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Trabalho de evento-resumo periodico
Neurobiological basis of sleep disturbances in tauopathies: human wake-promoting neurons degenerate more in Alzheimer’s disease (2019)
Oh, Jun; Eser, Rana A.; Ehrenberg, Alexander J.; Morales, Dulce; Petersen, Cathrine; Theofilas, Panos; Resende, Elisa; Cosme, Celica; Seeley, William W.; Spina, Salvatore; Walsh, Christine M.; Neylan, Thomas C.; Miller, Bruce L.; Bittencourt, Jackson Cioni ; Grinberg, Lea Tenenholz
Source: Sleep. Conference titles: Annual Meeting of the Associated Professional Sleep Societies. XIV Sleep and Neurodegeration. Unidades: ICB, FM
Subjects: ANATOMIA, TRANSTORNOS DO SONO, DOENÇA DE ALZHEIMER, DOENÇAS NEURODEGENERATIVAS, IMUNOHISTOQUÍMICA, NEURÔNIOS, SONO
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ABNT
OH, Jun et al. Neurobiological basis of sleep disturbances in tauopathies: human wake-promoting neurons degenerate more in Alzheimer’s disease. Sleep. North Carolina: Oxford University Press. Disponível em: https://doi.org/10.1093/sleep/zsz067.302. Acesso em: 10 nov. 2024. , 2019
APA
Oh, J., Eser, R. A., Ehrenberg, A. J., Morales, D., Petersen, C., Theofilas, P., et al. (2019). Neurobiological basis of sleep disturbances in tauopathies: human wake-promoting neurons degenerate more in Alzheimer’s disease. Sleep. North Carolina: Oxford University Press. doi:10.1093/sleep/zsz067.302
NLM
Oh J, Eser RA, Ehrenberg AJ, Morales D, Petersen C, Theofilas P, Resende E, Cosme C, Seeley WW, Spina S, Walsh CM, Neylan TC, Miller BL, Bittencourt JC, Grinberg LT. Neurobiological basis of sleep disturbances in tauopathies: human wake-promoting neurons degenerate more in Alzheimer’s disease [Internet]. Sleep. 2019 ; 42 A-123-124.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1093/sleep/zsz067.302
Vancouver
Oh J, Eser RA, Ehrenberg AJ, Morales D, Petersen C, Theofilas P, Resende E, Cosme C, Seeley WW, Spina S, Walsh CM, Neylan TC, Miller BL, Bittencourt JC, Grinberg LT. Neurobiological basis of sleep disturbances in tauopathies: human wake-promoting neurons degenerate more in Alzheimer’s disease [Internet]. Sleep. 2019 ; 42 A-123-124.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1093/sleep/zsz067.302
Artigo de periodico
In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology (2014)
Caso, Francesca; Mandelli, Maria Luisa; Henry, Maya; Gesierich, Benno; Bettcher, Brianne M.; Ogar, Jennifer; Filippi, Massimo; Comi, Giancarlo; Magnani, Giuseppe; Sidhu, Manu; Trojanowski, John Q.; Huang, Eric J.; Grinberg, Lea T.; Miller, Bruce L.; Dronkers, Nina; Seeley, William W.; Gorno-Tempini, Maria Luisa
Source: Neurology. Unidade: FM
Subjects: COGNIÇÃO (ANORMALIDADES), AFASIA PROGRESSIVA, AGRAMATISMO
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ABNT
CASO, Francesca et al. In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology. Neurology, v. 82, n. 3, p. 239-247, 2014Tradução . . Disponível em: https://doi.org/10.1212/WNL.0000000000000031. Acesso em: 10 nov. 2024.
APA
Caso, F., Mandelli, M. L., Henry, M., Gesierich, B., Bettcher, B. M., Ogar, J., et al. (2014). In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology. Neurology, 82( 3), 239-247. doi:10.1212/WNL.0000000000000031
NLM
Caso F, Mandelli ML, Henry M, Gesierich B, Bettcher BM, Ogar J, Filippi M, Comi G, Magnani G, Sidhu M, Trojanowski JQ, Huang EJ, Grinberg LT, Miller BL, Dronkers N, Seeley WW, Gorno-Tempini ML. In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology [Internet]. Neurology. 2014 ; 82( 3): 239-247.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1212/WNL.0000000000000031
Vancouver
Caso F, Mandelli ML, Henry M, Gesierich B, Bettcher BM, Ogar J, Filippi M, Comi G, Magnani G, Sidhu M, Trojanowski JQ, Huang EJ, Grinberg LT, Miller BL, Dronkers N, Seeley WW, Gorno-Tempini ML. In vivo signatures of nonfluent/agrammatic primary progressive aphasia caused by FTLD pathology [Internet]. Neurology. 2014 ; 82( 3): 239-247.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1212/WNL.0000000000000031
Artigo de periodico
TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia (2014)
Blitterswijk, Marka van; Mullen, Bianca; Nicholson, Alexandra M.; Bieniek, Kevin F.; Heckman, Michael G.; Baker, Matthew C.; DeJesus‑Hernandez, Mariely; Finch, NiCole A.; Brown, Patricia H.; Murray, Melissa E.; Hsiung, Ging‑Yuek R.; Stewart, Heather; Karydas, Anna M.; Finger, Elizabeth; Kertesz, Andrew; Bigio, Eileen H.; Weintraub, Sandra; Mesulam, Marsel; Hatanpaa, Kimmo J.; White III, Charles L.; Strong, Michael J.; Beach, Thomas G.; Wszolek, Zbigniew K.; Lippa, Carol; Caselli, Richard; Petrucelli, Leonard; Josephs, Keith A.; Parisi, Joseph E.; Knopman, David S.; Petersen, Ronald C.; Mackenzie, Ian R.; Seeley, William W.; Grinberg, Lea T.; Miller, Bruce L.; Boylan, Kevin B.; Graff‑Radford, Neill R.; Boeve, Bradley F.; Dickson, Dennis W.; Rademakers, Rosa
Source: Acta Neuropathologica. Unidade: FM
Subjects: POLIMORFISMO, DOENÇAS NEURODEGENERATIVAS (ETIOLOGIA), MUTAÇÃO GENÉTICA, DEMÊNCIA
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ABNT
BLITTERSWIJK, Marka van et al. TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia. Acta Neuropathologica, v. 127, n. 3, p. 397-406, 2014Tradução . . Disponível em: http://link.springer.com/article/10.1007/s00401-013-1240-4. Acesso em: 10 nov. 2024.
APA
Blitterswijk, M. van, Mullen, B., Nicholson, A. M., Bieniek, K. F., Heckman, M. G., Baker, M. C., et al. (2014). TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia. Acta Neuropathologica, 127( 3), 397-406. doi:10.1007/s00401-013-1240-4
NLM
Blitterswijk M van, Mullen B, Nicholson AM, Bieniek KF, Heckman MG, Baker MC, DeJesus‑Hernandez M, Finch NCA, Brown PH, Murray ME, Hsiung G‑YR, Stewart H, Karydas AM, Finger E, Kertesz A, Bigio EH, Weintraub S, Mesulam M, Hatanpaa KJ, White III CL, Strong MJ, Beach TG, Wszolek ZK, Lippa C, Caselli R, Petrucelli L, Josephs KA, Parisi JE, Knopman DS, Petersen RC, Mackenzie IR, Seeley WW, Grinberg LT, Miller BL, Boylan KB, Graff‑Radford NR, Boeve BF, Dickson DW, Rademakers R. TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia [Internet]. Acta Neuropathologica. 2014 ; 127( 3): 397-406.[citado 2024 nov. 10 ] Available from: http://link.springer.com/article/10.1007/s00401-013-1240-4
Vancouver
Blitterswijk M van, Mullen B, Nicholson AM, Bieniek KF, Heckman MG, Baker MC, DeJesus‑Hernandez M, Finch NCA, Brown PH, Murray ME, Hsiung G‑YR, Stewart H, Karydas AM, Finger E, Kertesz A, Bigio EH, Weintraub S, Mesulam M, Hatanpaa KJ, White III CL, Strong MJ, Beach TG, Wszolek ZK, Lippa C, Caselli R, Petrucelli L, Josephs KA, Parisi JE, Knopman DS, Petersen RC, Mackenzie IR, Seeley WW, Grinberg LT, Miller BL, Boylan KB, Graff‑Radford NR, Boeve BF, Dickson DW, Rademakers R. TMEM106B protects C9ORF72 expansion carriers against frontotemporal dementia [Internet]. Acta Neuropathologica. 2014 ; 127( 3): 397-406.[citado 2024 nov. 10 ] Available from: http://link.springer.com/article/10.1007/s00401-013-1240-4
Artigo de periodico
Practical utility of amyloid and FDG-PET in an academic dementia center (2014)
Sánchez-Juan, Pascual; Ghosh, Pia M.; Hagen, Jayne; Gesierich, Benno; Henry, Maya; Grinberg, Lea T.; O'Neil, James P.; Janabi, Mustafa; Huang, Eric J.; Trojanowski, John Q.; Vinters, Harry V.; Gorno-Tempini, Marilu; Seeley, William W.; Boxer, Adam L.; Rosen, Howard J.; Kramer, Joel H.; Miller, Bruce L.; Jagust, William J.; Rabinovici, Gil D.
Source: Neurology. Unidade: FM
Subjects: DEMÊNCIA, DIAGNÓSTICO POR IMAGEM, DOENÇAS DEGENERATIVAS
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ABNT
SÁNCHEZ-JUAN, Pascual et al. Practical utility of amyloid and FDG-PET in an academic dementia center. Neurology, v. 82, n. 3, p. 230-238, 2014Tradução . . Disponível em: https://doi.org/10.1212/WNL.0000000000000032. Acesso em: 10 nov. 2024.
APA
Sánchez-Juan, P., Ghosh, P. M., Hagen, J., Gesierich, B., Henry, M., Grinberg, L. T., et al. (2014). Practical utility of amyloid and FDG-PET in an academic dementia center. Neurology, 82( 3), 230-238. doi:10.1212/WNL.0000000000000032
NLM
Sánchez-Juan P, Ghosh PM, Hagen J, Gesierich B, Henry M, Grinberg LT, O'Neil JP, Janabi M, Huang EJ, Trojanowski JQ, Vinters HV, Gorno-Tempini M, Seeley WW, Boxer AL, Rosen HJ, Kramer JH, Miller BL, Jagust WJ, Rabinovici GD. Practical utility of amyloid and FDG-PET in an academic dementia center [Internet]. Neurology. 2014 ; 82( 3): 230-238.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1212/WNL.0000000000000032
Vancouver
Sánchez-Juan P, Ghosh PM, Hagen J, Gesierich B, Henry M, Grinberg LT, O'Neil JP, Janabi M, Huang EJ, Trojanowski JQ, Vinters HV, Gorno-Tempini M, Seeley WW, Boxer AL, Rosen HJ, Kramer JH, Miller BL, Jagust WJ, Rabinovici GD. Practical utility of amyloid and FDG-PET in an academic dementia center [Internet]. Neurology. 2014 ; 82( 3): 230-238.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1212/WNL.0000000000000032
Artigo de periodico
Progranulin Mutations as Risk Factors for Alzheimer Disease (2013)
Perry, David C.; Lehmann, Manja; Yokoyama, Jennifer S.; Karydas, Anna; Lee, Jason JiYong; Coppola, Giovanni; Grinberg, Lea T.; Geschwind, Dan; Seeley, William W.; Miller, Bruce L.; Rosen, Howard; Rabinovici, Gil
Source: JAMA Neurology. Unidade: FM
Subjects: FATORES DE RISCO, DOENÇAS NEURODEGENERATIVAS, DOENÇA DE ALZHEIMER, MUTAÇÃO GENÉTICA
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ABNT
PERRY, David C. et al. Progranulin Mutations as Risk Factors for Alzheimer Disease. JAMA Neurology, v. 70, n. 6, p. 774-778, 2013Tradução . . Disponível em: https://doi.org/10.1001/2013.jamaneurol.393. Acesso em: 10 nov. 2024.
APA
Perry, D. C., Lehmann, M., Yokoyama, J. S., Karydas, A., Lee, J. J. Y., Coppola, G., et al. (2013). Progranulin Mutations as Risk Factors for Alzheimer Disease. JAMA Neurology, 70( 6), 774-778. doi:10.1001/2013.jamaneurol.393
NLM
Perry DC, Lehmann M, Yokoyama JS, Karydas A, Lee JJY, Coppola G, Grinberg LT, Geschwind D, Seeley WW, Miller BL, Rosen H, Rabinovici G. Progranulin Mutations as Risk Factors for Alzheimer Disease [Internet]. JAMA Neurology. 2013 ; 70( 6): 774-778.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1001/2013.jamaneurol.393
Vancouver
Perry DC, Lehmann M, Yokoyama JS, Karydas A, Lee JJY, Coppola G, Grinberg LT, Geschwind D, Seeley WW, Miller BL, Rosen H, Rabinovici G. Progranulin Mutations as Risk Factors for Alzheimer Disease [Internet]. JAMA Neurology. 2013 ; 70( 6): 774-778.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1001/2013.jamaneurol.393
Artigo de periodico
TDP-43 frontotemporal lobar degeneration and autoimmune disease (2013)
Miller, Zachary A.; Rankin, Katherine P.; Graff-Radford, Neill R.; Takada, Leonel T.; Sturm, Virginia E.; Cleveland, Clare M.; Criswell, Lindsey A.; Jaeger, Philipp A.; Stan, Trisha; Heggeli, Kristin A.; Hsu, Sandy Chan; Karydas, Anna; Khan, Baber K.; Grinberg, Lea T.; Gorno-Tempini, Maria Luisa; Boxer, Adam L.; Rosen, Howard J.; Kramer, Joel H.; Coppola, Giovanni; Geschwind, Daniel H.; Rademakers, Rosa; Seeley, William W.; Wyss-Coray, Tony; Miller, Bruce L.
Source: Journal of Neurology, Neurosurgery and Psychiatry. Unidade: FM
Subjects: DOENÇAS AUTOIMUNES, DOENÇA DE ALZHEIMER, DEMÊNCIA, REGRESSÃO LOGÍSTICA
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ABNT
MILLER, Zachary A. et al. TDP-43 frontotemporal lobar degeneration and autoimmune disease. Journal of Neurology, Neurosurgery and Psychiatry, v. 84, n. 9, p. 956-962, 2013Tradução . . Disponível em: https://doi.org/10.1136/jnnp-2012-304644. Acesso em: 10 nov. 2024.
APA
Miller, Z. A., Rankin, K. P., Graff-Radford, N. R., Takada, L. T., Sturm, V. E., Cleveland, C. M., et al. (2013). TDP-43 frontotemporal lobar degeneration and autoimmune disease. Journal of Neurology, Neurosurgery and Psychiatry, 84( 9), 956-962. doi:10.1136/jnnp-2012-304644
NLM
Miller ZA, Rankin KP, Graff-Radford NR, Takada LT, Sturm VE, Cleveland CM, Criswell LA, Jaeger PA, Stan T, Heggeli KA, Hsu SC, Karydas A, Khan BK, Grinberg LT, Gorno-Tempini ML, Boxer AL, Rosen HJ, Kramer JH, Coppola G, Geschwind DH, Rademakers R, Seeley WW, Wyss-Coray T, Miller BL. TDP-43 frontotemporal lobar degeneration and autoimmune disease [Internet]. Journal of Neurology, Neurosurgery and Psychiatry. 2013 ; 84( 9): 956-962.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1136/jnnp-2012-304644
Vancouver
Miller ZA, Rankin KP, Graff-Radford NR, Takada LT, Sturm VE, Cleveland CM, Criswell LA, Jaeger PA, Stan T, Heggeli KA, Hsu SC, Karydas A, Khan BK, Grinberg LT, Gorno-Tempini ML, Boxer AL, Rosen HJ, Kramer JH, Coppola G, Geschwind DH, Rademakers R, Seeley WW, Wyss-Coray T, Miller BL. TDP-43 frontotemporal lobar degeneration and autoimmune disease [Internet]. Journal of Neurology, Neurosurgery and Psychiatry. 2013 ; 84( 9): 956-962.[citado 2024 nov. 10 ] Available from: https://doi.org/10.1136/jnnp-2012-304644
Artigo de periodico
Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation (2013)
Grinberg, Lea Tenenholz; Wang, Xuehua; Wang, Chao; Sohn, Peter Dongmin; Theofilas, Panos; Sidhu, Manu; Arevalo, John Benjamin; Heinsen, Helmut; Huang, Eric J.; Rosen, Howard; Miller, Bruce L.; Gan, Li; Seeley, William W.
Source: Acta Neuropathologica. Unidade: FM
Subjects: AUTÓPSIA, IMUNOHISTOQUÍMICA, ANTICORPOS MONOCLONAIS, SISTEMA NERVOSO CENTRAL
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ABNT
GRINBERG, Lea Tenenholz et al. Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation. Acta Neuropathologica, v. 125, n. 4, p. 581-593, 2013Tradução . . Disponível em: http://link.springer.com/content/pdf/10.1007%2Fs00401-013-1080-2.pdf. Acesso em: 10 nov. 2024.
APA
Grinberg, L. T., Wang, X., Wang, C., Sohn, P. D., Theofilas, P., Sidhu, M., et al. (2013). Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation. Acta Neuropathologica, 125( 4), 581-593. doi:10.1007/s00401-013-1080-2
NLM
Grinberg LT, Wang X, Wang C, Sohn PD, Theofilas P, Sidhu M, Arevalo JB, Heinsen H, Huang EJ, Rosen H, Miller BL, Gan L, Seeley WW. Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation [Internet]. Acta Neuropathologica. 2013 ; 125( 4): 581-593.[citado 2024 nov. 10 ] Available from: http://link.springer.com/content/pdf/10.1007%2Fs00401-013-1080-2.pdf
Vancouver
Grinberg LT, Wang X, Wang C, Sohn PD, Theofilas P, Sidhu M, Arevalo JB, Heinsen H, Huang EJ, Rosen H, Miller BL, Gan L, Seeley WW. Argyrophilic grain disease differs from other tauopathies by lacking tau acetylation [Internet]. Acta Neuropathologica. 2013 ; 125( 4): 581-593.[citado 2024 nov. 10 ] Available from: http://link.springer.com/content/pdf/10.1007%2Fs00401-013-1080-2.pdf

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