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1. MAPT H2 haplotype and risk of Pick's disease in the Pick's disease International Consortium: a genetic association study

Author

Warner, Thomas T, Jaunmuktane, Zane, Boeve, Bradley F, Duara, Ranjan, Graff-Radford, Neill R, Josephs, Keith A, Knopman, David S, Koga, Shunsuke, Murray, Melissa E, Lyons, Kelly E, Pahwa, Rajesh, Petersen, Ronald C, Whitwell, Jennifer L, Grinberg, Lea T, Miller, Bruce, Schlereth, Athena, Spina, Salvatore, Grossman, Murray, Irwin, David J, Suh, EunRan, Trojanowski, John Q, Van Deerlin, Vivianna M, Wolk, David A, Connors, Theresa R, Dooley, Patrick M, Oakley, Derek H, Aldecoa, Iban, Balasa, Mircea, Gelpi, Ellen, Borrego-Écija, Sergi, Gascon-Bayarri, Jordi, Sánchez-Valle, Raquel, Sanz-Cartagena, Pilar, Piñol-Ripoll, Gerard, Bigio, Eileen H, Flanagan, Margaret E, Rogalski, Emily J, Weintraub, Sandra, Schneider, Julie A, Peng, Lihua, Zhu, Xiongwei, Chang, Koping, Troncoso, Juan C, Prokop, Stefan, Newell, Kathy L, Jones, Matthew, Richardson, Anna, Roncaroli, Federico, Snowden, Julie, Allinson, Kieren, Singh, Poonam, Serrano, Geidy E, Flowers, Xena E, Goldman, James E, Heaps, Allison C, Leskinen, Sandra P, Black, Sandra E, Masellis, Mario, King, Andrew, Al-Sarraj, Safa, Troakes, Claire, Hodges, John R, Kril, Jillian J, Kwok, John B, Piguet, Olivier, Roeber, Sigrun, Attems, Johannes, Thomas, Alan J, Evers, Bret M., Bieniek, Kevin F, Sieben, Anne A, Cras, Patrick P, De Vil, Bart B, Bird, Thomas, Castellani, Rudolph J, Chaffee, Ann, Franklin, Erin, Haroutunian, Vahram, Jacobsen, Max, Keene, Dirk, Latimer, Caitlin S, Metcalf, Jeff, Perrin, Richard J, Purohit, Dushyant P, Rissman, Robert A, Schantz, Aimee, Walker, Jamie, De Deyn, Peter P, Duyckaerts, Charles, Le Ber, Isabelle, Seilhean, Danielle, Turbant-Leclere, Sabrina, Ervin, John F, Nennesmo, Inger, Riehl, James, Nacmias, Benedetta, Finger, Elizabeth C, Blauwendraat, Cornelis, Nalls, Mike A, Singleton, Andrew B, Vitale, Dan, Cunha, Cristina, Wszolek, Zbigniew K, Valentino, Rebecca R, Scotton, William J, Roemer, Shanu F, Lashley, Tammaryn, Heckman, Michael G, Shoai, Maryam, Martinez-Carrasco, Alejandro, Tamvaka, Nicole, Walton, Ronald L, Baker, Matthew C, Macpherson, Hannah L, Real, Raquel, Soto-Beasley, Alexandra I, Mok, Kin, Revesz, Tamas, Christopher, Elizabeth A, DeTure, Michael, Seeley, William W, Lee, Edward B, Frosch, Matthew P, Molina-Porcel, Laura, Gefen, Tamar, Redding-Ochoa, Javier, Ghetti, Bernardino, Robinson, Andrew C, Kobylecki, Christopher, Rowe, James B, Beach, Thomas G, Teich, Andrew F, Keith, Julia L, Bodi, Istvan, Halliday, Glenda M, Gearing, Marla, Arzberger, Thomas, Morris, Christopher M, White, Charles L, 3rd, Mechawar, Naguib, Boluda, Susana, MacKenzie, Ian R, McLean, Catriona, Cykowski, Matthew D, Wang, Shih-Hsiu J, Graff, Caroline, Nagra, Rashed M, Kovacs, Gabor G, Giaccone, Giorgio, Neumann, Manuela, Ang, Lee-Cyn, Carvalho, Agostinho, Morris, Huw R, Rademakers, Rosa, Hardy, John A, Dickson, Dennis W, Rohrer, Jonathan D, and Ross, Owen A

Published
2024
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3. MAPT H2 haplotype and risk of Pick's disease in the Pick's disease International Consortium: a genetic association study

Author

Valentino, Rebecca R, primary, Scotton, William J, additional, Roemer, Shanu F, additional, Lashley, Tammaryn, additional, Heckman, Michael G, additional, Shoai, Maryam, additional, Martinez-Carrasco, Alejandro, additional, Tamvaka, Nicole, additional, Walton, Ronald L, additional, Baker, Matthew C, additional, Macpherson, Hannah L, additional, Real, Raquel, additional, Soto-Beasley, Alexandra I, additional, Mok, Kin, additional, Revesz, Tamas, additional, Christopher, Elizabeth A, additional, DeTure, Michael, additional, Seeley, William W, additional, Lee, Edward B, additional, Frosch, Matthew P, additional, Molina-Porcel, Laura, additional, Gefen, Tamar, additional, Redding-Ochoa, Javier, additional, Ghetti, Bernardino, additional, Robinson, Andrew C, additional, Kobylecki, Christopher, additional, Rowe, James B, additional, Beach, Thomas G, additional, Teich, Andrew F, additional, Keith, Julia L, additional, Bodi, Istvan, additional, Halliday, Glenda M, additional, Gearing, Marla, additional, Arzberger, Thomas, additional, Morris, Christopher M, additional, White, Charles L, additional, Mechawar, Naguib, additional, Boluda, Susana, additional, MacKenzie, Ian R, additional, McLean, Catriona, additional, Cykowski, Matthew D, additional, Wang, Shih-Hsiu J, additional, Graff, Caroline, additional, Nagra, Rashed M, additional, Kovacs, Gabor G, additional, Giaccone, Giorgio, additional, Neumann, Manuela, additional, Ang, Lee-Cyn, additional, Carvalho, Agostinho, additional, Morris, Huw R, additional, Rademakers, Rosa, additional, Hardy, John A, additional, Dickson, Dennis W, additional, Rohrer, Jonathan D, additional, Ross, Owen A, additional, Warner, Thomas T, additional, Jaunmuktane, Zane, additional, Boeve, Bradley F, additional, Duara, Ranjan, additional, Graff-Radford, Neill R, additional, Josephs, Keith A, additional, Knopman, David S, additional, Koga, Shunsuke, additional, Murray, Melissa E, additional, Lyons, Kelly E, additional, Pahwa, Rajesh, additional, Petersen, Ronald C, additional, Whitwell, Jennifer L, additional, Grinberg, Lea T, additional, Miller, Bruce, additional, Schlereth, Athena, additional, Spina, Salvatore, additional, Grossman, Murray, additional, Irwin, David J, additional, Suh, EunRan, additional, Trojanowski, John Q, additional, Van Deerlin, Vivianna M, additional, Wolk, David A, additional, Connors, Theresa R, additional, Dooley, Patrick M, additional, Oakley, Derek H, additional, Aldecoa, Iban, additional, Balasa, Mircea, additional, Gelpi, Ellen, additional, Borrego-Écija, Sergi, additional, Gascon-Bayarri, Jordi, additional, Sánchez-Valle, Raquel, additional, Sanz-Cartagena, Pilar, additional, Piñol-Ripoll, Gerard, additional, Bigio, Eileen H, additional, Flanagan, Margaret E, additional, Rogalski, Emily J, additional, Weintraub, Sandra, additional, Schneider, Julie A, additional, Peng, Lihua, additional, Zhu, Xiongwei, additional, Chang, Koping, additional, Troncoso, Juan C, additional, Prokop, Stefan, additional, Newell, Kathy L, additional, Jones, Matthew, additional, Richardson, Anna, additional, Roncaroli, Federico, additional, Snowden, Julie, additional, Allinson, Kieren, additional, Singh, Poonam, additional, Serrano, Geidy E, additional, Flowers, Xena E, additional, Goldman, James E, additional, Heaps, Allison C, additional, Leskinen, Sandra P, additional, Black, Sandra E, additional, Masellis, Mario, additional, King, Andrew, additional, Al-Sarraj, Safa, additional, Troakes, Claire, additional, Hodges, John R, additional, Kril, Jillian J, additional, Kwok, John B, additional, Piguet, Olivier, additional, Roeber, Sigrun, additional, Attems, Johannes, additional, Thomas, Alan J, additional, Evers, Bret M., additional, Bieniek, Kevin F, additional, Sieben, Anne A, additional, Cras, Patrick P, additional, De Vil, Bart B, additional, Bird, Thomas, additional, Castellani, Rudolph J, additional, Chaffee, Ann, additional, Franklin, Erin, additional, Haroutunian, Vahram, additional, Jacobsen, Max, additional, Keene, Dirk, additional, Latimer, Caitlin S, additional, Metcalf, Jeff, additional, Perrin, Richard J, additional, Purohit, Dushyant P, additional, Rissman, Robert A, additional, Schantz, Aimee, additional, Walker, Jamie, additional, De Deyn, Peter P, additional, Duyckaerts, Charles, additional, Le Ber, Isabelle, additional, Seilhean, Danielle, additional, Turbant-Leclere, Sabrina, additional, Ervin, John F, additional, Nennesmo, Inger, additional, Riehl, James, additional, Nacmias, Benedetta, additional, Finger, Elizabeth C, additional, Blauwendraat, Cornelis, additional, Nalls, Mike A, additional, Singleton, Andrew B, additional, Vitale, Dan, additional, Cunha, Cristina, additional, and Wszolek, Zbigniew K, additional

Published
2024
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4. Author Response: Machine learning of dissection photographs and surface scanning for quantitative 3D neuropathology

Author

Gazula, Harshvardhan, primary, Tregidgo, Henry F. J., additional, Billot, Benjamin, additional, Balbastre, Yael, additional, William-Ramirez, Jonathan, additional, Herisse, Rogeny, additional, Deden-Binder, Lucas J, additional, Casamitjana, Adrià, additional, Melief, Erica J., additional, Latimer, Caitlin S., additional, Kilgore, Mitchell D., additional, Montine, Mark, additional, Robinson, Eleanor, additional, Blackburn, Emily, additional, Marshall, Michael S., additional, Connors, Theresa R., additional, Oakley, Derek H., additional, Frosch, Matthew P., additional, Young, Sean I., additional, Leemput, Koen Van, additional, Dalca, Adrian V., additional, Fischl, Bruce, additional, Mac Donald, Christine L., additional, Keene, C. Dirk, additional, Hyman, Bradley T., additional, and Iglesias, Juan Eugenio, additional

Published
2024
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5. Machine learning of dissection photographs and surface scanning for quantitative 3D neuropathology

Author

Gazula, Harshvardhan, primary, Tregidgo, Henry F. J., additional, Billot, Benjamin, additional, Balbastre, Yael, additional, William-Ramirez, Jonathan, additional, Herisse, Rogeny, additional, Deden-Binder, Lucas J, additional, Casamitjana, Adrià, additional, Melief, Erica J., additional, Latimer, Caitlin S., additional, Kilgore, Mitchell D., additional, Montine, Mark, additional, Robinson, Eleanor, additional, Blackburn, Emily, additional, Marshall, Michael S., additional, Connors, Theresa R., additional, Oakley, Derek H., additional, Frosch, Matthew P., additional, Young, Sean I., additional, Leemput, Koen Van, additional, Dalca, Adrian V., additional, Fischl, Bruce, additional, Mac Donald, Christine L., additional, Keene, C. Dirk, additional, Hyman, Bradley T., additional, and Iglesias, Juan Eugenio, additional

Published
2024
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6. Machine learning of dissection photographs and surface scanning for quantitative 3D neuropathology.

Author

Gazula, Harshvardhan, Tregidgo, Henry F. J., Billot, Benjamin, Balbastre, Yael, Williams-Ramirez, Jonathan, Herisse, Rogeny, Deden-Binder, Lucas J., Casamitjana, Adria, Melief, Erica J., Latimer, Caitlin S., Kilgore, Mitchell D., Montine, Mark, Robinson, Eleanor, Blackburn, Emily, Marshall, Michael S., Connors, Theresa R., Oakley, Derek H., Frosch, Matthew P., Young, Sean I., and Van Leemput, Koen

Published
2024
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7. Machine learning of dissection photographs and surface scanning for quantitative 3D neuropathology

Author

Gazula, Harshvardhan, primary, Tregidgo, Henry F. J., additional, Billot, Benjamin, additional, Balbastre, Yael, additional, William-Ramirez, Jonathan, additional, Herisse, Rogeny, additional, Deden-Binder, Lucas J, additional, Casamitjana, Adrià, additional, Melief, Erica J., additional, Latimer, Caitlin S., additional, Kilgore, Mitchell D., additional, Montine, Mark, additional, Robinson, Eleanor, additional, Blackburn, Emily, additional, Marshall, Michael S., additional, Connors, Theresa R., additional, Oakley, Derek H., additional, Frosch, Matthew P., additional, Young, Sean I., additional, Van Leemput, Koen, additional, Dalca, Adrian V., additional, Fischl, Bruce, additional, Mac Donald, Christine L., additional, Keene, C. Dirk, additional, Hyman, Bradley T., additional, and Iglesias, Juan Eugenio, additional

Published
2023
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8. Age-Dependent Increase in Tau Phosphorylation at Serine 396 in Huntington’s Disease Prefrontal Cortex

Author

Petrozziello, Tiziana, primary, Huntress, Sommer S., additional, Castillo-Torres, Ayleen L., additional, Quinn, James P., additional, Connors, Theresa R., additional, Auger, Corinne A., additional, Mills, Alexandra N., additional, Kim, Spencer E., additional, Liu, Sophia, additional, Mahmood, Farah, additional, Boudi, Adel, additional, Wu, Muzhou, additional, Sapp, Ellen, additional, Kivisäkk, Pia, additional, Sunderesh, Shekar R., additional, Pouladi, Mahmoud A., additional, Arnold, Steven E., additional, Hyman, Bradley T., additional, Rosas, H. Diana, additional, DiFiglia, Marian, additional, Mouro Pinto, Ricardo, additional, Kegel-Gleason, Kimberly, additional, and Sadri-Vakili, Ghazaleh, additional

Published
2023
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9. Age-dependent increase in tau phosphorylation at serine 396 in Huntington s disease pre-frontal cortex

Author

Petrozziello, Tiziana, primary, Huntress, Sommer S., additional, Castillo-Torres, Ayleen L., additional, Quinn, James P., additional, Connors, Theresa R., additional, Auger, Corinne A., additional, Mills, Alexandra N., additional, Kim, Spencer E., additional, Liu, Sophia, additional, Mahmood, Farah, additional, Boudi, Adel, additional, Wu, Muzhou, additional, Sapp, Ellen, additional, Kivisakk, Pia, additional, Sunderesh, Shekar R., additional, Pouladi, Mahmoud A., additional, Arnold, Steven E., additional, Hyman, Bradley T., additional, Rosas, H. Diana, additional, DiFiglia, Marian, additional, Mouro Pinto, Ricardo, additional, Kegel-Gleason, Kimberly, additional, and Sadri-Vakili, Ghazaleh, additional

Published
2023
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10. Creating the Pick’s disease International Consortium: Association study ofMAPTH2 haplotype with risk of Pick’s disease

Author

Valentino, Rebecca R, primary, Scotton, William J, additional, Roemer, Shanu F, additional, Lashley, Tammaryn, additional, Heckman, Michael G, additional, Shoai, Maryam, additional, Martinez-Carrasco, Alejandro, additional, Tamvaka, Nicole, additional, Walton, Ronald L, additional, Baker, Matthew C, additional, Macpherson, Hannah L, additional, Real, Raquel, additional, Soto-Beasley, Alexandra I, additional, Mok, Kin, additional, Revesz, Tamas, additional, Warner, Thomas T, additional, Jaunmuktane, Zane, additional, Boeve, Bradley F, additional, Christopher, Elizabeth A, additional, DeTure, Michael, additional, Duara, Ranjan, additional, Graff-Radford, Neill R, additional, Josephs, Keith A, additional, Knopman, David S, additional, Koga, Shunsuke, additional, Murray, Melissa E, additional, Lyons, Kelly E, additional, Pahwa, Rajesh, additional, Parisi, Joseph E, additional, Petersen, Ronald C, additional, Whitwell, Jennifer, additional, Grinberg, Lea T, additional, Miller, Bruce, additional, Schlereth, Athena, additional, Seeley, William W, additional, Spina, Salvatore, additional, Grossman, Murray, additional, Irwin, David J, additional, Lee, Edward B, additional, Suh, EunRan, additional, Trojanowski, John Q, additional, Van Deerlin, Vivianna M, additional, Wolk, David A, additional, Connors, Theresa R, additional, Dooley, Patrick M, additional, Frosch, Matthew P, additional, Oakley, Derek H, additional, Aldecoa, Iban, additional, Balasa, Mircea, additional, Gelpi, Ellen, additional, Borrego-Écija, Sergi, additional, de Eugenio Huélamo, Rosa Maria, additional, Gascon-Bayarri, Jordi, additional, Sánchez-Valle, Raquel, additional, Sanz-Cartagena, Pilar, additional, Piñol-Ripoll, Gerard, additional, Molina-Porcel, Laura, additional, Bigio, Eileen H, additional, Flanagan, Margaret E, additional, Gefen, Tamar, additional, Rogalski, Emily J, additional, Weintraub, Sandra, additional, Redding-Ochoa, Javier, additional, Chang, Koping, additional, Troncoso, Juan C, additional, Prokop, Stefan, additional, Newell, Kathy L, additional, Ghetti, Bernardino, additional, Jones, Matthew, additional, Richardson, Anna, additional, Robinson, Andrew C, additional, Roncaroli, Federico, additional, Snowden, Julie, additional, Allinson, Kieren, additional, Green, Oliver, additional, Rowe, James B, additional, Singh, Poonam, additional, Beach, Thomas G, additional, Serrano, Geidy E, additional, Flowers, Xena E, additional, Goldman, James E, additional, Heaps, Allison C, additional, Leskinen, Sandra P, additional, Teich, Andrew F, additional, Black, Sandra E, additional, Keith, Julia L, additional, Masellis, Mario, additional, Bodi, Istvan, additional, King, Andrew, additional, Sarraj, Safa-Al, additional, Troakes, Claire, additional, Halliday, Glenda M, additional, Hodges, John R, additional, Kril, Jillian J, additional, Kwok, John B, additional, Piguet, Olivier, additional, Gearing, Marla, additional, Arzberger, Thomas, additional, Roeber, Sigrun, additional, Attems, Johannes, additional, Morris, Christopher M, additional, Thomas, Alan J, additional, Evers, Bret M., additional, White, Charles L, additional, Mechawar, Naguib, additional, Sieben, Anne A, additional, Cras, Patrick P, additional, De Vil, Bart B, additional, De Deyn, Peter Paul P.P., additional, Duyckaerts, Charles, additional, Ber, Isabelle Le, additional, Seihean, Danielle, additional, Turbant-Leclere, Sabrina, additional, MacKenzie, Ian R, additional, McLean, Catriona, additional, Cykowski, Matthew D, additional, Ervin, John F, additional, Wang, Shih-Hsiu J, additional, Graff, Caroline, additional, Nennesmo, Inger, additional, Nagra, Rashed M, additional, Riehl, James, additional, Kovacs, Gabor G, additional, Giaccone, Giorgio, additional, Nacmias, Benedetta, additional, Neumann, Manuela, additional, Ang, Lee-Cyn, additional, Finger, Elizabeth C, additional, Blauwendraat, Cornelis, additional, Nalls, Mike A, additional, Singleton, Andrew B, additional, Vitale, Dan, additional, Cunha, Cristina, additional, Carvalho, Agostinho, additional, Wszolek, Zbigniew K, additional, Morris, Huw R, additional, Rademakers, Rosa, additional, Hardy, John A, additional, Dickson, Dennis W, additional, Rohrer, Jonathan D, additional, and Ross, Owen A, additional

Published
2023
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11. 3D analysis of dissection photographs with surface scanning and machine learning for quantitative neuropathology

Author

Gazula, Harshvardhan, Tregidgo, Henry F. J., Billot, Benjamin, Balbastre, Yael, William-Ramirez, Jonathan, Herisse, Rogeny, Casamitjana, Adrià, Melief, Erica J., Latimer, Caitlin S., Kilgore, Mitchell D., Montine, Mark, Robinson, Eleanor, Blackburn, Emily, Marshall, Michael S., Connors, Theresa R., Oakley, Derek H., Frosch, Matthew P., Van Leemput, Koen, Dalca, Adrian V., Fischl, Bruce, Mac Donald, Christine L., Keene, C. Dirk, Hyman, Bradley T., and Iglesias, Juan Eugenio

Subjects
Article
Abstract

Dissection photographs are routinely acquired in brain banks but seldom used for quantitative analysis. We present a publicly available, open-source toolbox of computational methods for 3D analysis of photographs of dissected slices of human brains. The toolbox includes methods for: (i) Geometric preprocessing of the photographs; (ii) 3D volumetric reconstruction of a human brain or hemisphere from the photographs and, optionally, a surface scan; and (iii) automatic 3D segmentation of nine bilateral brain regions using a novel machine learning method (“Photo-SynthSeg”), which is capable of “interpolating” the 3D segmentation across the gaps between photographs with large spacing in between. Our tools can be used for quantitative brain analysis at the macroscopic level (e.g., volumetry), as a substitute for ex vivo magnetic resonance imaging (MRI) – which requires access to an MRI scanner and ex vivo scanning expertise. Our tools are also helpful for computationally guided dissection of brain areas that are difficult to identify from the slices, e.g., defined by functional atlases. Finally, our tools also provide a spatial mapping between the a 3D MRI scan (when available) and the 2D slices, which enables accurate neuropathological-neuroimaging correlation. We evaluate our toolbox on a synthetic dataset and on dissection photographs from two NIH Alzheimer’s Disease Research Centers (ADRC). Our methodology yields accurate 3D reconstruction and automated segmentations that are highly correlated to those obtained from ex vivo MRI, and that can detect expected differences between brains with Alzheimer’s disease and controls. The tools are available as part of our widespread neuroimaging suite “FreeSurfer” ( https://surfer.nmr.mgh.harvard.edu/fswiki/PhotoTools ). SIGNIFICANCE STATEMENT: When donated human brains are dissected at brain banks, they are first cut into slabs that are routinely photographed just with archiving purposes. Here we present a set of novel, open-source computational tools that enable 3D reconstruction of these photographs into a volumetric dataset, as well as subsequent 3D segmentation of the reconstructed volumes (i.e., assigning neuroanatomical labels to every pixel in the images). Our tools enable quantitative analyses of the brain at the macroscopic level (e.g., measuring volumes of brain regions) without requiring MRI scans of the specimens. The tools also provide a spatial mapping between an MRI (if available) and the photographs, thus enabling the study of correlations between macroscopic and microscopic features (e.g., atrophy vs histology).

Published
2023

12. Age-dependent increase in tau phosphorylation at serine 396 in Huntington’s disease pre-frontal cortex

Author

Petrozziello, Tiziana, Huntress, Sommer S., Castillo-Torres, Ayleen L., Quinn, James P., Connors, Theresa R., Auger, Corinne A., Mills, Alexandra N., Kim, Spencer E., Liu, Sophia, Mahmood, Farah, Boudi, Adel, Wu, Muzhou, Sapp, Ellen, Kivisäkk, Pia, Sunderesh, Shekar R., Pouladi, Mahmoud A., Arnold, Steven E., Hyman, Bradley T., Rosas, H. Diana, DiFiglia, Marian, Pinto, Ricardo Mouro, Kegel-Gleason, Kimberly, and Sadri-Vakili, Ghazaleh

Subjects
Article
Abstract

BACKGROUND: To date, it is still controversial whether tau phosphorylation plays a role in Huntington’s disease (HD), as previous studies demonstrated either no alterations or increases in phosphorylated tau (pTau) in HD post-mortem brain and mouse models. OBJECTIVES: The goal of this study was to determine whether total tau and pTau levels are altered in HD. METHODS: Immunohistochemistry, cellular fractionations, and western blots were used to measure tau and pTau levels in a large cohort of HD and control post-mortem prefrontal cortex (PFC). Furthermore, western blots were performed to assess tau, and pTau levels in HD and control isogenic embryonic stem cell (ESC)-derived cortical neurons and neuronal stem cells (NSCs). Similarly, western blots were used to assess tau and pTau in Htt (Q111) and transgenic R6/2 mice. Lastly, total tau levels were assessed in HD and healthy control plasma using Quanterix Simoa assay. RESULTS: Our results revealed that, while there was no difference in tau or pTau levels in HD PFC compared to controls, tau phosphorylated at S396 levels were increased in PFC samples from HD patients 60 years or older at time of death. Additionally, tau and pTau levels were not changed in HD ESC-derived cortical neurons and NSCs. Similarly, tau or pTau levels were not altered in Htt (Q111) and transgenic R6/2 mice compared to wild-type littermates. Lastly, tau levels were not changed in plasma from a small cohort of HD patients compared to controls. CONCLUSION: Together these findings demonstrate that pTau-S396 levels increase significantly with age in HD PFC.

Published
2023

13. Structure–activity relationship of pyrazol-4-yl-pyridine derivatives and identification of a radiofluorinated probe for imaging the muscarinic acetylcholine receptor M4

Author

Haider, Ahmed, primary, Deng, Xiaoyun, additional, Mastromihalis, Olivia, additional, Pfister, Stefanie K., additional, Jeppesen, Troels E., additional, Xiao, Zhiwei, additional, Pham, Vi, additional, Sun, Shaofa, additional, Rong, Jian, additional, Zhao, Chunyu, additional, Chen, Jiahui, additional, Li, Yinlong, additional, Connors, Theresa R., additional, Davenport, April T., additional, Daunais, James B., additional, Hosseini, Vahid, additional, Ran, Wenqing, additional, Christopoulos, Arthur, additional, Wang, Lu, additional, Valant, Celine, additional, and Liang, Steven H., additional

Published
2023
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14. Additional file 5 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 5: Table S1. Overview of patient demographics of human BA46 tissue samples.

Published
2023
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15. Additional file 6 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 6: Table S2. Overview of PTMs of insoluble Tau species identified at different disease stages of human AD [20], the P301S and the P301L mouse model and human dementia patients carrying the P301L Tau mutation.

Published
2023
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16. Additional file 2 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 2. Figure S2. MS intensity of the APP protein in the soluble fraction. A Amount of APP in the soluble fraction of the cortex of the P301S model during progression (mean +- SD). B Amount of APP in the soluble fraction of the cortex of the P301L model during progression (mean +- SD). As the different models/species were analyzed in different experiments, a quantitative comparison of the results between the experiments is not possible.

Published
2023
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17. Additional file 4 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 4. Figure S4. Analysis of the quantitative modification extent (FLEXITau) and Pearson correlation identify regions and modifications of Tau that drive pathology in both models and human AD. A, C Euclidean hierarchical clustering of relative amounts of unmodified FLEX-peptide of pathological Tau derived from the P301S brain stem (A) and subcortical region (C). B, D Euclidean hierarchical clustering of relative amounts of unmodified FLEX-peptide of pathological Tau derived from the P301L hippocampus (B) and subcortical region (D). E Average relative amounts of unmodified FLEX-peptides per condition from pathological Tau derived from the P301S brain stem and subcortical region and the P301L hippocampus and subcortical region ordered from N- to C-terminus. F Pearson correlation between the amount of unmodified FLEX-peptide and logarithmic amount of pathological Tau ordered from N- to C-terminus for the P301S brain stem and subcortical region and the P301L hippocampus and subcortical region.A legend is provided for the extent of modification and the Pearson correlation coefficient of each peptide. And the in average top 5 correlating peptides.

Published
2023
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18. Additional file 3 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 3. Figure S3. PTM analyses of pathological Tau during the progression in P301S and P301L mouse models. A, C Euclidean hierarchical clustering of binary PTMs data from pathological Tau derived from the P301S brain stem (A) and subcortical region (C). B, D Euclidean hierarchical clustering of binary PTMs data from pathological Tau derived from the P301L hippocampus (B) and subcortical region (D). PTMs that were used for clustering were found in at least 50% of the biological replicates in at least one time point. Grey squares indicate the presence of a PTM. Annotated clusters represent PTMs identified at all time points (blue), pathological PTMs appearing with tangle formation (orange) and PTMs appearing before (yellow) or after (magenta) the onset of tangle formation.

Published
2023
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19. Additional file 1 of Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, Viode, Arthur, Schlaffner, Christoph N., van Zalm, Patrick, Cheng, Long, Dellovade, Tammy, Langlois, Xavier, Bannon, Anthony, Chang, Rui, Connors, Theresa R., Oakley, Derek, Renard, Bernhard, Rappsilber, Juri, Hyman, Bradley, Steen, Hanno, and Steen, Judith A.

Abstract

Additional file 1: Figure S1. Comparison of the FLEXITau assay to AT100 staining. A Average area covered by AT100 during disease progression in the cortex of both mouse models (mean +- SD). B Pearson correlation analyses of the absolute amount of insoluble Tau derived from the FLEXITau assay and the area covered by AT100 in the cortex of the P301S model. Comparison was performed between the two brain hemispheres of the same animal. C Pearson correlation analyses of the absolute amount of insoluble Tau derived from the FLEXITau assay and the area covered by AT100 in the cortex of the P301L model. Comparison was performed between the two brain hemispheres of the same animal.

Published
2023
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20. Assessment of cholesterol homeostasis in the living human brain

Author

Haider, Ahmed, primary, Zhao, Chunyu, additional, Wang, Lu, additional, Xiao, Zhiwei, additional, Rong, Jian, additional, Xia, Xiaotian, additional, Chen, Zhen, additional, Pfister, Stefanie K., additional, Mast, Natalia, additional, Yutuc, Eylan, additional, Chen, Jiahui, additional, Li, Yinlong, additional, Shao, Tuo, additional, Warnock, Geoffrey I., additional, Dawoud, Alyaa, additional, Connors, Theresa R., additional, Oakley, Derek H., additional, Wei, Huiyi, additional, Wang, Jinghao, additional, Zheng, Zhihua, additional, Xu, Hao, additional, Davenport, April T., additional, Daunais, James B., additional, Van, Richard S., additional, Shao, Yihan, additional, Wang, Yuqin, additional, Zhang, Ming-Rong, additional, Gebhard, Catherine, additional, Pikuleva, Irina, additional, Levey, Allan I., additional, Griffiths, William J., additional, and Liang, Steven H., additional

Published
2022
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21. Assessment of cholesterol homeostasis in the living human brain

Author

Haider, Ahmed, Zhao, Chunyu, Wang, Lu, Xiao, Zhiwei, Rong, Jian, Xia, Xiaotian, Chen, Zhen, Pfister, Stefanie K, Mast, Natalia, Yutuc, Eylan, Chen, Jiahui, Li, Yinlong, Shao, Tuo, Warnock, Geoffrey I, Dawoud, Alyaa, Connors, Theresa R, Oakley, Derek H, Wei, Huiyi, Wang, Jinghao, Zheng, Zhihua, Xu, Hao, Davenport, April T, Daunais, James B, Van, Richard S, Shao, Yihan, Wang, Yuqin, Zhang, Ming-Rong, Gebhard, Catherine, Pikuleva, Irina, Levey, Allan I, et al, and University of Zurich

Subjects
610 Medicine & health, 10181 Clinic for Nuclear Medicine, 2700 General Medicine
Published
2022

22. Common mouse models of tauopathy reflect early but not late human disease

Author

Wenger, Kathrin, primary, Viode, Arthur, additional, Schlaffner, Christoph N., additional, Zalm, Patrick van, additional, Cheng, Long, additional, Dellovade, Tammy, additional, Langlois, Xavier, additional, Bannon, Anthony, additional, Connors, Theresa R., additional, Oakley, Derek, additional, Renard, Bernhard, additional, Rappsilber, Juri, additional, Hyman, Bradley, additional, Steen, Hanno, additional, and Steen, Judith, additional

Published
2022
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23. Regional variability and genotypic and pharmacodynamic effects on PrP concentration in the CNS

Author

Mortberg, Meredith A., primary, Zhao, Hien T., additional, Reidenbach, Andrew G., additional, Gentile, Juliana E., additional, Kuhn, Eric, additional, O’Moore, Jill, additional, Dooley, Patrick M., additional, Connors, Theresa R., additional, Mazur, Curt, additional, Allen, Shona W., additional, Trombetta, Bianca A., additional, McManus, Alison, additional, Moore, Matthew R., additional, Liu, Jiewu, additional, Cabin, Deborah E., additional, Kordasiewicz, Holly B., additional, Mathews, Joel, additional, Arnold, Steven E., additional, Vallabh, Sonia M., additional, and Minikel, Eric Vallabh, additional

Published
2022
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25. Novel genetic variants in MAPT and alterations in tau phosphorylation in amyotrophic lateral sclerosis post‐mortem motor cortex and cerebrospinal fluid

Author

Petrozziello, Tiziana, primary, Amaral, Ana C., additional, Dujardin, Simon, additional, Farhan, Sali M. K., additional, Chan, James, additional, Trombetta, Bianca A., additional, Kivisäkk, Pia, additional, Mills, Alexandra N., additional, Bordt, Evan A., additional, Kim, Spencer E., additional, Dooley, Patrick M., additional, Commins, Caitlin, additional, Connors, Theresa R., additional, Oakley, Derek H., additional, Ghosal, Anubrata, additional, Gomez‐Isla, Teresa, additional, Hyman, Bradley T., additional, Arnold, Steven E., additional, Spires‐Jones, Tara, additional, Cudkowicz, Merit E., additional, Berry, James D., additional, and Sadri‐Vakili, Ghazaleh, additional

Published
2021
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26. PrP concentration in the central nervous system: regional variability, genotypic effects, and pharmacodynamic impact

Author

Mortberg, Meredith A, primary, Zhao, Hien T, additional, Reidenbach, Andrew G, additional, Gentile, Juliana E, additional, Kuhn, Eric, additional, O’Moore, Jill, additional, Dooley, Patrick M, additional, Connors, Theresa R, additional, Mazur, Curt, additional, Allen, Shona W, additional, Trombetta, Bianca A, additional, McManus, Alison, additional, Moore, Matthew R, additional, Liu, Jiewu, additional, Cabin, Deborah E, additional, Kordasiewicz, Holly B, additional, Mathews, Joel, additional, Arnold, Steven E, additional, Vallabh, Sonia M, additional, and Minikel, Eric Vallabh, additional

Published
2021
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27. Novel genetic variants in MAPT and alterations in tau phosphorylation in amyotrophic lateral sclerosis post‐mortem motor cortex and cerebrospinal fluid.

Author

Petrozziello, Tiziana, Amaral, Ana C., Dujardin, Simon, Farhan, Sali M. K., Chan, James, Trombetta, Bianca A., Kivisäkk, Pia, Mills, Alexandra N., Bordt, Evan A., Kim, Spencer E., Dooley, Patrick M., Commins, Caitlin, Connors, Theresa R., Oakley, Derek H., Ghosal, Anubrata, Gomez‐Isla, Teresa, Hyman, Bradley T., Arnold, Steven E., Spires‐Jones, Tara, and Cudkowicz, Merit E.

Subjects
AMYOTROPHIC lateral sclerosis, MOTOR cortex, MOTOR neuron diseases, CEREBROSPINAL fluid, NEUROFIBRILLARY tangles, GENETIC variation, TAU proteins
Abstract

Although the molecular mechanisms underlying amyotrophic lateral sclerosis (ALS) are not yet fully understood, several studies report alterations in tau phosphorylation in both sporadic and familial ALS. Recently, we have demonstrated that phosphorylated tau at S396 (pTau‐S396) is mislocalized to synapses in ALS motor cortex (mCTX) and contributes to mitochondrial dysfunction. Here, we demonstrate that while there was no overall increase in total tau, pTau‐S396, and pTau‐S404 in ALS post‐mortem mCTX, total tau and pTau‐S396 were increased in C9ORF72‐ALS. Additionally, there was a significant decrease in pTau‐T181 in ALS mCTX compared controls. Furthermore, we leveraged the ALS Knowledge Portal and Project MinE data sets and identified ALS‐specific genetic variants across MAPT, the gene encoding tau. Lastly, assessment of cerebrospinal fluid (CSF) samples revealed a significant increase in total tau levels in bulbar‐onset ALS together with a decrease in CSF pTau‐T181:tau ratio in all ALS samples, as reported previously. While increases in CSF tau levels correlated with a faster disease progression as measured by the revised ALS functional rating scale (ALSFRS‐R), decreases in CSF pTau‐T181:tau ratio correlated with a slower disease progression, suggesting that CSF total tau and pTau‐T181 ratio may serve as biomarkers of disease in ALS. Our findings highlight the potential role of pTau‐T181 in ALS, as decreases in CSF pTau‐T181:tau ratio may reflect the significant decrease in pTau‐T181 in post‐mortem mCTX. Taken together, these results indicate that tau phosphorylation is altered in ALS post‐mortem mCTX as well as in CSF and, importantly, the newly described pathogenic or likely pathogenic variants identified in MAPT in this study are adjacent to T181 and S396 phosphorylation sites further highlighting the potential role of these tau functional domains in ALS. Although the molecular mechanisms underlying amyotrophic lateral sclerosis (ALS) are not yet fully understood, recent studies report alterations in tau phosphorylation in ALS. Our study builds on these findings and demonstrates that tau phosphorylation is altered in post‐mortem ALS motor cortex and highlights new and ALS‐specific variants in MAPT, the gene encoding tau. Lastly, we report alterations in phosphorylated tau in ALS cerebrospinal fluid that may function as a predictive biomarker for ALS. [ABSTRACT FROM AUTHOR]

Published
2022
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28. Machine learning of dissection photographs and surface scanning for quantitative 3D neuropathology.

Author

Gazula H, Tregidgo HFJ, Billot B, Balbastre Y, William-Ramirez J, Herisse R, Deden-Binder LJ, Casamitjana A, Melief EJ, Latimer CS, Kilgore MD, Montine M, Robinson E, Blackburn E, Marshall MS, Connors TR, Oakley DH, Frosch MP, Young SI, Van Leemput K, Dalca AV, FIschl B, Mac Donald CL, Keene CD, Hyman BT, and Iglesias JE

Abstract

We present open-source tools for 3D analysis of photographs of dissected slices of human brains, which are routinely acquired in brain banks but seldom used for quantitative analysis. Our tools can: (i) 3D reconstruct a volume from the photographs and, optionally, a surface scan; and (ii) produce a high-resolution 3D segmentation into 11 brain regions per hemisphere (22 in total), independently of the slice thickness. Our tools can be used as a substitute for ex vivo magnetic resonance imaging (MRI), which requires access to an MRI scanner, ex vivo scanning expertise, and considerable financial resources. We tested our tools on synthetic and real data from two NIH Alzheimer's Disease Research Centers. The results show that our methodology yields accurate 3D reconstructions, segmentations, and volumetric measurements that are highly correlated to those from MRI. Our method also detects expected differences between post mortem confirmed Alzheimer's disease cases and controls. The tools are available in our widespread neuroimaging suite "FreeSurfer" ( https://surfer.nmr.mgh.harvard.edu/fswiki/PhotoTools ).

Published
2024
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29. Age-dependent increase in tau phosphorylation at serine 396 in Huntington's disease pre-frontal cortex.

Author

Petrozziello T, Huntress SS, Castillo-Torres AL, Quinn JP, Connors TR, Auger CA, Mills AN, Kim SE, Liu S, Mahmood F, Boudi A, Wu M, Sapp E, Kivisäkk P, Sunderesh SR, Pouladi MA, Arnold SE, Hyman BT, Rosas HD, DiFiglia M, Pinto RM, Kegel-Gleason K, and Sadri-Vakili G

Abstract

Background: To date, it is still controversial whether tau phosphorylation plays a role in Huntington's disease (HD), as previous studies demonstrated either no alterations or increases in phosphorylated tau (pTau) in HD post-mortem brain and mouse models., Objectives: The goal of this study was to determine whether total tau and pTau levels are altered in HD., Methods: Immunohistochemistry, cellular fractionations, and western blots were used to measure tau and pTau levels in a large cohort of HD and control post-mortem prefrontal cortex (PFC). Furthermore, western blots were performed to assess tau, and pTau levels in HD and control isogenic embryonic stem cell (ESC)-derived cortical neurons and neuronal stem cells (NSCs). Similarly, western blots were used to assess tau and pTau in Htt Q111 and transgenic R6/2 mice. Lastly, total tau levels were assessed in HD and healthy control plasma using Quanterix Simoa assay., Results: Our results revealed that, while there was no difference in tau or pTau levels in HD PFC compared to controls, tau phosphorylated at S396 levels were increased in PFC samples from HD patients 60 years or older at time of death. Additionally, tau and pTau levels were not changed in HD ESC-derived cortical neurons and NSCs. Similarly, tau or pTau levels were not altered in Htt Q111 and transgenic R6/2 mice compared to wild-type littermates. Lastly, tau levels were not changed in plasma from a small cohort of HD patients compared to controls., Conclusion: Together these findings demonstrate that pTau-S396 levels increase significantly with age in HD PFC.

Published
2023
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30. Creating the Pick's disease International Consortium: Association study of MAPT H2 haplotype with risk of Pick's disease.

Author

Valentino RR, Scotton WJ, Roemer SF, Lashley T, Heckman MG, Shoai M, Martinez-Carrasco A, Tamvaka N, Walton RL, Baker MC, Macpherson HL, Real R, Soto-Beasley AI, Mok K, Revesz T, Warner TT, Jaunmuktane Z, Boeve BF, Christopher EA, DeTure M, Duara R, Graff-Radford NR, Josephs KA, Knopman DS, Koga S, Murray ME, Lyons KE, Pahwa R, Parisi JE, Petersen RC, Whitwell J, Grinberg LT, Miller B, Schlereth A, Seeley WW, Spina S, Grossman M, Irwin DJ, Lee EB, Suh E, Trojanowski JQ, Van Deerlin VM, Wolk DA, Connors TR, Dooley PM, Frosch MP, Oakley DH, Aldecoa I, Balasa M, Gelpi E, Borrego-Écija S, de Eugenio Huélamo RM, Gascon-Bayarri J, Sánchez-Valle R, Sanz-Cartagena P, Piñol-Ripoll G, Molina-Porcel L, Bigio EH, Flanagan ME, Gefen T, Rogalski EJ, Weintraub S, Redding-Ochoa J, Chang K, Troncoso JC, Prokop S, Newell KL, Ghetti B, Jones M, Richardson A, Robinson AC, Roncaroli F, Snowden J, Allinson K, Green O, Rowe JB, Singh P, Beach TG, Serrano GE, Flowers XE, Goldman JE, Heaps AC, Leskinen SP, Teich AF, Black SE, Keith JL, Masellis M, Bodi I, King A, Sarraj SA, Troakes C, Halliday GM, Hodges JR, Kril JJ, Kwok JB, Piguet O, Gearing M, Arzberger T, Roeber S, Attems J, Morris CM, Thomas AJ, Evers BM, White CL, Mechawar N, Sieben AA, Cras PP, De Vil BB, De Deyn PPPP, Duyckaerts C, Le Ber I, Seihean D, Turbant-Leclere S, MacKenzie IR, McLean C, Cykowski MD, Ervin JF, Wang SJ, Graff C, Nennesmo I, Nagra RM, Riehl J, Kovacs GG, Giaccone G, Nacmias B, Neumann M, Ang LC, Finger EC, Blauwendraat C, Nalls MA, Singleton AB, Vitale D, Cunha C, Carvalho A, Wszolek ZK, Morris HR, Rademakers R, Hardy JA, Dickson DW, Rohrer JD, and Ross OA

Abstract

Background: Pick's disease (PiD) is a rare and predominantly sporadic form of frontotemporal dementia that is classified as a primary tauopathy. PiD is pathologically defined by argyrophilic inclusion Pick bodies and ballooned neurons in the frontal and temporal brain lobes. PiD is characterised by the presence of Pick bodies which are formed from aggregated, hyperphosphorylated, 3-repeat tau proteins, encoded by the MAPT gene. The MAPT H2 haplotype has consistently been associated with a decreased disease risk of the 4-repeat tauopathies of progressive supranuclear palsy and corticobasal degeneration, however its role in susceptibility to PiD is unclear. The primary aim of this study was to evaluate the association between MAPT H2 and risk of PiD., Methods: We established the Pick's disease International Consortium (PIC) and collected 338 (60.7% male) pathologically confirmed PiD brains from 39 sites worldwide. 1,312 neurologically healthy clinical controls were recruited from Mayo Clinic Jacksonville, FL (N=881) or Rochester, MN (N=431). For the primary analysis, subjects were directly genotyped for MAPT H1-H2 haplotype-defining variant rs8070723. In secondary analysis, we genotyped and constructed the six-variant MAPT H1 subhaplotypes (rs1467967, rs242557, rs3785883, rs2471738, rs8070723, and rs7521)., Findings: Our primary analysis found that the MAPT H2 haplotype was associated with increased risk of PiD (OR: 1.35, 95% CI: 1.12-1.64 P=0.002). In secondary analysis involving H1 subhaplotypes, a protective association with PiD was observed for the H1f haplotype (0.0% vs. 1.2%, P=0.049), with a similar trend noted for H1b (OR: 0.76, 95% CI: 0.58-1.00, P=0.051). The 4-repeat tauopathy risk haplotype MAPT H1c was not associated with PiD susceptibility (OR: 0.93, 95% CI: 0.70-1.25, P=0.65)., Interpretation: The PIC represents the first opportunity to perform relatively large-scale studies to enhance our understanding of the pathobiology of PiD. This study demonstrates that in contrast to its protective role in 4R tauopathies, the MAPT H2 haplotype is associated with an increased risk of PiD. This finding is critical in directing isoform-related therapeutics for tauopathies., Competing Interests: M.A.N. and D.V.’s participation in this project was part of a competitive contract awarded to Data Tecnica International LLC by the National Institutes of Health to support open science research. M.A.N. also currently serves on the scientific advisory board for Character Bio Inc. and Neuron23 Inc.

Published
2023
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