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101. Moderate‐Severe Traumatic Brain Injury History and Chronic Traumatic Encephalopathy Neuropathology in Brain Donors Exposed to Repetitive Head Impacts

Author

Culhane, Julia E, primary, Abdolmohammadi, Bobak, additional, Nair, Evan S, additional, Saltiel, Nicole, additional, Tripodis, Yorghos, additional, Martin, Brett M, additional, Palmisano, Joseph, additional, Katz, Douglas I, additional, Dwyer, Brigid, additional, Daneshvar, Daniel H, additional, Goldstein, Lee E, additional, Dams‐O'Connor, Kristen, additional, Kowall, Neil W, additional, Stern, Robert A, additional, Huber, Bertrand R., additional, Stein, Thor D., additional, Mez, Jesse B., additional, McKee, Ann C., additional, and Alosco, Michael L, additional

Published
2022
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102. Leveraging American football helmet accelerometer data to estimate associations between cumulative repetitive head impact exposure and chronic traumatic encephalopathy

Author

Nair, Evan S, primary, Daneshvar, Daniel H, additional, Rasch, Abigail, additional, Abdolmohammadi, Bobak, additional, Saltiel, Nicole, additional, Uretsky, Madeline, additional, Shah, Arsal, additional, Baucom, Zachary H., additional, Martin, Brett M, additional, Palmisano, Joseph, additional, Cherry, Jonathan D, additional, Alvarez, Victor E., additional, Huber, Bertrand R., additional, Alosco, Michael L, additional, Tripodis, Yorghos, additional, Crary, John F., additional, Stein, Thor D., additional, McKee, Ann C., additional, and Mez, Jesse B., additional

Published
2022
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103. Volumetric Characterization of Microvasculature in Ex Vivo Human Brain Samples By Serial Sectioning Optical Coherence Tomography

Author

Yang, Jiarui, primary, Chang, Shuaibin, additional, Chen, Ichun Anderson, additional, Kura, Sreekanth, additional, Rosen, Grace A., additional, Saltiel, Nicole A., additional, Huber, Bertrand R., additional, Varadarajan, Divya, additional, Balbastre, Yael, additional, Magnain, Caroline, additional, Chen, Shih-chi, additional, Fischl, Bruce, additional, McKee, Ann C., additional, Boas, David A., additional, and Wang, Hui, additional

Published
2022
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105. Neuroimmune proteins can differentiate between tauopathies

Author

Cherry, Jonathan D., primary, Baucom, Zach H., additional, Eppich, Kaleb G., additional, Kirsch, Daniel, additional, Dixon, Erin R., additional, Tripodis, Yorghos, additional, Bieniek, Kevin F., additional, Farrell, Kurt, additional, Whitney, Kristen, additional, Uretsky, Madeline, additional, Crary, John F., additional, Dickson, Dennis, additional, and McKee, Ann C., additional

Published
2022
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106. Association of APOE Genotypes and Chronic Traumatic Encephalopathy

Author

Atherton, Kathryn, primary, Han, Xudong, additional, Chung, Jaeyoon, additional, Cherry, Jonathan D., additional, Baucom, Zachary, additional, Saltiel, Nicole, additional, Nair, Evan, additional, Abdolmohammadi, Bobak, additional, Uretsky, Madeline, additional, Khan, Mohammed Muzamil, additional, Shea, Conor, additional, Durape, Shruti, additional, Martin, Brett M., additional, Palmisano, Joseph N., additional, Farrell, Kurt, additional, Nowinski, Christopher J., additional, Alvarez, Victor E., additional, Dwyer, Brigid, additional, Daneshvar, Daniel H., additional, Katz, Douglas I., additional, Goldstein, Lee E., additional, Cantu, Robert C., additional, Kowall, Neil W., additional, Alosco, Michael L., additional, Huber, Bertrand R., additional, Tripodis, Yorghos, additional, Crary, John F., additional, Farrer, Lindsay, additional, Stern, Robert A., additional, Stein, Thor D., additional, McKee, Ann C., additional, and Mez, Jesse, additional

Published
2022
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110. Concussion, microvascular injury, and early tauopathy in young athletes after impact head injury and an impact concussion mouse model

Author

Tagge, Chad A, Fisher, Andrew M, Minaeva, Olga V, Gaudreau-Balderrama, Amanda, Moncaster, Juliet A, Zhang, Xiao-Lei, Wojnarowicz, Mark W, Casey, Noel, Lu, Haiyan, Kokiko-Cochran, Olga N, Saman, Sudad, Ericsson, Maria, Onos, Kristen D, Veksler, Ronel, Senatorov, Vladimir V, Jr, Kondo, Asami, Zhou, Xiao Z, Miry, Omid, Vose, Linnea R, Gopaul, Katisha R, Upreti, Chirag, Nowinski, Christopher J, Cantu, Robert C, Alvarez, Victor E, Hildebrandt, Audrey M, Franz, Erich S, Konrad, Janusz, Hamilton, James A, Hua, Ning, Tripodis, Yorghos, Anderson, Andrew T, Howell, Gareth R, Kaufer, Daniela, Hall, Garth F, Lu, Kun P, Ransohoff, Richard M, Cleveland, Robin O, Kowall, Neil W, Stein, Thor D, Lamb, Bruce T, Huber, Bertrand R, Moss, William C, Friedman, Alon, Stanton, Patric K, McKee, Ann C, and Goldstein, Lee E

Published
2018
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111. Flortaucipir tau PET in former American football players.

Author

Su, Yi, Protas, Hillary D., Luo, Ji, Chen, Kewei, Alosco, Michael L, Adler, Charles, Balcer, Laura, Bernick, Charles B., Au, Rhoda, Banks, Sarah J, Barr, William, Coleman, Michael J, Dodick, David W., Katz, Douglas I, Marek, Kenneth, Mariani, Megan, McClean, Michael D, McKee, Ann C., Mez, Jesse B., and Daneshvar, Daniel H

Abstract

Background: Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease thought to be caused, in part, by repetitive head impact (RHI) exposure and characterized by phosphorylated tau deposition with varying patterns in the cerebral cortex. Flortaucipir tau PET data from the DIAGNOSE CTE Research Project was examined to investigate tau PET patterns and its relation to RHI exposure in former professional and college American football players. Method: In this study, 218 DIAGNOSE CTE participants, ages 45‐74, with flortaucipir PET were included; 104 were former National Football League players (PRO), 58 were former college football players (COL), and 56 had no history of contact sports, other exposure to RHI, or traumatic brain injury (UE). Regional flortaucipir uptake was quantified using established procedures for three previously defined statistical regions (superior frontal, left parietal, and medial temporal) and compared across the three groups. Association analyses were also performed to examine the relationship between flortaucipir uptake and exposure to RHI using the cumulative head impact index for linear acceleration g‐force (CHII‐G). The potential clinical utility of flortaucipir PET for CTE was also investigated by examining its ability to differentiate participants meeting criteria for traumatic encephalopathy syndrome (TES) and probable or possible level of certainty for CTE pathology from those who do not meet those criteria. Result: Significantly higher flortaucipir uptake was observed in former football players than in participants without RHI exposure, controlling for age and race for the superior frontal region (Fig. 1A), left parietal, and medial temporal regions. Association between regional flortaucipir uptake and CHII‐G was only observed in the superior frontal region in former players (PRO+COL) 60 years and older (Fig. 1B) and no association was observed in the full PRO+COL group. Flortaucipir PET was not able to differentiate TES groups in former football players (Fig. 1C). Conclusion: Elevated flortaucipir uptake was observed in former American football players to a group of unexposed men. The association between flortaucipir uptake and exposure to RHI may require a long latent period to manifest. Further investigation of more sensitive tau PET tracers and quantification techniques is warranted to better characterize CTE related tau pathology. [ABSTRACT FROM AUTHOR]

Published
2023
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112. Florbetapir amyloid PET in cognitively impaired former professional and college American football players.

Author

Stern, Robert A, Trujillo‐Rodriguez, Diana, Tripodis, Yorghos, Pulukuri, Surya V, Alosco, Michael L, Adler, Charles, Balcer, Laura, Bernick, Charles B., Baucom, Zachary H., Marek, Kenneth, McClean, Michael D, Johnson, Keith A., McKee, Ann C., Stein, Thor D., Mez, Jesse B., Palmisano, Joseph N, Cummings, Jeffrey L., Shenton, Martha E, and Reiman, Eric M.

Abstract

Background: Repetitive head impact (RHI) exposure from the routine play of American football increases the risk of later‐life cognitive impairment and dementia from the neurodegenerative disease, chronic traumatic encephalopathy (CTE). Although neuropathological studies of CTE have found comorbid neurodegenerative and other pathologies, neuritic Aβ plaques are infrequent, particularly in early stages. However, amyloid PET imaging has not been fully characterized in cognitively impaired former American football players. Method: In this cross‐sectional, observational cohort study from the DIAGNOSE CTE Research Project, florbetapir PET mean cortical standard uptake value ratios (SUVR) and positivity (defined by average SUVR >1.10, indicative of moderate‐to‐frequent neuritic Aβ plaques), were analyzed in 119 former professional (PRO) National Football League players, 60 former college football players (COL), and 58 men unexposed (UE) to RHI who were cognitively asymptomatic. Former players were categorized into one of four diagnostic groups: cognitively normal (CN), subjective memory complaints (SMC), mild cognitive impairment (MCI), and dementia (DEM). All participants were 45‐74 yo. Multivariable linear and logistic regressions were conducted, with race, education, age, and APOE4 genotype included as covariates. A priori power calculations demonstrated adequate power to detect significant findings Result: No differences between the three exposure groups in average florbetapir SUVR or proportion of elevated florbetapir uptake were found. Pairwise group comparisons resulted in no differences in average SUVR between PRO and COL (‐0.01, 95% CI [‐0.033, 0.025], p = 0.95), PRO and UE (0.02, 95% CI [‐0.010, 0.029], p = 0.41), and COL and UE (0.02, 95% CI [0.0004, 0.039], p = 0.36). Analysis of covariance resulted in no differences among diagnostic groups (F = 0.94, p = 0.43). Neither years of playing football nor measures of cognition and daily functioning showed significant associations with florbetapir SUVR. Conclusion: Former professional and college American football players with cognitive impairment and dementia did not have elevated florbetapir amyloid PET compared to a group of men without RHI exposure. Their rates of florbetapir positivity in the football players were lower than expected for a group of men this age. These findings suggest that cognitive impairment in former elite football players may not be due to Alzheimer's disease pathology. [ABSTRACT FROM AUTHOR]

Published
2023
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113. Author Correction: Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing

Author

Kunkle, Brian W., Grenier-Boley, Benjamin, Sims, Rebecca, Bis, Joshua C., Damotte, Vincent, Naj, Adam C., Boland, Anne, Vronskaya, Maria, van der Lee, Sven J., Amlie-Wolf, Alexandre, Bellenguez, Céline, Frizatti, Aura, Chouraki, Vincent, Martin, Eden R., Sleegers, Kristel, Badarinarayan, Nandini, Jakobsdottir, Johanna, Hamilton-Nelson, Kara L., Moreno-Grau, Sonia, Olaso, Robert, Raybould, Rachel, Chen, Yuning, Kuzma, Amanda B., Hiltunen, Mikko, Morgan, Taniesha, Ahmad, Shahzad, Vardarajan, Badri N., Epelbaum, Jacques, Hoffmann, Per, Boada, Merce, Beecham, Gary W., Garnier, Jean-Guillaume, Harold, Denise, Fitzpatrick, Annette L., Valladares, Otto, Moutet, Marie-Laure, Gerrish, Amy, Smith, Albert V., Qu, Liming, Bacq, Delphine, Denning, Nicola, Jian, Xueqiu, Zhao, Yi, Del Zompo, Maria, Fox, Nick C., Choi, Seung-Hoan, Mateo, Ignacio, Hughes, Joseph T., Adams, Hieab H., Malamon, John, Sanchez-Garcia, Florentino, Patel, Yogen, Brody, Jennifer A., Dombroski, Beth A., Naranjo, Maria Candida Deniz, Daniilidou, Makrina, Eiriksdottir, Gudny, Mukherjee, Shubhabrata, Wallon, David, Uphill, James, Aspelund, Thor, Cantwell, Laura B., Garzia, Fabienne, Galimberti, Daniela, Hofer, Edith, Butkiewicz, Mariusz, Fin, Bertrand, Scarpini, Elio, Sarnowski, Chloe, Bush, Will S., Meslage, Stéphane, Kornhuber, Johannes, White, Charles C., Song, Yuenjoo, Barber, Robert C., Engelborghs, Sebastiaan, Sordon, Sabrina, Voijnovic, Dina, Adams, Perrie M., Vandenberghe, Rik, Mayhaus, Manuel, Cupples, L. Adrienne, Albert, Marilyn S., De Deyn, Peter P., Gu, Wei, Himali, Jayanadra J., Beekly, Duane, Squassina, Alessio, Hartmann, Annette M., Orellana, Adelina, Blacker, Deborah, Rodriguez-Rodriguez, Eloy, Lovestone, Simon, Garcia, Melissa E., Doody, Rachelle S., Munoz-Fernadez, Carmen, Sussams, Rebecca, Lin, Honghuang, Fairchild, Thomas J., Benito, Yolanda A., Holmes, Clive, Karamujić-Čomić, Hata, Frosch, Matthew P., Thonberg, Hakan, Maier, Wolfgang, Roshchupkin, Gennady, Ghetti, Bernardino, Giedraitis, Vilmantas, Kawalia, Amit, Li, Shuo, Huebinger, Ryan M., Kilander, Lena, Moebus, Susanne, Hernández, Isabel, Kamboh, M. Ilyas, Brundin, RoseMarie, Turton, James, Yang, Qiong, Katz, Mindy J., Concari, Letizia, Lord, Jenny, Beiser, Alexa S., Keene, C. Dirk, Helisalmi, Seppo, Kloszewska, Iwona, Kukull, Walter A., Koivisto, Anne Maria, Lynch, Aoibhinn, Tarraga, Lluís, Larson, Eric B., Haapasalo, Annakaisa, Lawlor, Brian, Mosley, Thomas H., Lipton, Richard B., Solfrizzi, Vincenzo, Gill, Michael, Longstreth, Jr, W. T., Montine, Thomas J., Frisardi, Vincenza, Diez-Fairen, Monica, Rivadeneira, Fernando, Petersen, Ronald C., Deramecourt, Vincent, Alvarez, Ignacio, Salani, Francesca, Ciaramella, Antonio, Boerwinkle, Eric, Reiman, Eric M., Fievet, Nathalie, Rotter, Jerome I., Reisch, Joan S., Hanon, Olivier, Cupidi, Chiara, Uitterlinden, A. G. Andre, Royall, Donald R., Dufouil, Carole, Maletta, Raffaele Giovanni, de Rojas, Itziar, Sano, Mary, Brice, Alexis, Cecchetti, Roberta, George-Hyslop, Peter St, Ritchie, Karen, Tsolaki, Magda, Tsuang, Debby W., Dubois, Bruno, Craig, David, Wu, Chuang-Kuo, Soininen, Hilkka, Avramidou, Despoina, Albin, Roger L., Fratiglioni, Laura, Germanou, Antonia, Apostolova, Liana G., Keller, Lina, Koutroumani, Maria, Arnold, Steven E., Panza, Francesco, Gkatzima, Olymbia, Asthana, Sanjay, Hannequin, Didier, Whitehead, Patrice, Atwood, Craig S., Caffarra, Paolo, Hampel, Harald, Quintela, Inés, Carracedo, Ángel, Lannfelt, Lars, Rubinsztein, David C., Barnes, Lisa L., Pasquier, Florence, Frölich, Lutz, Barral, Sandra, McGuinness, Bernadette, Beach, Thomas G., Johnston, Janet A., Becker, James T., Passmore, Peter, Bigio, Eileen H., Schott, Jonathan M., Bird, Thomas D., Warren, Jason D., Boeve, Bradley F., Lupton, Michelle K., Bowen, James D., Proitsi, Petra, Boxer, Adam, Powell, John F., Burke, James R., Kauwe, John S. K., Burns, Jeffrey M., Mancuso, Michelangelo, Buxbaum, Joseph D., Bonuccelli, Ubaldo, Cairns, Nigel J., McQuillin, Andrew, Cao, Chuanhai, Livingston, Gill, Carlson, Chris S., Bass, Nicholas J., Carlsson, Cynthia M., Hardy, John, Carney, Regina M., Bras, Jose, Carrasquillo, Minerva M., Guerreiro, Rita, Allen, Mariet, Chui, Helena C., Fisher, Elizabeth, Masullo, Carlo, Crocco, Elizabeth A., DeCarli, Charles, Bisceglio, Gina, Dick, Malcolm, Ma, Li, Duara, Ranjan, Graff-Radford, Neill R., Evans, Denis A., Hodges, Angela, Faber, Kelley M., Scherer, Martin, Fallon, Kenneth B., Riemenschneider, Matthias, Fardo, David W., Heun, Reinhard, Farlow, Martin R., Kölsch, Heike, Ferris, Steven, Leber, Markus, Foroud, Tatiana M., Heuser, Isabella, Galasko, Douglas R., Giegling, Ina, Gearing, Marla, Hüll, Michael, Geschwind, Daniel H., Gilbert, John R., Morris, John, Green, Robert C., Mayo, Kevin, Growdon, John H., Feulner, Thomas, Hamilton, Ronald L., Harrell, Lindy E., Drichel, Dmitriy, Honig, Lawrence S., Cushion, Thomas D., Huentelman, Matthew J., Hollingworth, Paul, Hulette, Christine M., Hyman, Bradley T., Marshall, Rachel, Jarvik, Gail P., Meggy, Alun, Abner, Erin, Menzies, Georgina E., Jin, Lee-Way, Leonenko, Ganna, Real, Luis M., Jun, Gyungah R., Baldwin, Clinton T., Grozeva, Detelina, Karydas, Anna, Russo, Giancarlo, Kaye, Jeffrey A., Kim, Ronald, Jessen, Frank, Kowall, Neil W., Vellas, Bruno, Kramer, Joel H., Vardy, Emma, LaFerla, Frank M., Jöckel, Karl-Heinz, Lah, James J., Dichgans, Martin, Leverenz, James B., Mann, David, Levey, Allan I., Pickering-Brown, Stuart, Lieberman, Andrew P., Klopp, Norman, Lunetta, Kathryn L., Wichmann, H-Erich, Lyketsos, Constantine G., Morgan, Kevin, Marson, Daniel C., Brown, Kristelle, Martiniuk, Frank, Medway, Christopher, Mash, Deborah C., Nöthen, Markus M., Masliah, Eliezer, Hooper, Nigel M., McCormick, Wayne C., Daniele, Antonio, McCurry, Susan M., Bayer, Anthony, McDavid, Andrew N., Gallacher, John, McKee, Ann C., van den Bussche, Hendrik, Mesulam, Marsel, Brayne, Carol, Miller, Bruce L., Riedel-Heller, Steffi, Miller, Carol A., Miller, Joshua W., Al-Chalabi, Ammar, Morris, John C., Shaw, Christopher E., Myers, Amanda J., Wiltfang, Jens, O’Bryant, Sid, Olichney, John M., Alvarez, Victoria, Parisi, Joseph E., Singleton, Andrew B., Paulson, Henry L., Collinge, John, Perry, William R., Mead, Simon, Peskind, Elaine, Cribbs, David H., Rossor, Martin, Pierce, Aimee, Ryan, Natalie S., Poon, Wayne W., Nacmias, Benedetta, Potter, Huntington, Sorbi, Sandro, Quinn, Joseph F., Sacchinelli, Eleonora, Raj, Ashok, Spalletta, Gianfranco, Raskind, Murray, Caltagirone, Carlo, Bossù, Paola, Orfei, Maria Donata, Reisberg, Barry, Clarke, Robert, Reitz, Christiane, Smith, A David, Ringman, John M., Warden, Donald, Roberson, Erik D., Wilcock, Gordon, Rogaeva, Ekaterina, Bruni, Amalia Cecilia, Rosen, Howard J., Gallo, Maura, Rosenberg, Roger N., Ben-Shlomo, Yoav, Sager, Mark A., Mecocci, Patrizia, Saykin, Andrew J., Pastor, Pau, Cuccaro, Michael L., Vance, Jeffery M., Schneider, Julie A., Schneider, Lori S., Slifer, Susan, Seeley, William W., Smith, Amanda G., Sonnen, Joshua A., Spina, Salvatore, Stern, Robert A., Swerdlow, Russell H., Tang, Mitchell, Tanzi, Rudolph E., Trojanowski, John Q., Troncoso, Juan C., Van Deerlin, Vivianna M., Van Eldik, Linda J., Vinters, Harry V., Vonsattel, Jean Paul, Weintraub, Sandra, Welsh-Bohmer, Kathleen A., Wilhelmsen, Kirk C., Williamson, Jennifer, Wingo, Thomas S., Woltjer, Randall L., Wright, Clinton B., Yu, Chang-En, Yu, Lei, Saba, Yasaman, Alzheimer Disease Genetics Consortium (ADGC), The European Alzheimer’s Disease Initiative (EADI), Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (CHARGE), Genetic and Environmental Risk in AD/Defining Genetic, Polygenic and Environmental Risk for Alzheimer’s Disease Consortium (GERAD/PERADES), Pilotto, Alberto, Bullido, Maria J., Peters, Oliver, Crane, Paul K., Bennett, David, Bosco, Paola, Coto, Eliecer, Boccardi, Virginia, De Jager, Phil L., Lleo, Alberto, Warner, Nick, Lopez, Oscar L., Ingelsson, Martin, Deloukas, Panagiotis, Cruchaga, Carlos, Graff, Caroline, Gwilliam, Rhian, Fornage, Myriam, Goate, Alison M., Sanchez-Juan, Pascual, Kehoe, Patrick G., Amin, Najaf, Ertekin-Taner, Nilifur, Berr, Claudine, Debette, Stéphanie, Love, Seth, Launer, Lenore J., Younkin, Steven G., Dartigues, Jean-Francois, Corcoran, Chris, Ikram, M. Arfan, Dickson, Dennis W., Nicolas, Gael, Campion, Dominique, Tschanz, JoAnn, Schmidt, Helena, Hakonarson, Hakon, Clarimon, Jordi, Munger, Ron, Schmidt, Reinhold, Farrer, Lindsay A., Van Broeckhoven, Christine, O’Donovan, Michael C., DeStefano, Anita L., Jones, Lesley, Haines, Jonathan L., Deleuze, Jean-Francois, Owen, Michael J., Gudnason, Vilmundur, Mayeux, Richard, Escott-Price, Valentina, Psaty, Bruce M., Ramirez, Alfredo, Wang, Li-San, Ruiz, Agustin, van Duijn, Cornelia M., Holmans, Peter A., Seshadri, Sudha, Williams, Julie, Amouyel, Phillippe, Schellenberg, Gerard D., Lambert, Jean-Charles, and Pericak-Vance, Margaret A.

Published
2019
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114. The Spectrum of Disease in Chronic Traumatic Encephalopathy

Author

McKee, Ann C., Stein, Thor D., and Nowinski, Christopher J.

Abstract

Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behaviour. Eighteen age- and gender-matched individuals without a history of repetitive mild traumatic brain injury served as control subjects. In chronic traumatic encephalopathy, the spectrum of hyperphosphorylated tau pathology ranged in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including the medial temporal lobe, thereby allowing a progressive staging of pathology from stages I-IV. Multifocal axonal varicosities and axonal loss were found in deep cortex and subcortical white matter at all stages of chronic traumatic encephalopathy. TAR DNA-binding protein 43 immunoreactive inclusions and neurites were also found in 85% of cases, ranging from focal pathology in stages I-III to widespread inclusions and neurites in stage IV. Symptoms in stage I chronic traumatic encephalopathy included headache and loss of attention and concentration. Additional symptoms in stage II included depression, explosivity and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and in stage IV, dementia, word-finding difficulty and aggression were characteristic. Data on athletic exposure were available for 34 American football players; the stage of chronic traumatic encephalopathy correlated with increased duration of football play, survival after football and age at death. Chronic traumatic encephalopathy was the sole diagnosis in 43 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lobar degeneration (6%). There is an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in chronic traumatic encephalopathy that occurs in conjunction with widespread axonal disruption and loss. The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein. (Contains 4 tables and 6 figures.)

Published
2013
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117. White matter hyperintensities in former American football players.

Author

Alosco, Michael L., Tripodis, Yorghos, Baucom, Zachary H., Adler, Charles H., Balcer, Laura J., Bernick, Charles, Mariani, Megan L., Au, Rhoda, Banks, Sarah J., Barr, William B., Wethe, Jennifer V., Cantu, Robert C., Coleman, Michael J., Dodick, David W., McClean, Michael D., McKee, Ann C., Mez, Jesse, Palmisano, Joseph N., Martin, Brett, and Hartlage, Kaitlin

Abstract

Introduction: The presentation, risk factors, and etiologies of white matter hyperintensities (WMH) in people exposed to repetitive head impacts are unknown. We examined the burden and distribution of WMH, and their association with years of play, age of first exposure, and clinical function in former American football players. Methods: A total of 149 former football players and 53 asymptomatic unexposed participants (all men, 45–74 years) completed fluid‐attenuated inversion recovery magnetic resonance imaging, neuropsychological testing, and self‐report neuropsychiatric measures. Lesion Segmentation Toolbox estimated WMH. Analyses were performed in the total sample and stratified by age 60. Results: In older but not younger participants, former football players had greater total, frontal, temporal, and parietal log‐WMH compared to asymptomatic unexposed men. In older but not younger former football players, greater log‐WMH was associated with younger age of first exposure to football and worse executive function. Discussion: In older former football players, WMH may have unique presentations, risk factors, and etiologies. Highlights: Older but not younger former football players had greater total, frontal, temporal, and parietal lobe white matter hyperintensities (WMH) compared to same‐age asymptomatic unexposed men.Younger age of first exposure to football was associated with greater WMH in older but not younger former American football players.In former football players, greater WMH was associated with worse executive function and verbal memory. [ABSTRACT FROM AUTHOR]

Published
2023
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118. Associations between near end-of-life flortaucipir PET and postmortem CTE-related tau neuropathology in six former American football players

Author

Alosco, Michael L, Su, Yi, Stein, Thor D, Protas, Hillary, Cherry, Jonathan D, Adler, Charles H, Balcer, Laura J, Bernick, Charles, Pulukuri, Surya Vamsi, Abdolmohammadi, Bobak, Coleman, Michael J, Palmisano, Joseph N, Tripodis, Yorghos, Mez, Jesse, Rabinovici, Gil D, Marek, Kenneth L, Beach, Thomas G, Johnson, Keith A, Huber, Bertrand Russell, Koerte, Inga, Lin, Alexander P, Bouix, Sylvain, Cummings, Jeffrey L, Shenton, Martha E, Reiman, Eric M, McKee, Ann C, Stern, Robert A, and DIAGNOSE C. T. E. Research Project

Subjects
Traumatic, Aging, Physical Injury - Accidents and Adverse Effects, DIAGNOSE C. T. E. Research Project, Clinical Sciences, Football, tau Proteins, Neurodegenerative, Neurodegenerative disease, Alzheimer's Disease, Chronic Traumatic Encephalopathy, Alzheimer Disease, Acquired Cognitive Impairment, Humans, Positron emission tomography imaging, Flortaucipir, Neurosciences, Brain, Repetitive head impacts, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Brain Disorders, Death, Other Physical Sciences, Nuclear Medicine & Medical Imaging, Positron-Emission Tomography, Brain Injuries, Neurological, Dementia, Autopsy, Tau, Biomarkers
Abstract

PurposeFlourine-18-flortaucipir tau positron emission tomography (PET) was developed for the detection for Alzheimer's disease. Human imaging studies have begun to investigate its use in chronic traumatic encephalopathy (CTE). Flortaucipir-PET to autopsy correlation studies in CTE are needed for diagnostic validation. We examined the association between end-of-life flortaucipir PET and postmortem neuropathological measurements of CTE-related tau in six former American football players.MethodsThree former National Football League players and three former college football players who were part of the DIAGNOSE CTE Research Project died and agreed to have their brains donated. The six players had flortaucipir (tau) and florbetapir (amyloid) PET prior to death. All brains from the deceased participants were neuropathologically evaluated for the presence of CTE. On average, the participants were 59.0 (SD = 9.32) years of age at time of PET. PET scans were acquired 20.33 (SD = 13.08) months before their death. Using Spearman correlation analyses, we compared flortaucipir standard uptake value ratios (SUVRs) to digital slide-based AT8 phosphorylated tau (p-tau) density in a priori selected composite cortical, composite limbic, and thalamic regions-of-interest (ROIs).ResultsFour brain donors had autopsy-confirmed CTE, all with high stage disease (n = 3 stage III, n = 1 stage IV). Three of these four met criteria for the clinical syndrome of CTE, known as traumatic encephalopathy syndrome (TES). Two did not have CTE at autopsy and one of these met criteria for TES. Concomitant pathology was only present in one of the non-CTE cases (Lewy body) and one of the CTE cases (motor neuron disease). There was a strong association between flortaucipir SUVRs and p-tau density in the composite cortical (ρ = 0.71) and limbic (ρ = 0.77) ROIs. Although there was a strong association in the thalamic ROI (ρ = 0.83), this is a region with known off-target binding. SUVRs were modest and CTE and non-CTE cases had overlapping SUVRs and discordant p-tau density for some regions.ConclusionsFlortaucipir-PET could be useful for detecting high stage CTE neuropathology, but specificity to CTE p-tau is uncertain. Off-target flortaucipir binding in the hippocampus and thalamus complicates interpretation of these associations. In vivo biomarkers that can detect the specific p-tau of CTE across the disease continuum are needed.

Published
2022

121. Utility of the ALSFRS‐R for predicting ALS and comorbid disease neuropathology: The Veterans Affairs Biorepository Brain Bank

Author

Colvin, Leigh E., primary, Foster, Zachariah W., additional, Stein, Thor D., additional, Thakore‐James, Manisha, additional, Salajegheh, Mohammad Kian, additional, Carr, Kendall, additional, Spencer, Keith R., additional, Abdul Rauf, Nazifa, additional, Adams, Latease, additional, Averill, James G., additional, Walker, Sean E., additional, Robey, Ian, additional, Alvarez, Victor E., additional, Huber, Bertrand R., additional, McKee, Ann C., additional, Kowall, Neil W., additional, and Brady, Christopher B., additional

Published
2022
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122. MicroRNA Alterations in Chronic Traumatic Encephalopathy and Amyotrophic Lateral Sclerosis

Author

Alvia, Marcela, primary, Aytan, Nurgul, additional, Spencer, Keith R., additional, Foster, Zachariah W., additional, Rauf, Nazifa Abdul, additional, Guilderson, Latease, additional, Robey, Ian, additional, Averill, James G., additional, Walker, Sean E., additional, Alvarez, Victor E., additional, Huber, Bertrand R., additional, Mathais, Rebecca, additional, Cormier, Kerry A., additional, Nicks, Raymond, additional, Pothast, Morgan, additional, Labadorf, Adam, additional, Agus, Filisia, additional, Alosco, Michael L., additional, Mez, Jesse, additional, Kowall, Neil W., additional, McKee, Ann C., additional, Brady, Christopher B., additional, and Stein, Thor D., additional

Published
2022
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123. Ante-mortem plasma phosphorylated tau (181) predicts Alzheimer’s disease neuropathology and regional tau at autopsy

Author

Morrison, Madeline S, primary, Aparicio, Hugo J, additional, Blennow, Kaj, additional, Zetterberg, Henrik, additional, Ashton, Nicholas J, additional, Karikari, Thomas K, additional, Tripodis, Yorghos, additional, Martin, Brett, additional, Palmisano, Joseph N, additional, Sugarman, Michael A, additional, Frank, Brandon, additional, Steinberg, Eric G, additional, Turk, Katherine W, additional, Budson, Andrew E, additional, Au, Rhoda, additional, Goldstein, Lee E, additional, Jun, Gyungah R, additional, Kowall, Neil W, additional, Killiany, Ronald, additional, Qiu, Wei Qiao, additional, Stern, Robert A, additional, Mez, Jesse, additional, McKee, Ann C, additional, Stein, Thor D, additional, and Alosco, Michael L, additional

Published
2022
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126. Additional file 1 of Neuroimmune proteins can differentiate between tauopathies

Author

Cherry, Jonathan D., Baucom, Zach H., Eppich, Kaleb G., Kirsch, Daniel, Dixon, Erin R., Tripodis, Yorghos, Bieniek, Kevin F., Farrell, Kurt, Whitney, Kristen, Uretsky, Madeline, Crary, John F., Dickson, Dennis, and McKee, Ann C.

Abstract

Additional file 1: Figure S1. CCL21 is still elevated in the CTE CSF in the male subset of cases. To determine if gender was driving the CSF related CCL21 elevation, only males from the CTE and AD groups were compared. Although the AD male sample size was reduced to 5 cases, CCL21 concentrations still trended towards significant increases in CTE as measured with a Mann–Whitney test. Each dot represents 1 case. Error bars represent mean ± SEM.

Published
2022
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127. Additional file 4 of A comparison between tau and amyloid-�� cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease

Author

Turk, Katherine W., Geada, Alexandra, Alvarez, Victor E., Xia, Weiming, Cherry, Jonathan D., Nicks, Raymond, Meng, Gaoyuan, Daley, Sarah, Tripodis, Yorghos, Huber, Bertrand R., Budson, Andrew E., Dwyer, Brigid, Kowall, Neil W., Cantu, Robert C., Goldstein, Lee E., Katz, Douglas I., Stern, Robert A., Alosco, Michael L., Mez, Jesse, McKee, Ann C., and Stein, Thor D.

Abstract

Additional file 4: Table e-1. Estimated Marginal Means and SEM in parentheses for rank normalized CSF analyte measurements from No CTE/no AD (control) group; showing ANCOVA adjusted for age, p

Published
2022
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129. Additional file 1 of A comparison between tau and amyloid-�� cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease

Author

Turk, Katherine W., Geada, Alexandra, Alvarez, Victor E., Xia, Weiming, Cherry, Jonathan D., Nicks, Raymond, Meng, Gaoyuan, Daley, Sarah, Tripodis, Yorghos, Huber, Bertrand R., Budson, Andrew E., Dwyer, Brigid, Kowall, Neil W., Cantu, Robert C., Goldstein, Lee E., Katz, Douglas I., Stern, Robert A., Alosco, Michael L., Mez, Jesse, McKee, Ann C., and Stein, Thor D.

Abstract

Additional file 1. Supplemental results

Published
2022
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131. Additional file 1 of Interpretable deep learning of myelin histopathology in age-related cognitive impairment

Author

McKenzie, Andrew T., Marx, Gabriel A., Koenigsberg, Daniel, Sawyer, Mary, Iida, Megan A., Walker, Jamie M., Richardson, Timothy E., Campanella, Gabriele, Attems, Johannes, McKee, Ann C., Stein, Thor D., Fuchs, Thomas J., White, Charles L., Farrell, Kurt, and Crary, John F.

Abstract

Additional file 1: Figure S1 Annotation procedure of blue hue ranges in Luxol fast blue, hematoxylin, and eosin-stained tiles. Representative tiles show the annotation method used for positive pixel counting in the Luxol fast blue, hematoxylin, and eosin (LH&E) stained histology tiles. For the annotation heatmap, the darker blue pixel range is highlighted as red while the lighter blue pixel range is highlighted as light blue. Figure S2 Correlation of slide-level probability estimates of cognitive impairment in matched brain donors between the two brain regions. Scatter plots showing the probability estimates of cognitive impairment by the top-performing models in the same brain donors between WSIs in the hippocampus and frontal cortex data sets. The blue line shows predictions from a linear model and grey error envelopes show 95% confidence intervals for the linear model. Figure S3 Scatterplot matrix of deep histopathology features with clinicopathologic features in the frontal cortex. Correlation analysis of deep histopathology results and clinicopathologic features: age, Braak score, ARTAG positivity in the hippocampus (coded as 0 = not present and 1 = present), cognitive label (coded as 0 = not cognitively impaired and 1 = cognitively impaired), probability of cognitive impairment as predicted by the top-performing model trained on the frontal cortex data, and median LFB staining intensity (pixel counts) in the top attention tiles in the frontal cortex data set. Upper right: rank correlation values and associated p-values (* = p < 0.05, ** = p < 0.01, *** = p < 0.001). Diagonal: histograms of variables. Lower left: Scatterplots with linear model trend lines for the variable pairs (red lines) and 95% confidence intervals (blue envelopes). This plot was made using the R package GGally (v. 2.1.2). CI = Cognitive impairment; ARTAG = Aging-related tau astrogliopathy; LFB = Luxol Fast Blue.

Published
2022
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134. Antibody against early driver of neurodegeneration cis P-tau blocks brain injury and tauopathy

Author

Kondo, Asami, Shahpasand, Koorosh, Mannix, Rebekah, Qiu, Jianhua, Moncaster, Juliet, Chen, Chun-Hau, Yao, Yandan, Lin, Yu-Min, Driver, Jane A., Sun, Yan, Wei, Shuo, Luo, Man-Li, Albayram, Onder, Huang, Pengyu, Rotenberg, Alexander, Ryo, Akihide, Goldstein, Lee E., Pascual-Leone, Alvaro, McKee, Ann C., Meehan, William, Zhou, Xiao Zhen, and Lu, Kun Ping

Subjects
Nerve degeneration -- Care and treatment, Antibodies -- Usage -- Health aspects, Tau proteins -- Health aspects, Brain injuries -- Care and treatment, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Traumatic brain injury (TBI), characterized by acute neurological dysfunction, is one of the best known environmental risk factors for chronic traumatic encephalopathy and Alzheimer's disease, the defining pathologic features of which include tauopathy made of phosphorylated tau protein (P-tau). However, tauopathy has not been detected in the early stages after TBI, and how TBI leads to tauopathy is unknown. Here we find robust cis P-tau pathology after TBI in humans and mice. After TBI in mice and stress in vitro, neurons acutely produce cis P-tau, which disrupts axonal microtubule networks and mitochondrial transport, spreads to other neurons, and leads to apoptosis. This process, which we term 'cistauosis', appears long before other tauopathy. Treating TBI mice with cis antibody blocks cistauosis, prevents tauopathy development and spread, and restores many TBI-related structural and functional sequelae. Thus, cis P-tau is a major early driver of disease after TBI and leads to tauopathy in chronic traumatic encephalopathy and Alzheimer's disease. The cis antibody may be further developed to detect and treat TBI, and prevent progressive neurodegeneration after injury., Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults (1), and in the USA approximately 2.5 million people suffer TBI each year [...]

Published
2015

135. Beta-amyloid deposition in chronic traumatic encephalopathy

Author

Stein, Thor D., Montenigro, Philip H., Alvarez, Victor E., Xia, Weiming, Crary, John F., Tripodis, Yorghos, Daneshvar, Daniel H., Mez, Jesse, Solomon, Todd, Meng, Gaoyuan, Kubilus, Caroline A., Cormier, Kerry A., Meng, Steven, Babcock, Katharine, Kiernan, Patrick, Murphy, Lauren, Nowinski, Christopher J., Martin, Brett, Dixon, Diane, Stern, Robert A., Cantu, Robert C., Kowall, Neil W., and McKee, Ann C.

Published
2015
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137. Erratum to Letters to the Editor regarding: The Second NINDS/NIBIB Consensus Meeting to Define Neuropathological Criteria for the Diagnosis of Chronic Traumatic Encephalopathy. J Neuropathol Exp Neurol 2021;80(3):210–9

Author

Glass, Jonathan D, primary, Hammers, Jennifer L, additional, Omalu, Bennet L, additional, Bieniek, Kevin F, additional, Crary, John F, additional, Dickson, Dennis W, additional, Stein, Thor D, additional, Mez, Jesse, additional, Alosco, Michael E, additional, and McKee, Ann C, additional

Published
2022
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138. Imaging post-mortem neurodegenerative human brains with serial sectioning optical coherence tomography

Author

Yang, Jiarui, primary, Chang, Shuaibin, additional, Rosen, Grace A., additional, Saltiel, Nicole A., additional, Wang, Hui, additional, Magnain, Caroline, additional, Chen, Shih-chi, additional, Fischl, Bruce, additional, Huber, Bertrand R., additional, McKee, Ann C., additional, Chen, Ichun Anderson, additional, and Boas, David A., additional

Published
2022
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144. Incidence of and Mortality From Amyotrophic Lateral Sclerosis in National Football League Athletes

Author

Daneshvar, Daniel H., primary, Mez, Jesse, additional, Alosco, Michael L., additional, Baucom, Zachary H., additional, Mahar, Ian, additional, Baugh, Christine M., additional, Valle, Jhaqueline P., additional, Weuve, Jennifer, additional, Paganoni, Sabrina, additional, Cantu, Robert C., additional, Zafonte, Ross D., additional, Stern, Robert A., additional, Stein, Thor D., additional, Tripodis, Yorghos, additional, Nowinski, Christopher J., additional, and McKee, Ann C., additional

Published
2021
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145. Plasma p‐tau 181 shows stronger network association to Alzheimer's disease dementia than neurofilament light and total tau

Author

Frank, Brandon, primary, Ally, Madeline, additional, Brekke, Bailee, additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Sugarman, Michael A., additional, Ashton, Nicholas J., additional, Karikari, Thomas K., additional, Tripodis, Yorghos, additional, Martin, Brett, additional, Palmisano, Joseph N., additional, Steinberg, Eric G., additional, Simkina, Irene, additional, Turk, Katherine W., additional, Budson, Andrew E., additional, O'Connor, Maureen K., additional, Au, Rhoda, additional, Goldstein, Lee E., additional, Jun, Gyungah R., additional, Kowall, Neil W., additional, Stein, Thor D., additional, McKee, Ann C., additional, Killiany, Ronald, additional, Qiu, Wei Qiao, additional, Stern, Robert A., additional, Mez, Jesse, additional, and Alosco, Michael L., additional

Published
2021
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146. Tau phosphorylation sites serine202 and serine396 are differently altered in chronic traumatic encephalopathy and Alzheimer's disease

Author

Stathas, SpiroAnthony, primary, Alvarez, Victor E., additional, Xia, Weiming, additional, Nicks, Raymond, additional, Meng, Gaoyuan, additional, Daley, Sarah, additional, Pothast, Morgan, additional, Shah, Arsal, additional, Kelley, Hunter, additional, Esnault, Camille, additional, McCormack, Robert, additional, Dixon, Erin, additional, Fishbein, Lucas, additional, Cherry, Jonathan D., additional, Huber, Bertrand R., additional, Tripodis, Yorghos, additional, Alosco, Michael L., additional, Mez, Jesse, additional, McKee, Ann C., additional, and Stein, Thor D., additional

Published
2021
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147. Plasma P‐tau181 and NfL are central nodes in a network of diagnostic, biomarker, and demographic data

Author

Frank, Brandon E., primary, Ally, Madeline, additional, Brekke, Bailee, additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Sugarman, Michael, additional, Ashton, Nicholas J., additional, Karikari, Thomas K., additional, Tripodis, Yorghos, additional, McKee, Ann C., additional, Stein, Thor D., additional, Martin, Brett M., additional, Palmisano, Joseph, additional, Steinberg, Eric, additional, Simkin, Irene, additional, Turk, Katherine W., additional, Budson, Andrew, additional, O'Connor, Maureen K., additional, Au, Rhoda, additional, Qiu, Wendy, additional, Goldstein, Lee E., additional, Killiany, Ronald J., additional, Kowall, Neil W., additional, Mez, Jesse, additional, Stern, Robert A., additional, and Alosco, Michael L., additional

Published
2021
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148. A comparison between tau and amyloid‐b cerebrospinal fluid biomarkers in chronic traumatic encephalopathy and Alzheimer disease

Author

Turk, Katherine W., primary, Geada, Alexandra W., additional, Alvarez, Victor E., additional, Xia, Weiming, additional, Cherry, Jonathan D., additional, Huber, Bertrand R., additional, Mez, Jesse, additional, Alosco, Michael L., additional, Meng, Gaoyuan, additional, Nicks, Raymond W., additional, Tripodis, Yorghos, additional, Budson, Andrew, additional, Dwyer, Brigid, additional, Kowall, Neil W., additional, Cantu, Robert, additional, Goldstein, Lee E., additional, Katz, Douglas I., additional, Stern, Robert A., additional, McKee, Ann C., additional, and Stein, Thor D., additional

Published
2021
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149. Long‐term effects of repetitive head impacts on gray matter cortical thickness

Author

Brekke, Bailee, primary, DeVivo, Renee, additional, McKee, Ann C., additional, Stein, Thor D., additional, Tripodis, Yorghos, additional, Phelps, Alyssa, additional, Weller, Jason, additional, Martin, Brett M, additional, Palmisano, Joseph, additional, Steinberg, Eric, additional, Turk, Katherine W, additional, Budson, Andrew, additional, O'Connor, Maureen K, additional, Au, Rhoda, additional, Qiu, Wendy, additional, Goldstein, Lee E, additional, Kowall, Neil W, additional, Stern, Robert A, additional, Killiany, Ronald J, additional, Mez, Jesse, additional, and Alosco, Michael L, additional

Published
2021
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150. Genome-wide association study and functional validation implicates JADE1 in tauopathy

Author

Farrell, Kurt, primary, Kim, SoongHo, additional, Han, Natalia, additional, Iida, Megan A., additional, Gonzalez, Elias M., additional, Otero-Garcia, Marcos, additional, Walker, Jamie M., additional, Richardson, Timothy E., additional, Renton, Alan E., additional, Andrews, Shea J., additional, Fulton-Howard, Brian, additional, Humphrey, Jack, additional, Vialle, Ricardo A., additional, Bowles, Kathryn R., additional, de Paiva Lopes, Katia, additional, Whitney, Kristen, additional, Dangoor, Diana K., additional, Walsh, Hadley, additional, Marcora, Edoardo, additional, Hefti, Marco M., additional, Casella, Alicia, additional, Sissoko, Cheick T., additional, Kapoor, Manav, additional, Novikova, Gloriia, additional, Udine, Evan, additional, Wong, Garrett, additional, Tang, Weijing, additional, Bhangale, Tushar, additional, Hunkapiller, Julie, additional, Ayalon, Gai, additional, Graham, Robert R., additional, Cherry, Jonathan D., additional, Cortes, Etty P., additional, Borukov, Valeriy Y., additional, McKee, Ann C., additional, Stein, Thor D., additional, Vonsattel, Jean-Paul, additional, Teich, Andy F., additional, Gearing, Marla, additional, Glass, Jonathan, additional, Troncoso, Juan C., additional, Frosch, Matthew P., additional, Hyman, Bradley T., additional, Dickson, Dennis W., additional, Murray, Melissa E., additional, Attems, Johannes, additional, Flanagan, Margaret E., additional, Mao, Qinwen, additional, Mesulam, M.-Marsel, additional, Weintraub, Sandra, additional, Woltjer, Randy L., additional, Pham, Thao, additional, Kofler, Julia, additional, Schneider, Julie A., additional, Yu, Lei, additional, Purohit, Dushyant P., additional, Haroutunian, Vahram, additional, Hof, Patrick R., additional, Gandy, Sam, additional, Sano, Mary, additional, Beach, Thomas G., additional, Poon, Wayne, additional, Kawas, Claudia H., additional, Corrada, María M., additional, Rissman, Robert A., additional, Metcalf, Jeff, additional, Shuldberg, Sara, additional, Salehi, Bahar, additional, Nelson, Peter T., additional, Trojanowski, John Q., additional, Lee, Edward B., additional, Wolk, David A., additional, McMillan, Corey T., additional, Keene, C. Dirk, additional, Latimer, Caitlin S., additional, Montine, Thomas J., additional, Kovacs, Gabor G., additional, Lutz, Mirjam I., additional, Fischer, Peter, additional, Perrin, Richard J., additional, Cairns, Nigel J., additional, Franklin, Erin E., additional, Cohen, Herbert T., additional, Raj, Towfique, additional, Cobos, Inma, additional, Frost, Bess, additional, Goate, Alison, additional, White III, Charles L., additional, and Crary, John F., additional

Published
2021
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