, Ironside, James W., King, Andrew, Kofler, Julia, Kovari, Eniko, Kril, Jillian J., Love, Seth, Mackenzie, Ian R., Mao, Qinwen, Matej, Radoslav, McLean, Catriona, Munoz, David G., Murray, Melissa E., Neltner, Janna, Nelson, Peter T., Ritchie, Diane, Rodriguez, Roberta D., Rohan, Zdenek, Rozemuller, Annemieke, Sakai, Kenji, Schultz, Christian, Seilhean, Danielle, Smith, Vanessa, Tacik, Pawel, Takahashi, Hitoshi, Takao, Masaki, Thal, Dietmar Rudolf, Weis, Serge, Wharton, Stephen B., White, Charles L., III, Woulfe, John M., Yamada, Masahito, and Trojanowski, John Q.

Abstract

Aging-related tau astrogliopathy (ARTAG) is a recently introduced terminology. To facilitate the consistent identification of ARTAG and to distinguish it from astroglial tau pathologies observed in the primary frontotemporal lobar degeneration tauopathies we evaluated how consistently neuropathologists recognize (1) different astroglial tau immunoreactivities, including those of ARTAG and those associated with primary tauopathies (Study 1); (2) ARTAG types (Study 2A); and (3) ARTAG severity (Study 2B). Microphotographs and scanned sections immunostained for phosphorylated tau (AT8) were made available for download and preview. Percentage of agreement and kappa values with 95% confidence interval (CI) were calculated for each evaluation. The overall agreement for Study 1 was > 60% with a kappa value of 0.55 (95% CI 0.433-0.645). Moderate agreement (> 90%, kappa 0.48, 95% CI 0.457-0.900) was reached in Study 2A for the identification of ARTAG pathology for each ARTAG subtype (kappa 0.37-0.72), whereas fair agreement (kappa 0.40, 95% CI 0.341-0.445) was reached for the evaluation of ARTAG severity. The overall assessment of ARTAG showed moderate agreement (kappa 0.60, 95% CI 0.534-0.653) among raters. Our study supports the application of the current harmonized evaluation strategy for ARTAG with a slight modification of the evaluation of its severity.

Published
2017
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35. Aging-related tau astrogliopathy (ARTAG) : harmonized evaluation strategy

Author

Kovacs, Gabor G., Ferrer, Isidro, Grinberg, Lea T., Alafuzoff, Irina, Attems, Johannes, Budka, Herbert, Cairns, Nigel J., Crary, John F., Duyckaerts, Charles, Ghetti, Bernardino, Halliday, Glenda M., Ironside, James W., Love, Seth, Mackenzie, Ian R., Munoz, David G., Murray, Melissa E., Nelson, Peter T., Takahashi, Hitoshi, Trojanowski, John Q., Ansorge, Olaf, Arzberger, Thomas, Baborie, Atik, Beach, Thomas G., Bieniek, Kevin F., Bigio, Eileen H., Bodi, Istvan, Dugger, Brittany N., Feany, Mel, Gelpi, Ellen, Gentleman, Stephen M., Giaccone, Giorgio, Hatanpaa, Kimmo J., Heale, Richard, Hof, Patrick R., Hofer, Monika, Hortobagyi, Tibor, Jellinger, Kurt, Jicha, Gregory A., Ince, Paul, Kofler, Julia, Koevari, Enikoe, Kril, Jillian J., Mann, David M., Matej, Radoslav, McKee, Ann C., McLean, Catriona, Milenkovic, Ivan, Montine, Thomas J., Murayama, Shigeo, Lee, Edward B., Rahimi, Jasmin, Rodriguez, Roberta D., Rozemuller, Annemieke, Schneider, Julie A., Schultz, Christian, Seeley, William, Seilhean, Danielle, Smith, Colin, Tagliavini, Fabrizio, Takao, Masaki, Thal, Dietmar Rudolf, Toledo, Jon B., Tolnay, Markus, Troncoso, Juan C., Vinters, Harry V., Weis, Serge, Wharton, Stephen B., White, Charles L., III, Wisniewski, Thomas, Woulfe, John M., Yamada, Masahito, Dickson, Dennis W., Kovacs, Gabor G., Ferrer, Isidro, Grinberg, Lea T., Alafuzoff, Irina, Attems, Johannes, Budka, Herbert, Cairns, Nigel J., Crary, John F., Duyckaerts, Charles, Ghetti, Bernardino, Halliday, Glenda M., Ironside, James W., Love, Seth, Mackenzie, Ian R., Munoz, David G., Murray, Melissa E., Nelson, Peter T., Takahashi, Hitoshi, Trojanowski, John Q., Ansorge, Olaf, Arzberger, Thomas, Baborie, Atik, Beach, Thomas G., Bieniek, Kevin F., Bigio, Eileen H., Bodi, Istvan, Dugger, Brittany N., Feany, Mel, Gelpi, Ellen, Gentleman, Stephen M., Giaccone, Giorgio, Hatanpaa, Kimmo J., Heale, Richard, Hof, Patrick R., Hofer, Monika, Hortobagyi, Tibor, Jellinger, Kurt, Jicha, Gregory A., Ince, Paul, Kofler, Julia, Koevari, Enikoe, Kril, Jillian J., Mann, David M., Matej, Radoslav, McKee, Ann C., McLean, Catriona, Milenkovic, Ivan, Montine, Thomas J., Murayama, Shigeo, Lee, Edward B., Rahimi, Jasmin, Rodriguez, Roberta D., Rozemuller, Annemieke, Schneider, Julie A., Schultz, Christian, Seeley, William, Seilhean, Danielle, Smith, Colin, Tagliavini, Fabrizio, Takao, Masaki, Thal, Dietmar Rudolf, Toledo, Jon B., Tolnay, Markus, Troncoso, Juan C., Vinters, Harry V., Weis, Serge, Wharton, Stephen B., White, Charles L., III, Wisniewski, Thomas, Woulfe, John M., Yamada, Masahito, and Dickson, Dennis W.

Abstract

Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of astrogli

Published
2016
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36. [18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation

Author

Bevan Jones, W. Richard, primary, Cope, Thomas E., additional, Passamonti, Luca, additional, Fryer, Tim D., additional, Hong, Young T., additional, Aigbirhio, Franklin, additional, Kril, Jillian J., additional, Forrest, Shelley L., additional, Allinson, Kieren, additional, Coles, Jonathan P., additional, Simon Jones, P., additional, Spillantini, Maria G., additional, Hodges, John R., additional, O'Brien, John T., additional, and Rowe, James B., additional

Published
2016
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39. [18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation.

Author

Bevan Jones, W. Richard, Cope, Thomas E., Passamonti, Luca, Fryer, Tim D., Hong, Young T., Aigbirhio, Franklin, Kril, Jillian J., Forrest, Shelley L., Allinson, Kieren, Coles, Jonathan P., Simon Jones, P., Spillantini, Maria G., Hodges, John R., O'Brien, John T., and Rowe, James B.

Subjects
FRONTOTEMPORAL dementia, RADIOLIGAND assay, NEUROLOGICAL disorders, HUMAN chromosome abnormality diagnosis, GENETIC mutation
Abstract

The validation of tau radioligands could improve the diagnosis of frontotemporal lobar degeneration and the assessment of disease-modifying therapies. Here, we demonstrate that binding of the tau radioligand [18F] AV-1451 was significantly abnormal in both magnitude and distribution in a patient with familial frontotemporal dementia due to a MAPT 10 + 16C>T gene mutation, recapitulating the pattern of neuropathology seen in her father. Given the genetic diagnosis and the non-Alzheimer's pathology, these findings suggest that [18F] AV-1451 might be a useful biomarker in primary tauopathies. Largerscale in vivo and post-mortem studies will be needed to assess the technique's specificity. [ABSTRACT FROM AUTHOR]

Published
2016
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40. Increased apolipoprotein D dimer formation in Alzheimer's disease hippocampus is associated with lipid conjugated diene levels

Author

Bhatia, Surabhi, Jenner, Andrew M, Li, Hongyun, Ruberu, Kalani, Spiro, Adena S, Shepherd, Claire E, Kril, Jillian J, Kain, Nupur, Don, Anthony, Garner, Brett, Bhatia, Surabhi, Jenner, Andrew M, Li, Hongyun, Ruberu, Kalani, Spiro, Adena S, Shepherd, Claire E, Kril, Jillian J, Kain, Nupur, Don, Anthony, and Garner, Brett

Abstract

Previous studies indicate that apolipoprotein D (apoD) may have a lipid antioxidant function in the brain. We have shown that apoD can reduce free radical-generating lipid hydroperoxides to inert lipid hydroxides in a reaction that involves conversion of surface exposed apoD methione-93 (Met93) residue to Met93-sulfoxide (Met93-SO). One consequence of this reaction is the formation of a stable dimerized form of apoD. As cerebral lipid peroxidation is associated with Alzheimer's disease (AD), in the present study we aimed to assess the possible presence of apoD dimers in postmortem hippocampal and cerebellar tissues derived from a cohort of pathologically defined cases ranging from control to late stage AD. Both soluble and insoluble (requiring guanidine HCl extraction) fractions of tissue homogenates were analyzed for apoD and its dimerized form. We also assessed amyloid-β levels by ELISA and levels of lipid peroxidation by lipid conjugated diene and F2-isoprostane analysis. Our studies reveal a significant association between soluble apoD levels and AD Braak stage whereas apoD dimer formation appears to increase predominantly in the advanced stages of disease. The formation of apoD dimers is closely correlated to lipid conjugated diene levels and occurs in the hippocampus but not in the cerebellum. These results are consistent with the hypothesis that apoD acts as a lipid antioxidant in the brain.

Published
2013

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

Author

Van Deerlin, Vivian M, Sleiman, Patrick M. A., 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 M. A., 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 R. A., 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 B. J., 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., Lee, Virginia M-Y., Van Deerlin, Vivian M, Sleiman, Patrick M. A., 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 M. A., 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 R. A., 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 B. J., 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.

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
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44. Pick Bodies in a Family with Presenilin-1 Alzheimer's Disease

Author

Halliday, Glenda M, Song, Yun Ju C, Lepar, Gila, Brooks, William S, Kwok, John B, Kersaitis, Cindy, Gregory, Gillian, Shepherd, Claire E, Rahimi, Ahmed (Farid), Schofield, Peter, Kril, Jillian J, Halliday, Glenda M, Song, Yun Ju C, Lepar, Gila, Brooks, William S, Kwok, John B, Kersaitis, Cindy, Gregory, Gillian, Shepherd, Claire E, Rahimi, Ahmed (Farid), Schofield, Peter, and Kril, Jillian J

Abstract

Presenilin-1 (PS-1) mutations can cause Pick's disease without evidence of Alzheimer's disease (AD). We describe a family with a PS-1 M146L mutation and both Pick bodies and AD. Sarkosyl-insoluble hyperphosphorylated tau showed three bands consistent with AD, although dephosphorylation showed primarily three-repeat isoforms. M146L mutant PS-1 may predispose to both Pick's disease and AD by affecting multiple intracellular pathways involving tau phosphorylation and amyloid metabolism.

Published
2005

48. Alzheimer disease: Alzheimer disease neuropathology in the oldest old.

Author

Kril, Jillian J.

Subjects
*DEMENTIA, *NEUROLOGICAL disorders, *AGE factors in disease, *DISEASES in older people, *ALZHEIMER'S disease, *NERVE fibers
Abstract

The article focuses on the need to understand the relationship between dementia neuropathology and age. It notes that a body of medical literature implies that the link between Alzheimer's disease (AD)-type pathology and dementia does not apply in people above 95 years of age. It examines the results of a study on the impact of age on the association between AD-type pathology and dementia which suggests that the capability to predict dementia based on neurofibrillary tangle (NFT) and neuritic plaque (NP) densities decreases among people beyond 70 years.

Published
2009
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50. [ 18 F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation.

Author

Bevan Jones WR, Cope TE, Passamonti L, Fryer TD, Hong YT, Aigbirhio F, Kril JJ, Forrest SL, Allinson K, Coles JP, Simon Jones P, Spillantini MG, Hodges JR, O'Brien JT, and Rowe JB

Abstract

The validation of tau radioligands could improve the diagnosis of frontotemporal lobar degeneration and the assessment of disease-modifying therapies. Here, we demonstrate that binding of the tau radioligand [ 18 F]AV-1451 was significantly abnormal in both magnitude and distribution in a patient with familial frontotemporal dementia due to a MAPT 10 + 16C>T gene mutation, recapitulating the pattern of neuropathology seen in her father. Given the genetic diagnosis and the non-Alzheimer's pathology, these findings suggest that [ 18 F]AV-1451 might be a useful biomarker in primary tauopathies. Largerscale in vivo and post-mortem studies will be needed to assess the technique's specificity.

Published
2016
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