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359 results on '"Ikeuchi T"'

1. Positron emission tomography and magnetic resonance imaging methods and datasets within the Dominantly Inherited Alzheimer Network (DIAN).

Author: McKay, NS, Gordon, BA, Hornbeck, RC, Dincer, A, Flores, S, Keefe, SJ, Joseph-Mathurin, N, Jack, CR, Koeppe, R, Millar, PR, Ances, BM, Chen, CD, Daniels, A, Hobbs, DA, Jackson, K, Koudelis, D, Massoumzadeh, P, McCullough, A, Nickels, ML, Rahmani, F, Swisher, L, Wang, Q, Allegri, RF, Berman, SB, Brickman, AM, Brooks, WS, Cash, DM, Chhatwal, JP, Day, GS, Farlow, MR, la Fougère, C, Fox, NC, Fulham, M, Ghetti, B, Graff-Radford, N, Ikeuchi, T, Klunk, W, Lee, J-H, Levin, J, Martins, R, Masters, CL, McConathy, J, Mori, H, Noble, JM, Reischl, G, Rowe, C, Salloway, S, Sanchez-Valle, R, Schofield, PR, Shimada, H, Shoji, M, Su, Y, Suzuki, K, Vöglein, J, Yakushev, I, Cruchaga, C, Hassenstab, J, Karch, C, McDade, E, Perrin, RJ, Xiong, C, Morris, JC, Bateman, RJ, Benzinger, TLS, Dominantly Inherited Alzheimer Network, McKay, NS, Gordon, BA, Hornbeck, RC, Dincer, A, Flores, S, Keefe, SJ, Joseph-Mathurin, N, Jack, CR, Koeppe, R, Millar, PR, Ances, BM, Chen, CD, Daniels, A, Hobbs, DA, Jackson, K, Koudelis, D, Massoumzadeh, P, McCullough, A, Nickels, ML, Rahmani, F, Swisher, L, Wang, Q, Allegri, RF, Berman, SB, Brickman, AM, Brooks, WS, Cash, DM, Chhatwal, JP, Day, GS, Farlow, MR, la Fougère, C, Fox, NC, Fulham, M, Ghetti, B, Graff-Radford, N, Ikeuchi, T, Klunk, W, Lee, J-H, Levin, J, Martins, R, Masters, CL, McConathy, J, Mori, H, Noble, JM, Reischl, G, Rowe, C, Salloway, S, Sanchez-Valle, R, Schofield, PR, Shimada, H, Shoji, M, Su, Y, Suzuki, K, Vöglein, J, Yakushev, I, Cruchaga, C, Hassenstab, J, Karch, C, McDade, E, Perrin, RJ, Xiong, C, Morris, JC, Bateman, RJ, Benzinger, TLS, and Dominantly Inherited Alzheimer Network
Abstract: The Dominantly Inherited Alzheimer Network (DIAN) is an international collaboration studying autosomal dominant Alzheimer disease (ADAD). ADAD arises from mutations occurring in three genes. Offspring from ADAD families have a 50% chance of inheriting their familial mutation, so non-carrier siblings can be recruited for comparisons in case-control studies. The age of onset in ADAD is highly predictable within families, allowing researchers to estimate an individual's point in the disease trajectory. These characteristics allow candidate AD biomarker measurements to be reliably mapped during the preclinical phase. Although ADAD represents a small proportion of AD cases, understanding neuroimaging-based changes that occur during the preclinical period may provide insight into early disease stages of 'sporadic' AD also. Additionally, this study provides rich data for research in healthy aging through inclusion of the non-carrier controls. Here we introduce the neuroimaging dataset collected and describe how this resource can be used by a range of researchers.
Published: 2023

2. Patterns and implications of neurological examination findings in autosomal dominant Alzheimer disease

Author: Voeglein, J, Franzmeier, N, Morris, JC, Dieterich, M, McDade, E, Simons, M, Preische, O, Hofmann, A, Hassenstab, J, Benzinger, TL, Fagan, A, Noble, JM, Berman, SB, Graff-Radford, NR, Ghetti, B, Farlow, MR, Chhatwal, JP, Salloway, S, Xiong, C, Karch, CM, Cairns, N, Perrin, RJ, Day, G, Martins, R, Sanchez-Valle, R, Mori, H, Shimada, H, Ikeuchi, T, Suzuki, K, Schofield, PR, Masters, CL, Goate, A, Buckles, V, Fox, NC, Chrem, P, Allegri, R, Ringman, JM, Yakushev, I, Laske, C, Jucker, M, Hoglinger, G, Bateman, RJ, Danek, A, Levin, J, Voeglein, J, Franzmeier, N, Morris, JC, Dieterich, M, McDade, E, Simons, M, Preische, O, Hofmann, A, Hassenstab, J, Benzinger, TL, Fagan, A, Noble, JM, Berman, SB, Graff-Radford, NR, Ghetti, B, Farlow, MR, Chhatwal, JP, Salloway, S, Xiong, C, Karch, CM, Cairns, N, Perrin, RJ, Day, G, Martins, R, Sanchez-Valle, R, Mori, H, Shimada, H, Ikeuchi, T, Suzuki, K, Schofield, PR, Masters, CL, Goate, A, Buckles, V, Fox, NC, Chrem, P, Allegri, R, Ringman, JM, Yakushev, I, Laske, C, Jucker, M, Hoglinger, G, Bateman, RJ, Danek, A, and Levin, J
Abstract: INTRODUCTION: As knowledge about neurological examination findings in autosomal dominant Alzheimer disease (ADAD) is incomplete, we aimed to determine the frequency and significance of neurological examination findings in ADAD. METHODS: Frequencies of neurological examination findings were compared between symptomatic mutation carriers and non mutation carriers from the Dominantly Inherited Alzheimer Network (DIAN) to define AD neurological examination findings. AD neurological examination findings were analyzed regarding frequency, association with and predictive value regarding cognitive decline, and association with brain atrophy in symptomatic mutation carriers. RESULTS: AD neurological examination findings included abnormal deep tendon reflexes, gait disturbance, pathological cranial nerve examination findings, tremor, abnormal finger to nose and heel to shin testing, and compromised motor strength. The frequency of AD neurological examination findings was 65.1%. Cross-sectionally, mutation carriers with AD neurological examination findings showed a more than two-fold faster cognitive decline and had greater parieto-temporal atrophy, including hippocampal atrophy. Longitudinally, AD neurological examination findings predicted a significantly greater decline over time. DISCUSSION: ADAD features a distinct pattern of neurological examination findings that is useful to estimate prognosis and may inform clinical care and therapeutic trial designs.
Published: 2023

3. Grain orientation dependence of deformation microstructure evolution and mechanical properties in face-centered cubic high/medium entropy alloys

Author: Yoshida, S, primary, Fu, R, additional, Gong, W, additional, Ikeuchi, T, additional, Bai, Y, additional, Feng, Z, additional, Wu, G, additional, Shibata, A, additional, Hansen, N, additional, Huang, X, additional, and Tsuji, N, additional
Published: 2022
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4. Evidence that dog ownership protects against the onset of disability in an older community-dwelling Japanese population

Author: Mogi, M, Taniguchi, Y, Seino, S, Headey, B, Hata, T, Ikeuchi, T, Abe, T, Shinkai, S, Kitamura, A, Mogi, M, Taniguchi, Y, Seino, S, Headey, B, Hata, T, Ikeuchi, T, Abe, T, Shinkai, S, and Kitamura, A
Abstract: OBJECTIVES: This study examined the association between dog and cat ownership, the onset of disability and all-cause mortality in an older population. Dog and cat owners take more regular exercise and have closer social relationships than non-owners. We further assess the beneficial effects of these moderating variables on the onset of disability and mortality. METHODS: Dog and cat ownership data were collected from 11233 community-dwelling adults age 65 years and older. These data were matched with data about the onset of disability held by the Japanese long-term care insurance system. Local registry data were used to ascertain all-cause mortality. RESULTS: During the approximately 3.5 year follow-up period, 17.1% of the sample suffered onset of disability, and 5.2% died. Logistic regression analysis indicated that, compared with a reference group of those who had never owned a dog (odds ratio fixed at 1.0), older adults who were currently dog owners had a significantly lower odds ratio of onset of disability (OR = 0.54 95% CI: 0.37-0.79). Our results further show that regular exercise interacts with dog ownership to reduce the risk of disability. The association of dog and/or cat ownership with all-cause mortality was not statistically significant. CONCLUSIONS: Dog ownership appears to protect against incident disability among older Japanese adults. Additional benefits are gained from ownership combined with regular exercise. Daily dog care may have an important role to play in health promotion and successful aging.
Published: 2022

5. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview

Author: Delaby, C, Teunissen, CE, Blennow, K, Alcolea, D, Arisi, I, Amar, EB, Beaume, A, Bedel, A, Bellomo, G, Bigot-Corbel, E, Bjerke, M, Blanc-Quintin, M-C, Boada, M, Bousiges, O, Chapman, MD, DeMarco, ML, D'Onofrio, M, Dumurgier, J, Dufour-Rainfray, D, Engelborghs, S, Esselmann, H, Fogli, A, Gabelle, A, Galloni, E, Gondolf, C, Grandhomme, F, Grau-Rivera, O, Hart, M, Ikeuchi, T, Jeromin, A, Kasuga, K, Keshavan, A, Khalil, M, Koertvelyessy, P, Kulczynska-Przybik, A, Laplanche, J-L, Lewczuk, P, Li, Q-X, Lleo, A, Malaplate, C, Marquie, M, Masters, CL, Mroczko, B, Nogueira, L, Orellana, A, Otto, M, Oudart, J-B, Paquet, C, Paoletti, FP, Parnetti, L, Perret-Liaudet, A, Peoc'h, K, Poesen, K, Puig-Pijoan, A, Quadrio, I, Quillard-Muraine, M, Rucheton, B, Schraen, S, Schott, JM, Shaw, LM, Suarez-Calvet, M, Tsolaki, M, Tumani, H, Udeh-Momoh, CT, Vaudran, L, Verbeek, MM, Verde, F, Vermunt, L, Vogelgsang, J, Wiltfang, J, Zetterberg, H, Lehmann, S, Delaby, C, Teunissen, CE, Blennow, K, Alcolea, D, Arisi, I, Amar, EB, Beaume, A, Bedel, A, Bellomo, G, Bigot-Corbel, E, Bjerke, M, Blanc-Quintin, M-C, Boada, M, Bousiges, O, Chapman, MD, DeMarco, ML, D'Onofrio, M, Dumurgier, J, Dufour-Rainfray, D, Engelborghs, S, Esselmann, H, Fogli, A, Gabelle, A, Galloni, E, Gondolf, C, Grandhomme, F, Grau-Rivera, O, Hart, M, Ikeuchi, T, Jeromin, A, Kasuga, K, Keshavan, A, Khalil, M, Koertvelyessy, P, Kulczynska-Przybik, A, Laplanche, J-L, Lewczuk, P, Li, Q-X, Lleo, A, Malaplate, C, Marquie, M, Masters, CL, Mroczko, B, Nogueira, L, Orellana, A, Otto, M, Oudart, J-B, Paquet, C, Paoletti, FP, Parnetti, L, Perret-Liaudet, A, Peoc'h, K, Poesen, K, Puig-Pijoan, A, Quadrio, I, Quillard-Muraine, M, Rucheton, B, Schraen, S, Schott, JM, Shaw, LM, Suarez-Calvet, M, Tsolaki, M, Tumani, H, Udeh-Momoh, CT, Vaudran, L, Verbeek, MM, Verde, F, Vermunt, L, Vogelgsang, J, Wiltfang, J, Zetterberg, H, and Lehmann, S
Abstract: INTRODUCTION: The current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. METHODS: We obtained a description of (pre-)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. RESULTS: The (pre-)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. DISCUSSION: This is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD.
Published: 2022

6. Clinical reporting following the quantification of cerebrospinal fluid biomarkers in Alzheimer's disease: An international overview

Author: Delaby, C., Teunissen, C.E., Blennow, K., Alcolea, D., Arisi, I., Amar, E.B., Beaume, A., Bedel, A., Bellomo, G., Bigot-Corbel, E., Bjerke, M., Blanc-Quintin, M.C., Boada, M., Bousiges, O., Chapman, M.D., DeMarco, M.L., D'Onofrio, M., Dumurgier, J., Dufour-Rainfray, D., Engelborghs, S., Esselmann, H., Fogli, A., Gabelle, A., Galloni, E., Gondolf, C., Grandhomme, F., Grau-Rivera, O., Hart, M., Ikeuchi, T., Jeromin, A., Kasuga, K., Keshavan, A., Khalil, M., Körtvelyessy, P., Kulczynska-Przybik, A., Laplanche, J.L., Lewczuk, P., Li, Q.X., Lleó, A., Malaplate, C., Marquié, M., Masters, C.L., Mroczko, B., Nogueira, L., Orellana, A., Otto, M., Oudart, J.B., Paquet, C., Paoletti, F.P., Parnetti, L., Perret-Liaudet, A., Peoc'h, K., Poesen, K., Puig-Pijoan, A., Quadrio, I., Quillard-Muraine, M., Rucheton, B., Schraen, S., Schott, J.M., Shaw, L.M., Suárez-Calvet, M., Tsolaki, M., Tumani, H., Udeh-Momoh, C.T., Vaudran, L., Verbeek, M.M., Verde, F., Vermunt, L., Vogelgsang, J., Wiltfang, J., Zetterberg, H., Lehmann, S., Delaby, C., Teunissen, C.E., Blennow, K., Alcolea, D., Arisi, I., Amar, E.B., Beaume, A., Bedel, A., Bellomo, G., Bigot-Corbel, E., Bjerke, M., Blanc-Quintin, M.C., Boada, M., Bousiges, O., Chapman, M.D., DeMarco, M.L., D'Onofrio, M., Dumurgier, J., Dufour-Rainfray, D., Engelborghs, S., Esselmann, H., Fogli, A., Gabelle, A., Galloni, E., Gondolf, C., Grandhomme, F., Grau-Rivera, O., Hart, M., Ikeuchi, T., Jeromin, A., Kasuga, K., Keshavan, A., Khalil, M., Körtvelyessy, P., Kulczynska-Przybik, A., Laplanche, J.L., Lewczuk, P., Li, Q.X., Lleó, A., Malaplate, C., Marquié, M., Masters, C.L., Mroczko, B., Nogueira, L., Orellana, A., Otto, M., Oudart, J.B., Paquet, C., Paoletti, F.P., Parnetti, L., Perret-Liaudet, A., Peoc'h, K., Poesen, K., Puig-Pijoan, A., Quadrio, I., Quillard-Muraine, M., Rucheton, B., Schraen, S., Schott, J.M., Shaw, L.M., Suárez-Calvet, M., Tsolaki, M., Tumani, H., Udeh-Momoh, C.T., Vaudran, L., Verbeek, M.M., Verde, F., Vermunt, L., Vogelgsang, J., Wiltfang, J., Zetterberg, H., and Lehmann, S.
Abstract: Item does not contain fulltext, INTRODUCTION: The current practice of quantifying cerebrospinal fluid (CSF) biomarkers as an aid in the diagnosis of Alzheimer's disease (AD) varies from center to center. For a same biochemical profile, interpretation and reporting of results may differ, which can lead to misunderstandings and raises questions about the commutability of tests. METHODS: We obtained a description of (pre-)analytical protocols and sample reports from 40 centers worldwide. A consensus approach allowed us to propose harmonized comments corresponding to the different CSF biomarker profiles observed in patients. RESULTS: The (pre-)analytical procedures were similar between centers. There was considerable heterogeneity in cutoff definitions and report comments. We therefore identified and selected by consensus the most accurate and informative comments regarding the interpretation of CSF biomarkers in the context of AD diagnosis. DISCUSSION: This is the first time that harmonized reports are proposed across worldwide specialized laboratories involved in the biochemical diagnosis of AD.
Published: 2022

7. Grain orientation dependence of deformation microstructure evolution and mechanical properties in face-centered cubic high/medium entropy alloys

Author: Yoshida, S., Fu, R., Gong, W., Ikeuchi, T., Bai, Y., Feng, Z., Wu, G., Shibata, A., Hansen, N., Huang, X., Tsuji, N., Yoshida, S., Fu, R., Gong, W., Ikeuchi, T., Bai, Y., Feng, Z., Wu, G., Shibata, A., Hansen, N., Huang, X., and Tsuji, N.
Abstract: This study revealed characteristics of the deformation behavior in high/medium entropy alloys (HEAs/MEAs) with face-centered cubic (FCC) structure. A Co60Ni40 alloy and a Co20Cr40Ni40 MEA having low and high friction stresses (fundamental resistance to dislocation glide in solid solutions), respectively, but similar in other properties, including their stacking fault energy and grain sizes, were compared. The MEA exhibited a higher yield strength and work-hardening ability than those in the Co60Ni40 alloy at room temperature. Deformation microstructures of the Co60Ni40 alloy were composed of coarse dislocation cells (DCs) in most grains, and a few deformation twins (DTs) formed in grains with tensile axis (TA) nearly parallel to . In the MEA, three microstructure types were found depending on the grain orientations: (1) fine DCs developed in TA similar to//-oriented grains; (2) planar dislocation structures (PDSs) formed in grains with other orientations; and (3) dense DTs adding to the PDSs developed in TA similar to//-oriented grains. The results imply difficulty in cross-slip of screw dislocations and dynamic recovery in the MEA, leading to an increase in the dislocation density and work-hardening rate. Our results suggest that FCC high-alloy systems with high friction stress inherently develop characteristic deformation microstructures advantageous for achieving high strength and large ductility.
Published: 2022

8. State-of-the-art of lumbar puncture and its place in the journey of patients with Alzheimer's disease

Author: Hampel, H, Shaw, LM, Aisen, P, Chen, C, Lleo, A, Iwatsubo, T, Iwata, A, Yamada, M, Ikeuchi, T, Jia, JP, Wang, HL, Teunissen, CE, Peskind, E, Blennow, K, Cummings, J, and Vergallo, A
Subjects: system readiness, diagnosis, biomarker, lumbar puncture, Alzheimer's disease, evidence-based guidelines, cerebrospinal fluid
Abstract: Recent advances in developing disease-modifying therapies (DMT) for Alzheimer's disease (AD), and the recognition that AD pathophysiology emerges decades before clinical symptoms, necessitate a paradigm shift of health-care systems toward biomarker-guided early detection, diagnosis, and therapeutic decision-making. Appropriate incorporation of cerebrospinal fluid biomarker analysis in clinical practice is an essential step toward system readiness for accommodating the demand of AD diagnosis and proper use of DMTs-once they become available. However, the use of lumbar puncture (LP) in individuals with suspected neurodegenerative diseases such as AD is inconsistent, and the perception of its utility and safety differs considerably among medical specialties as well as among regions and countries. This review describes the state-of-the-art evidence concerning the safety profile of LP in older adults, discusses the risk factors for LP-associated adverse events, and provides recommendations and an outlook for optimized use and global implementation of LP in individuals with suspected AD.
Published: 2022

9. χ2-based AlGaAs phase sensitive amplifier with record gain, noise, and sensitivity

Author: Yan, Zhizhong, primary, He, Haoyu, additional, Liu, Han, additional, Iu, M., additional, Ahmed, O., additional, Chen, E., additional, Blakey, P., additional, Akasaka, Youichi, additional, Ikeuchi, T., additional, and Helmy, Amr S., additional
Published: 2022
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10. Using global team science to identify genetic parkinson's disease worldwide

Author: Vollstedt, E, Kasten, M, Klein, C, Aasly, J, Adler, C, Ahmad-Annuar, A, Albanese, A, Alcalay, R, Al-Mubarak, B, Alvarez, V, Andree-Munoz, B, Annesi, G, Appel-Cresswell, S, Arkadir, D, Armasu, S, Barber, T, Bardien, S, Barkhuizen, M, Barrett, M, Basak, A, Beach, T, Benitez, B, Berg, D, Bhatia, K, Binkofski, F, Blauwendraat, C, Bonifati, V, Borges, V, Bozi, M, Brice, A, Brighina, L, Brockmann, K, Brucke, T, Bruggemann, N, Camacho, M, Cardoso, F, Belin, A, Carr, J, Chan, P, Chang-Castello, J, Chase, B, Chen-Plotkin, A, Ju Chung, S, Cilia, R, Clarimon, J, Clark, L, Cornejo-Olivas, M, Corvol, J, Cosentino, C, Cras, P, Crosiers, D, Damasio, J, Das, P, de Carvalho Aguiar, P, De Michele, G, De Rosa, A, Dieguez, E, Dorszewska, J, Erer, S, Ertan, S, Farrer, M, Fedotova, E, Ferese, R, Ferrarese, C, Ferraz, H, Fiala, O, Foroud, T, Friedman, A, Frigerio, R, Funayama, M, Gambardella, S, Garraux, G, Gatto, E, Genc, G, Giladi, N, Goldwurm, S, Gomez-Esteban, J, Gomez-Garre, P, Gorostidi, A, Grosset, D, Hanagasi, H, Hardy, J, Hassan, A, Hattori, N, Hauser, R, Hedera, P, Hentati, F, Hertz, J, Holton, J, Houlden, H, Hutz, M, Ikeuchi, T, Illarioshkin, S, Inca-Martinez, M, Infante, J, Jankovic, J, Jeon, B, Jesus, S, Jimenez-Del-Rio, M, Kaasinen, V, Kataoka, H, Kawakami, H, Kim, Y, Klivenyi, P, Koks, S, Konig, I, Kostic, V, Koziorowski, D, Kruger, R, Krygowska-Wajs, A, Kulisevsky, J, Lai, D, Lang, A, Ledoux, M, Lesage, S, Lim, S, Lin, C, Lohmann, K, Lopera, F, Lopez, G, Lu, C, Lynch, T, Machaczka, M, Madoev, H, Magalhaes, M, Majamaa, K, Maraganore, D, Marder, K, Markopoulou, K, Martikainen, M, Mata, I, Mazzetti, P, Mellick, G, Menendez-Gonzalez, M, Micheli, F, Mirelman, A, Mir, P, Morino, H, Morris, H, Munhoz, R, Naito, A, Olszewska, D, Ozelius, L, Padmanabhan, S, Paisan-Ruiz, C, Payami, H, Peluso, S, Petkovic, S, Petrucci, S, Pezzoli, G, Pimentel, M, Pirker, W, Pramstaller, P, Pulkes, T, Puschmann, A, Quattrone, A, Raggio, V, Ransmayr, G, Rieder, C, Riess, O, Rodriguez-Porcel, F, Rogaeva, E, Ross, O, Ruiz-Martinez, J, Sammler, E, San Luciano, M, Satake, W, Saunders-Pullman, R, Sazci, A, Scherzer, C, Schrag, A, Schumacher-Schuh, A, Sharma, M, Sidransky, E, Singleton, A, Petersen, M, Smolders, S, Spitz, M, Stefanis, L, Struhal, W, Sue, C, Swan, M, Swanberg, M, Taba, P, Taipa, R, Tan, M, Tan, A, Tan, E, Tang, B, Tayebi, N, Thaler, A, Thomas, A, Toda, T, Toft, M, Torres, L, Tumas, V, Valente, E, Van Broeckhoven, C, Vecsei, L, Velez-Pardo, C, Vidailhet, M, Warner, T, Williams-Gray, C, Winkelmann, J, Woitalla, D, Wood, N, Wszolek, Z, Wu, R, Wu, Y, Xie, T, Yoshino, H, Zhang, B, Zimprich, A, Vollstedt E. -J., Kasten M., Klein C., Aasly J., Adler C., Ahmad-Annuar A., Albanese A., Alcalay R. N., Al-Mubarak B., Alvarez V., Andree-Munoz B., Annesi G., Appel-Cresswell S., Arkadir D., Armasu S., Barber T. R., Bardien S., Barkhuizen M., Barrett M. J., Basak A. N., Beach T., Benitez B. A., Berg D., Bhatia K., Binkofski F., Blauwendraat C., Bonifati V., Borges V., Bozi M., Brice A., Brighina L., Brockmann K., Brucke T., Bruggemann N., Camacho M., Cardoso F., Belin A. C., Carr J., Chan P., Chang-Castello J., Chase B., Chen-Plotkin A., Ju Chung S., Cilia R., Clarimon J., Clark L., Cornejo-Olivas M., Corvol J. -C., Cosentino C., Cras P., Crosiers D., Damasio J., Das P., de Carvalho Aguiar P., De Michele G., De Rosa A., Dieguez E., Dorszewska J., Erer S., Ertan S., Farrer M., Fedotova E., Ferese R., Ferrarese C., Ferraz H., Fiala O., Foroud T., Friedman A., Frigerio R., Funayama M., Gambardella S., Garraux G., Gatto E. M., Genc G., Giladi N., Goldwurm S., Gomez-Esteban J. C., Gomez-Garre P., Gorostidi A., Grosset D., Hanagasi H., Hardy J., Hassan A., Hattori N., Hauser R. A., Hedera P., Hentati F., Hertz J. M., Holton J. L., Houlden H., Hutz M. H., Ikeuchi T., Illarioshkin S., Inca-Martinez M., Infante J., Jankovic J., Jeon B. S., Jesus S., Jimenez-Del-Rio M., Kaasinen V., Kataoka H., Kawakami H., Kim Y. J., Klivenyi P., Koks S., Konig I. R., Kostic V., Koziorowski D., Kruger R., Krygowska-Wajs A., Kulisevsky J., Lai D., Lang A., LeDoux M., Lesage S., Lim S. -Y., Lin C. -H., Lohmann K., Lopera F., Lopez G., Lu C. -S., Lynch T., Machaczka M., Madoev H., Magalhaes M., Majamaa K., Maraganore D., Marder K., Markopoulou K., Martikainen M. H., Mata I., Mazzetti P., Mellick G., Menendez-Gonzalez M., Micheli F., Mirelman A., Mir P., Morino H., Morris H., Munhoz R. P., Naito A., Olszewska D. A., Ozelius L. J., Padmanabhan S., Paisan-Ruiz C., Payami H., Peluso S., Petkovic S., Petrucci S., Pezzoli G., Pimentel M., Pirker W., Pramstaller P. P., Pulkes T., Puschmann A., Quattrone A., Raggio V., Ransmayr G., Rieder C., Riess O., Rodriguez-Porcel F., Rogaeva E., Ross O. A., Ruiz-Martinez J., Sammler E., San Luciano M., Satake W., Saunders-Pullman R., Sazci A., Scherzer C., Schrag A., Schumacher-Schuh A., Sharma M., Sidransky E., Singleton A. B., Petersen M. S., Smolders S., Spitz M., Stefanis L., Struhal W., Sue C. M., Swan M., Swanberg M., Taba P., Taipa R., Tan M., Tan A. H., Tan E. -K., Tang B., Tayebi N., Thaler A., Thomas A., Toda T., Toft M., Torres L., Tumas V., Valente E. M., Van Broeckhoven C., Vecsei L., Velez-Pardo C., Vidailhet M., Warner T. T., Williams-Gray C. H., Winkelmann J., Woitalla D., Wood N. W., Wszolek Z. K., Wu R. -M., Wu Y. -R., Xie T., Yoshino H., Zhang B., Zimprich A., Vollstedt, E, Kasten, M, Klein, C, Aasly, J, Adler, C, Ahmad-Annuar, A, Albanese, A, Alcalay, R, Al-Mubarak, B, Alvarez, V, Andree-Munoz, B, Annesi, G, Appel-Cresswell, S, Arkadir, D, Armasu, S, Barber, T, Bardien, S, Barkhuizen, M, Barrett, M, Basak, A, Beach, T, Benitez, B, Berg, D, Bhatia, K, Binkofski, F, Blauwendraat, C, Bonifati, V, Borges, V, Bozi, M, Brice, A, Brighina, L, Brockmann, K, Brucke, T, Bruggemann, N, Camacho, M, Cardoso, F, Belin, A, Carr, J, Chan, P, Chang-Castello, J, Chase, B, Chen-Plotkin, A, Ju Chung, S, Cilia, R, Clarimon, J, Clark, L, Cornejo-Olivas, M, Corvol, J, Cosentino, C, Cras, P, Crosiers, D, Damasio, J, Das, P, de Carvalho Aguiar, P, De Michele, G, De Rosa, A, Dieguez, E, Dorszewska, J, Erer, S, Ertan, S, Farrer, M, Fedotova, E, Ferese, R, Ferrarese, C, Ferraz, H, Fiala, O, Foroud, T, Friedman, A, Frigerio, R, Funayama, M, Gambardella, S, Garraux, G, Gatto, E, Genc, G, Giladi, N, Goldwurm, S, Gomez-Esteban, J, Gomez-Garre, P, Gorostidi, A, Grosset, D, Hanagasi, H, Hardy, J, Hassan, A, Hattori, N, Hauser, R, Hedera, P, Hentati, F, Hertz, J, Holton, J, Houlden, H, Hutz, M, Ikeuchi, T, Illarioshkin, S, Inca-Martinez, M, Infante, J, Jankovic, J, Jeon, B, Jesus, S, Jimenez-Del-Rio, M, Kaasinen, V, Kataoka, H, Kawakami, H, Kim, Y, Klivenyi, P, Koks, S, Konig, I, Kostic, V, Koziorowski, D, Kruger, R, Krygowska-Wajs, A, Kulisevsky, J, Lai, D, Lang, A, Ledoux, M, Lesage, S, Lim, S, Lin, C, Lohmann, K, Lopera, F, Lopez, G, Lu, C, Lynch, T, Machaczka, M, Madoev, H, Magalhaes, M, Majamaa, K, Maraganore, D, Marder, K, Markopoulou, K, Martikainen, M, Mata, I, Mazzetti, P, Mellick, G, Menendez-Gonzalez, M, Micheli, F, Mirelman, A, Mir, P, Morino, H, Morris, H, Munhoz, R, Naito, A, Olszewska, D, Ozelius, L, Padmanabhan, S, Paisan-Ruiz, C, Payami, H, Peluso, S, Petkovic, S, Petrucci, S, Pezzoli, G, Pimentel, M, Pirker, W, Pramstaller, P, Pulkes, T, Puschmann, A, Quattrone, A, Raggio, V, Ransmayr, G, Rieder, C, Riess, O, Rodriguez-Porcel, F, Rogaeva, E, Ross, O, Ruiz-Martinez, J, Sammler, E, San Luciano, M, Satake, W, Saunders-Pullman, R, Sazci, A, Scherzer, C, Schrag, A, Schumacher-Schuh, A, Sharma, M, Sidransky, E, Singleton, A, Petersen, M, Smolders, S, Spitz, M, Stefanis, L, Struhal, W, Sue, C, Swan, M, Swanberg, M, Taba, P, Taipa, R, Tan, M, Tan, A, Tan, E, Tang, B, Tayebi, N, Thaler, A, Thomas, A, Toda, T, Toft, M, Torres, L, Tumas, V, Valente, E, Van Broeckhoven, C, Vecsei, L, Velez-Pardo, C, Vidailhet, M, Warner, T, Williams-Gray, C, Winkelmann, J, Woitalla, D, Wood, N, Wszolek, Z, Wu, R, Wu, Y, Xie, T, Yoshino, H, Zhang, B, Zimprich, A, Vollstedt E. -J., Kasten M., Klein C., Aasly J., Adler C., Ahmad-Annuar A., Albanese A., Alcalay R. N., Al-Mubarak B., Alvarez V., Andree-Munoz B., Annesi G., Appel-Cresswell S., Arkadir D., Armasu S., Barber T. R., Bardien S., Barkhuizen M., Barrett M. J., Basak A. N., Beach T., Benitez B. A., Berg D., Bhatia K., Binkofski F., Blauwendraat C., Bonifati V., Borges V., Bozi M., Brice A., Brighina L., Brockmann K., Brucke T., Bruggemann N., Camacho M., Cardoso F., Belin A. C., Carr J., Chan P., Chang-Castello J., Chase B., Chen-Plotkin A., Ju Chung S., Cilia R., Clarimon J., Clark L., Cornejo-Olivas M., Corvol J. -C., Cosentino C., Cras P., Crosiers D., Damasio J., Das P., de Carvalho Aguiar P., De Michele G., De Rosa A., Dieguez E., Dorszewska J., Erer S., Ertan S., Farrer M., Fedotova E., Ferese R., Ferrarese C., Ferraz H., Fiala O., Foroud T., Friedman A., Frigerio R., Funayama M., Gambardella S., Garraux G., Gatto E. M., Genc G., Giladi N., Goldwurm S., Gomez-Esteban J. C., Gomez-Garre P., Gorostidi A., Grosset D., Hanagasi H., Hardy J., Hassan A., Hattori N., Hauser R. A., Hedera P., Hentati F., Hertz J. M., Holton J. L., Houlden H., Hutz M. H., Ikeuchi T., Illarioshkin S., Inca-Martinez M., Infante J., Jankovic J., Jeon B. S., Jesus S., Jimenez-Del-Rio M., Kaasinen V., Kataoka H., Kawakami H., Kim Y. J., Klivenyi P., Koks S., Konig I. R., Kostic V., Koziorowski D., Kruger R., Krygowska-Wajs A., Kulisevsky J., Lai D., Lang A., LeDoux M., Lesage S., Lim S. -Y., Lin C. -H., Lohmann K., Lopera F., Lopez G., Lu C. -S., Lynch T., Machaczka M., Madoev H., Magalhaes M., Majamaa K., Maraganore D., Marder K., Markopoulou K., Martikainen M. H., Mata I., Mazzetti P., Mellick G., Menendez-Gonzalez M., Micheli F., Mirelman A., Mir P., Morino H., Morris H., Munhoz R. P., Naito A., Olszewska D. A., Ozelius L. J., Padmanabhan S., Paisan-Ruiz C., Payami H., Peluso S., Petkovic S., Petrucci S., Pezzoli G., Pimentel M., Pirker W., Pramstaller P. P., Pulkes T., Puschmann A., Quattrone A., Raggio V., Ransmayr G., Rieder C., Riess O., Rodriguez-Porcel F., Rogaeva E., Ross O. A., Ruiz-Martinez J., Sammler E., San Luciano M., Satake W., Saunders-Pullman R., Sazci A., Scherzer C., Schrag A., Schumacher-Schuh A., Sharma M., Sidransky E., Singleton A. B., Petersen M. S., Smolders S., Spitz M., Stefanis L., Struhal W., Sue C. M., Swan M., Swanberg M., Taba P., Taipa R., Tan M., Tan A. H., Tan E. -K., Tang B., Tayebi N., Thaler A., Thomas A., Toda T., Toft M., Torres L., Tumas V., Valente E. M., Van Broeckhoven C., Vecsei L., Velez-Pardo C., Vidailhet M., Warner T. T., Williams-Gray C. H., Winkelmann J., Woitalla D., Wood N. W., Wszolek Z. K., Wu R. -M., Wu Y. -R., Xie T., Yoshino H., Zhang B., and Zimprich A.
Published: 2019

11. BubR1 localizes to centrosomes and suppresses centrosome amplification via regulating Plk1 activity in interphase cells

Author: Izumi, H, Matsumoto, Y, Ikeuchi, T, Saya, H, Kajii, T, and Matsuura, S
Published: 2009
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12. Amyloid and tau pathology associations with personality traits, neuropsychiatric symptoms, and cognitive lifestyle in the preclinical phases of sporadic and autosomal dominant Alzheimer’s disease

Author: Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., Bedetti, C., Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., and Bedetti, C.
Abstract: Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.
Published: 2020

13. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease

Author: Barthélemy, N.R., Li, Y., Joseph-Mathurin, N., Gordon, B.A., Hassenstab, J., Benzinger, T.L.S., Buckles, V., Fagan, A.M., Perrin, R.J., Goate, A.M., Morris, J.C., Karch, C.M., Xiong, C., Allegri, R., Mendez, P.C., Berman, S.B., Ikeuchi, T., Mori, H., Shimada, H., Shoji, M., Suzuki, K., Noble, J., Farlow, M., Chhatwal, J., Graff-Radford, N.R., Salloway, S., Schofield, P.R., Masters, C.L., Martins, R.N., O’Connor, A., Fox, N.C., Levin, J., Jucker, M., Gabelle, A., Lehmann, S., Sato, C., Bateman, R.J., McDade, E., Bateman, R., Bechara, J., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Chea, S., Chrem Mendez, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Fitzpatrick, C., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Groves, A., Hoechst-Swisher, L., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., Morris, J., Nagamatsu, A., Neimeyer, K., Norton, J., Perrin, R., Raichle, M., Renton, A., Ringman, J., Roh, J.H., Schofield, P., Sigurdson, W., Sohrabi, H., Sparks, P., Taddei, K., Wang, P., Xu, X., Barthélemy, N.R., Li, Y., Joseph-Mathurin, N., Gordon, B.A., Hassenstab, J., Benzinger, T.L.S., Buckles, V., Fagan, A.M., Perrin, R.J., Goate, A.M., Morris, J.C., Karch, C.M., Xiong, C., Allegri, R., Mendez, P.C., Berman, S.B., Ikeuchi, T., Mori, H., Shimada, H., Shoji, M., Suzuki, K., Noble, J., Farlow, M., Chhatwal, J., Graff-Radford, N.R., Salloway, S., Schofield, P.R., Masters, C.L., Martins, R.N., O’Connor, A., Fox, N.C., Levin, J., Jucker, M., Gabelle, A., Lehmann, S., Sato, C., Bateman, R.J., McDade, E., Bateman, R., Bechara, J., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Chea, S., Chrem Mendez, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Fitzpatrick, C., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Groves, A., Hoechst-Swisher, L., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., Morris, J., Nagamatsu, A., Neimeyer, K., Norton, J., Perrin, R., Raichle, M., Renton, A., Ringman, J., Roh, J.H., Schofield, P., Sigurdson, W., Sohrabi, H., Sparks, P., Taddei, K., Wang, P., and Xu, X.
Abstract: Development of tau-based therapies for Alzheimer’s disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer’s disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments.
Published: 2020

14. Clinical, molecular and histopathological features of short stature syndrome with novel CUL7 mutation in Yakuts: new population isolate in Asia

Author: Maksimova, N, Hara, K, Miyashia, A, Nikolaeva, I, Shiga, A, Nogovicina, A, Sukhomyasova, A, Argunov, V, Shvedova, A, Ikeuchi, T, Nishizawa, M, Kuwano, R, and Onodera, O
Published: 2007

15. Close associations between prevalences of dominantly inherited spinocerebellar ataxias with CAG-repeat expansions and frequencies of large normal CAG alleles in Japanese and Caucasian populations

Author: Takano, H., Cancel, G., Ikeuchi, T., Lorenzetti, D., Mawad, R., Stevanin, G., Didierjean, O., Durr, A., Oyake, M., Shimohata, T., Sasaki, R., Koide, R., Igarashi, S., Hayashi, S., Takiyama, Y., Nishizawa, M., Tanaka, H., Zoghbi, H., Brice, A., and Tsuji, S.
Subjects: United States -- Health aspects, Japan -- Health aspects, Cerebellar ataxia -- Research, Genetic disorders -- Research, Movement disorders -- Research, Biological sciences
Abstract: Research on Caucasian and Japanese subjects shows a correlation between large normal CAG allele frequencies and the CAG-repeat expansions coinciding with dominantly inherited spinocerebellar ataxias (SCAs). Dominant SCA types and dentatorubralpallidoluysian atrophy were found primarily in Caucasian and Japanese populations respectively, with prevalences matching comparatively large numbers of normal alleles.
Published: 1998

16. Serum neurofilament dynamics predicts neurodegeneration and clinical progression in presymptomatic Alzheimer’s disease

Author: Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Preische, O., Schultz, S.A., Apel, A., Kuhle, J., Kaeser, S.A., Barro, C., Gräber, S., Kuder-Buletta, E., LaFougere, C., Laske, C., Vöglein, J., Levin, J., Masters, C.L., Martins, R., Schofield, P.R., Rossor, M.N., Graff-Radford, N.R., Salloway, S., Ghetti, B., Ringman, J.M., Noble, J.M., Chhatwal, J., Goate, A.M., Benzinger, T.L.S., Morris, J.C., Bateman, R.J., Wang, G., Fagan, A.M., McDade, E.M., Gordon, B.A., Jucker, M., Allegri, R., Amtashar, F., Bateman, R., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D’Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Lee, J-H, Marcus, D., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Morris, J., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., and Xu, X.
Abstract: Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. Here we leverage the unique characteristics of the Dominantly Inherited Alzheimer Network and ultrasensitive immunoassay technology to demonstrate that NfL levels in the cerebrospinal fluid (n = 187) and serum (n = 405) are correlated with one another and are elevated at the presymptomatic stages of familial Alzheimer’s disease. Longitudinal, within-person analysis of serum NfL dynamics (n = 196) confirmed this elevation and further revealed that the rate of change of serum NfL could discriminate mutation carriers from non-mutation carriers almost a decade earlier than cross-sectional absolute NfL levels (that is, 16.2 versus 6.8 years before the estimated symptom onset). Serum NfL rate of change peaked in participants converting from the presymptomatic to the symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging, but less so with amyloid-β deposition or glucose metabolism (assessed by positron emission tomography). Serum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the Mini–Mental State Examination and Logical Memory test. Thus, NfL dynamics in serum predict disease progression and brain neurodegeneration at the early presymptomatic stages of familial Alzheimer’s disease, which supports its potential utility as a clinically useful biomarker.
Published: 2019

17. Using global team science to identify genetic Parkinson's disease worldwide

Author: Vollstedt, E‐J, Kasten, M., Klein, C., Aasly, J., Adler, C., Ahmad‐Annuar, A., Albanese, A., Alcalay, R., Al‐Mubarak, B., Alvarez, V., Andree‐Muñoz, B., Annesi, G., Appel‐Cresswell, S., Arkadir, D., Armasu, S., Barber, T.R., Bardien, S., Barkhuizen, M., Barrett, M.J., BaŞak, A.N., Beach, T., Benitez, B.A., Berg, D., Bhatia, K., Binkofski, F., Blauwendraat, C., Bonifati, V., Borges, V., Bozi, M., Brice, A., Brighina, L., Brockmann, K., Brüggemann, N., Camacho, M., Cardoso, F., Belin, A.C., Carr, J., Chan, P., Chang‐Castello, J., Chase, B., Chen‐Plotkin, A., Chung, S.J., Cilia, R., Clarimon, J., Clark, L., Cornejo‐Olivas, M., Corvol, J‐C, Cosentino, C., Cras, P., Crosiers, D., Damásio, J., Das, P., Carvalho Aguiar, P., De Michele, G., De Rosa, A., Dieguez, E., Dorszewska, J., Erer, S., Ertan, S., Farrer, M., Fedotova, E., Ferese, R., Ferrarese, C., Ferraz, H., Fiala, O., Foroud, T., Friedman, A., Frigerio, R., Funayama, M., Gambardella, S., Garraux, G., Gatto, E.M., Genç, G., Goldwurm, S., Gomez‐Esteban, J.C., Gómez‐Garre, P., Gorostidi, A., Grosset, D., Hanagasi, H., Hardy, J., Hassan, A., Hattori, N., Hauser, R.A., Hedera, P., Hentati, F., Hertz, J.M., Holton, J.L., Houlden, H., Hutz, M.H., Ikeuchi, T., Illarioshkin, S., Inca‐Martinez, M., Infante, J., Jankovic, J., Jeon, B.S., Jesús, S., Jimenez‐Del‐Rio, M., Kataoka, H., Kawakami, H., Kim, Y.J., Klivényi, P., Kõks, S., König, I.R., KostiĆ, V., Koziorowski, D., Krüger, R., Krygowska‐Wajs, A., Kulisevsky, J., Lang, A., LeDoux, M., Lesage, S., Lim, S‐Y, Lin, C‐H, Lohmann, K., Lopera, F., Lopez, G., Lu, C‐S, Lynch, T., Machaczka, M., Madoev, H., Magalhães, M., Majamaa, K., Maraganore, D., Marder, K., Markopoulou, K., Martikainen, M.H., Mata, I., Mazzetti, P., Mellick, G., Menéndez‐González, M., Micheli, F., Mirelman, A., Mir, P., Morino, H., Morris, H., Munhoz, R.P., Naito, A., Olszewska, D.A., Ozelius, L.J., Padmanabhan, S., Paisán‐Ruiz, C., Payami, H., Peluso, S., Petkovic, S., Petrucci, S., Pezzoli, G., Pimentel, M., Pirker, W., Pramstaller, P.P., Pulkes, T., Puschmann, A., Quattrone, A., Raggio, V., Ransmayr, G., Rieder, C., Riess, O., Rodriguez‐Porcel, F., Rogaeva, E., Ross, O.A., Ruiz‐Martinez, J., Sammler, E., Luciano, M.S., Satake, W., Saunders‐Pullman, R., Sazci, A., Scherzer, C., Schrag, A., Schumacher‐Schuh, A., Sharma, M., Sidransky, E., Singleton, A.B., Petersen, M.S., Smolders, S., Spitz, M., Stefanis, L., Struhal, W., Sue, C., Swan, M., Swanberg, M., Taba, P., Taipa, R., Tan, M., Tan, A.H., Tan, E‐K, Tang, B., Tayebi, N., Thaler, A., Thomas, A., Toda, T., Toft, M., Torres, L., Tumas, V., Valente, E.M., Van Broeckhoven, C., Vecsei, L., Velez‐Pardo, C., Vidailhet, M., Warner, T.T., Williams‐Gray, C.H., Winkelmann, J., Woitalla, D., Wood, N.W., Wszolek, Z.K., Wu, R‐M, Wu, Y‐R, Xie, T., Yoshino, H., Zhang, B., Zimprich, A., Vollstedt, E‐J, Kasten, M., Klein, C., Aasly, J., Adler, C., Ahmad‐Annuar, A., Albanese, A., Alcalay, R., Al‐Mubarak, B., Alvarez, V., Andree‐Muñoz, B., Annesi, G., Appel‐Cresswell, S., Arkadir, D., Armasu, S., Barber, T.R., Bardien, S., Barkhuizen, M., Barrett, M.J., BaŞak, A.N., Beach, T., Benitez, B.A., Berg, D., Bhatia, K., Binkofski, F., Blauwendraat, C., Bonifati, V., Borges, V., Bozi, M., Brice, A., Brighina, L., Brockmann, K., Brüggemann, N., Camacho, M., Cardoso, F., Belin, A.C., Carr, J., Chan, P., Chang‐Castello, J., Chase, B., Chen‐Plotkin, A., Chung, S.J., Cilia, R., Clarimon, J., Clark, L., Cornejo‐Olivas, M., Corvol, J‐C, Cosentino, C., Cras, P., Crosiers, D., Damásio, J., Das, P., Carvalho Aguiar, P., De Michele, G., De Rosa, A., Dieguez, E., Dorszewska, J., Erer, S., Ertan, S., Farrer, M., Fedotova, E., Ferese, R., Ferrarese, C., Ferraz, H., Fiala, O., Foroud, T., Friedman, A., Frigerio, R., Funayama, M., Gambardella, S., Garraux, G., Gatto, E.M., Genç, G., Goldwurm, S., Gomez‐Esteban, J.C., Gómez‐Garre, P., Gorostidi, A., Grosset, D., Hanagasi, H., Hardy, J., Hassan, A., Hattori, N., Hauser, R.A., Hedera, P., Hentati, F., Hertz, J.M., Holton, J.L., Houlden, H., Hutz, M.H., Ikeuchi, T., Illarioshkin, S., Inca‐Martinez, M., Infante, J., Jankovic, J., Jeon, B.S., Jesús, S., Jimenez‐Del‐Rio, M., Kataoka, H., Kawakami, H., Kim, Y.J., Klivényi, P., Kõks, S., König, I.R., KostiĆ, V., Koziorowski, D., Krüger, R., Krygowska‐Wajs, A., Kulisevsky, J., Lang, A., LeDoux, M., Lesage, S., Lim, S‐Y, Lin, C‐H, Lohmann, K., Lopera, F., Lopez, G., Lu, C‐S, Lynch, T., Machaczka, M., Madoev, H., Magalhães, M., Majamaa, K., Maraganore, D., Marder, K., Markopoulou, K., Martikainen, M.H., Mata, I., Mazzetti, P., Mellick, G., Menéndez‐González, M., Micheli, F., Mirelman, A., Mir, P., Morino, H., Morris, H., Munhoz, R.P., Naito, A., Olszewska, D.A., Ozelius, L.J., Padmanabhan, S., Paisán‐Ruiz, C., Payami, H., Peluso, S., Petkovic, S., Petrucci, S., Pezzoli, G., Pimentel, M., Pirker, W., Pramstaller, P.P., Pulkes, T., Puschmann, A., Quattrone, A., Raggio, V., Ransmayr, G., Rieder, C., Riess, O., Rodriguez‐Porcel, F., Rogaeva, E., Ross, O.A., Ruiz‐Martinez, J., Sammler, E., Luciano, M.S., Satake, W., Saunders‐Pullman, R., Sazci, A., Scherzer, C., Schrag, A., Schumacher‐Schuh, A., Sharma, M., Sidransky, E., Singleton, A.B., Petersen, M.S., Smolders, S., Spitz, M., Stefanis, L., Struhal, W., Sue, C., Swan, M., Swanberg, M., Taba, P., Taipa, R., Tan, M., Tan, A.H., Tan, E‐K, Tang, B., Tayebi, N., Thaler, A., Thomas, A., Toda, T., Toft, M., Torres, L., Tumas, V., Valente, E.M., Van Broeckhoven, C., Vecsei, L., Velez‐Pardo, C., Vidailhet, M., Warner, T.T., Williams‐Gray, C.H., Winkelmann, J., Woitalla, D., Wood, N.W., Wszolek, Z.K., Wu, R‐M, Wu, Y‐R, Xie, T., Yoshino, H., Zhang, B., and Zimprich, A.
Abstract: Talks on rare diseases in the field of neurology often start with a statement like this: “About 80% of all rare diseases have a neurologic manifestation and about 80% of those are genetic in origin.” Although these numbers probably represent more of an estimate than well‐documented evidence, rapidly advancing and cost‐effective sequencing technologies have led to the quickly growing identification of patients with hereditary neurological diseases...
Published: 2019

18. An atlas of cortical circular RNA expression in Alzheimer disease brains demonstrates clinical and pathological associations

Author: Dube, U., Del-Aguila, J.L., Li, Z., Budde, J.P., Jiang, S., Hsu, S., Ibanez, L., Fernandez, M.V., Farias, F., Norton, J., Gentsch, J., Wang, F., Allegri, R., Amtashar, F., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., D'Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Kasuga, K., Kawarabayashi, T., Klunk, W., koeppe, R., Kuder-Buletta, E., Laske, C., Levin, J., Marcus, D., Martins, R., Mason, N.S., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Dube, U., Del-Aguila, J.L., Li, Z., Budde, J.P., Jiang, S., Hsu, S., Ibanez, L., Fernandez, M.V., Farias, F., Norton, J., Gentsch, J., Wang, F., Allegri, R., Amtashar, F., Benzinger, T., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, J., Buckles, V., Chea, S., Chrem, P., Chui, H., Cinco, J., Clifford, J., D'Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., Houeland DiBari, S., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Kasuga, K., Kawarabayashi, T., Klunk, W., koeppe, R., Kuder-Buletta, E., Laske, C., Levin, J., Marcus, D., Martins, R., Mason, N.S., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Perrin, R., Raichle, M., Ringman, J., Roh, J-H, Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., and Xu, X.
Abstract: Parietal cortex RNA-sequencing (RNA-seq) data were generated from individuals with and without Alzheimer disease (AD; ncontrol = 13; nAD = 83) from the Knight Alzheimer Disease Research Center (Knight ADRC). Using this and an independent (Mount Sinai Brain Bank (MSBB)) AD RNA-seq dataset, cortical circular RNA (circRNA) expression was quantified in the context of AD. Significant associations were identified between circRNA expression and AD diagnosis, clinical dementia severity and neuropathological severity. It was demonstrated that most circRNA–AD associations are independent of changes in cognate linear messenger RNA expression or estimated brain cell-type proportions. Evidence was provided for circRNA expression changes occurring early in presymptomatic AD and in autosomal dominant AD. It was also observed that AD-associated circRNAs co-expressed with known AD genes. Finally, potential microRNA-binding sites were identified in AD-associated circRNAs for miRNAs predicted to target AD genes. Together, these results highlight the importance of analyzing non-linear RNAs and support future studies exploring the potential roles of circRNAs in AD pathogenesis.
Published: 2019

19. Using global team science to identify genetic parkinson's disease worldwide

Author: Vollstedt, E. -J., Kasten, M., Klein, C., Aasly, J., Adler, C., Ahmad-Annuar, A., Albanese, Alberto, Alcalay, R. N., Al-Mubarak, B., Alvarez, V., Andree-Munoz, B., Annesi, G., Appel-Cresswell, S., Arkadir, D., Armasu, S., Barber, T. R., Bardien, S., Barkhuizen, M., Barrett, M. J., Basak, A. N., Beach, T., Benitez, B. A., Berg, D., Bhatia, K., Binkofski, F., Blauwendraat, C., Bonifati, V., Borges, V., Bozi, M., Brice, A., Brighina, L., Brockmann, K., Brucke, T., Bruggemann, N., Camacho, M., Cardoso, F., Belin, A. C., Carr, J., Chan, P., Chang-Castello, J., Chase, B., Chen-Plotkin, A., Ju Chung, S., Cilia, R., Clarimon, J., Clark, L., Cornejo-Olivas, M., Corvol, J. -C., Cosentino, C., Cras, P., Crosiers, D., Damasio, J., Das, P., de Carvalho Aguiar, P., De Michele, G., De Rosa, A., Dieguez, E., Dorszewska, J., Erer, S., Ertan, S., Farrer, M., Fedotova, E., Ferese, R., Ferrarese, C., Ferraz, H., Fiala, O., Foroud, T., Friedman, A., Frigerio, R., Funayama, M., Gambardella, S., Garraux, G., Gatto, E. M., Genc, G., Giladi, N., Goldwurm, S., Gomez-Esteban, J. C., Gomez-Garre, P., Gorostidi, A., Grosset, D., Hanagasi, H., Hardy, J., Hassan, A., Hattori, N., Hauser, R. A., Hedera, P., Hentati, F., Hertz, J. M., Holton, J. L., Houlden, H., Hutz, M. H., Ikeuchi, T., Illarioshkin, S., Inca-Martinez, M., Infante, J., Jankovic, J., Jeon, B. S., Jesus, S., Jimenez-Del-Rio, M., Kaasinen, V., Kataoka, H., Kawakami, H., Kim, Y. J., Klivenyi, P., Koks, S., Konig, I. R., Kostic, V., Koziorowski, D., Kruger, R., Krygowska-Wajs, A., Kulisevsky, J., Lai, D., Lang, A., Ledoux, M., Lesage, S., Lim, S. -Y., Lin, C. -H., Lohmann, K., Lopera, F., Lopez, G., Lu, C. -S., Lynch, T., Machaczka, M., Madoev, H., Magalhaes, M., Majamaa, K., Maraganore, D., Marder, K., Markopoulou, K., Martikainen, M. H., Mata, I., Mazzetti, P., Mellick, G., Menendez-Gonzalez, M., Micheli, F., Mirelman, A., Mir, P., Morino, H., Morris, H., Munhoz, R. P., Naito, A., Olszewska, D. A., Ozelius, L. J., Padmanabhan, S., Paisan-Ruiz, C., Payami, H., Peluso, S., Petkovic, S., Petrucci, S., Pezzoli, G., Pimentel, M., Pirker, W., Pramstaller, P. P., Pulkes, T., Puschmann, A., Quattrone, A., Raggio, V., Ransmayr, G., Rieder, C., Riess, O., Rodriguez-Porcel, F., Rogaeva, E., Ross, O. A., Ruiz-Martinez, J., Sammler, E., San Luciano, M., Satake, W., Saunders-Pullman, R., Sazci, A., Scherzer, C., Schrag, A., Schumacher-Schuh, A., Sharma, M., Sidransky, E., Singleton, A. B., Petersen, M. S., Smolders, S., Spitz, M., Stefanis, L., Struhal, W., Sue, C. M., Swan, M., Swanberg, M., Taba, P., Taipa, R., Tan, M., Tan, A. H., Tan, E. -K., Tang, B., Tayebi, N., Thaler, A., Thomas, A., Toda, T., Toft, M., Torres, L., Tumas, V., Valente, E. M., Van Broeckhoven, C., Vecsei, L., Velez-Pardo, C., Vidailhet, M., Warner, T. T., Williams-Gray, C. H., Winkelmann, J., Woitalla, D., Wood, N. W., Wszolek, Z. K., Wu, R. -M., Wu, Y. -R., Xie, T., Yoshino, H., Zhang, B., Zimprich, A., Albanese A. (ORCID:0000-0002-5864-0006), Vollstedt, E. -J., Kasten, M., Klein, C., Aasly, J., Adler, C., Ahmad-Annuar, A., Albanese, Alberto, Alcalay, R. N., Al-Mubarak, B., Alvarez, V., Andree-Munoz, B., Annesi, G., Appel-Cresswell, S., Arkadir, D., Armasu, S., Barber, T. R., Bardien, S., Barkhuizen, M., Barrett, M. J., Basak, A. N., Beach, T., Benitez, B. A., Berg, D., Bhatia, K., Binkofski, F., Blauwendraat, C., Bonifati, V., Borges, V., Bozi, M., Brice, A., Brighina, L., Brockmann, K., Brucke, T., Bruggemann, N., Camacho, M., Cardoso, F., Belin, A. C., Carr, J., Chan, P., Chang-Castello, J., Chase, B., Chen-Plotkin, A., Ju Chung, S., Cilia, R., Clarimon, J., Clark, L., Cornejo-Olivas, M., Corvol, J. -C., Cosentino, C., Cras, P., Crosiers, D., Damasio, J., Das, P., de Carvalho Aguiar, P., De Michele, G., De Rosa, A., Dieguez, E., Dorszewska, J., Erer, S., Ertan, S., Farrer, M., Fedotova, E., Ferese, R., Ferrarese, C., Ferraz, H., Fiala, O., Foroud, T., Friedman, A., Frigerio, R., Funayama, M., Gambardella, S., Garraux, G., Gatto, E. M., Genc, G., Giladi, N., Goldwurm, S., Gomez-Esteban, J. C., Gomez-Garre, P., Gorostidi, A., Grosset, D., Hanagasi, H., Hardy, J., Hassan, A., Hattori, N., Hauser, R. A., Hedera, P., Hentati, F., Hertz, J. M., Holton, J. L., Houlden, H., Hutz, M. H., Ikeuchi, T., Illarioshkin, S., Inca-Martinez, M., Infante, J., Jankovic, J., Jeon, B. S., Jesus, S., Jimenez-Del-Rio, M., Kaasinen, V., Kataoka, H., Kawakami, H., Kim, Y. J., Klivenyi, P., Koks, S., Konig, I. R., Kostic, V., Koziorowski, D., Kruger, R., Krygowska-Wajs, A., Kulisevsky, J., Lai, D., Lang, A., Ledoux, M., Lesage, S., Lim, S. -Y., Lin, C. -H., Lohmann, K., Lopera, F., Lopez, G., Lu, C. -S., Lynch, T., Machaczka, M., Madoev, H., Magalhaes, M., Majamaa, K., Maraganore, D., Marder, K., Markopoulou, K., Martikainen, M. H., Mata, I., Mazzetti, P., Mellick, G., Menendez-Gonzalez, M., Micheli, F., Mirelman, A., Mir, P., Morino, H., Morris, H., Munhoz, R. P., Naito, A., Olszewska, D. A., Ozelius, L. J., Padmanabhan, S., Paisan-Ruiz, C., Payami, H., Peluso, S., Petkovic, S., Petrucci, S., Pezzoli, G., Pimentel, M., Pirker, W., Pramstaller, P. P., Pulkes, T., Puschmann, A., Quattrone, A., Raggio, V., Ransmayr, G., Rieder, C., Riess, O., Rodriguez-Porcel, F., Rogaeva, E., Ross, O. A., Ruiz-Martinez, J., Sammler, E., San Luciano, M., Satake, W., Saunders-Pullman, R., Sazci, A., Scherzer, C., Schrag, A., Schumacher-Schuh, A., Sharma, M., Sidransky, E., Singleton, A. B., Petersen, M. S., Smolders, S., Spitz, M., Stefanis, L., Struhal, W., Sue, C. M., Swan, M., Swanberg, M., Taba, P., Taipa, R., Tan, M., Tan, A. H., Tan, E. -K., Tang, B., Tayebi, N., Thaler, A., Thomas, A., Toda, T., Toft, M., Torres, L., Tumas, V., Valente, E. M., Van Broeckhoven, C., Vecsei, L., Velez-Pardo, C., Vidailhet, M., Warner, T. T., Williams-Gray, C. H., Winkelmann, J., Woitalla, D., Wood, N. W., Wszolek, Z. K., Wu, R. -M., Wu, Y. -R., Xie, T., Yoshino, H., Zhang, B., Zimprich, A., and Albanese A. (ORCID:0000-0002-5864-0006)
Abstract: Talks on rare diseases in the field of neurology often start with a statement like this: “About 80% of all rare diseases have a neurologic manifestation and about 80% of those are genetic in origin.” Although these numbers probably represent more of an estimate than well-documented evidence, rapidly advancing and cost-effective sequencing technologies have led to the quickly growing identification of patients with hereditary neurological diseases. Although the importance of genetics for diagnosis and genetic counseling is undisputed, the recent development of first genetargeted therapies entering clinical trial1,2 is adding an important new layer to the (re-)consideration of genetic testing in neurology. However, establishing accurate genotype– phenotype and genotype–treatment relationships requires large sample sizes. Systematic reviews can serve as instruments to combine information from several small samples, but unfortunately, this is often complicated by inconsistent and incomplete reporting of clinical and genetic data across studies. Thus, large multicenter approaches are necessary to systematically and uniformly characterize patients with genetic neurologic conditions and to eventually establish sizable clinical trial-ready cohorts.
Published: 2019

20. A sporadic case of dentatorubral pallidoluysian atrophy (DRPLA) with CAG repeat expansion but no clinical abnormalities in the father

Author: Shimizu, N., Yamami, T., Nakayama, M., Ikeuchi, T., Koide, R., and Tsuji, S.
Published: 1996

21. Increase in xylitol production by Candida tropicalis upon addition of salt

Author: Azuma, M, Ikeuchi, T, Kiritani, R, Kato, J, and Ooshima, H
Published: 2000
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22. UTILIZING SOCIAL ROBOT TO REDUCE WORKLOAD OF HEALTHCARE PROFESSIONALS IN PSYCHIATRIC HOSPITAL: A PRELIMINARY STUDY

Author: Ikeuchi, T, primary, Sakurai, R, additional, Furuta, K, additional, Kasahara, Y, additional, Imamura, Y, additional, and Shinkai, S, additional
Published: 2018
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23. Screening of microorganisms for xylitol production and fermentation behavior in high concentrations of xylose

Author: Ikeuchi, T, Azuma, M, Kato, J, and Ooshima, H
Published: 1999
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24. Ultrasound And Embryonic Chromosomes

Author: Ikeuchi, T., Sasaki, M., Oshimura, M., Azumi, J., Tsuji, K., and Shimizu, T.
Published: 1973

25. THE ROLE OF SOCIAL CONTACT IN THE ASSOCIATION OF AGE AND WELL-BEING

Author: Ikeuchi, T., primary, Kobayashi, E., additional, and Fujiwara, Y., additional
Published: 2017
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26. FUTURE TIME PERSPECTIVE OF OLDER GERMANS AND JAPANESE LIVING ALONE

Author: Ikeuchi, T., primary, Lang, F.R., additional, and Osada, H., additional
Published: 2017
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27. Clinical and genetic characterization of adult‐onset leukoencephalopathy with axonal spheroids and pigmented glia associated with CSF1R mutation

Author: Konno, T., Yoshida, K., Mizuno, T., Kawarai, Toshitaka, Tada, M., Nozaki, H., Ikeda, S.-I., Nishizawa, M., Onodera, O., Wszolek, Z. K., Ikeuchi, T., Konno, T., Yoshida, K., Mizuno, T., Kawarai, Toshitaka, Tada, M., Nozaki, H., Ikeda, S.-I., Nishizawa, M., Onodera, O., Wszolek, Z. K., and Ikeuchi, T.
Abstract: Background and purpose: The clinical characteristics of colony stimulating factor 1 receptor (CSF1R) related adult‐onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) have been only partially elucidated. Methods: Clinical data from CSF1R mutation carriers who had been seen at our institutions or reported elsewhere were collected and analysed using a specific investigation sheet to standardize the data. Results: In all, 122 cases from 90 families with CSF1R mutations were identified. The mean age of onset was 43 years (range 18–78 years), the mean age at death was 53 years (range 23–84 years) and the mean disease duration was 6.8 years (range 1–29 years). Women had a significantly younger age of onset than men (40 vs. 47 years, P = 0.0006, 95% confidence interval 3.158–11.177). There was an age‐dependent penetrance that was significantly different between the sexes (P = 0.0013). Motor dysfunctions were the most frequent initial symptom in women whose diseases began in their 20s. Thinning of the corpus callosum, abnormal signalling in pyramidal tracts, diffusion‐restricted lesions and calcifications in the white matter were characteristic imaging findings of ALSP. The calcifications were more frequently reported in our case series than in the literature (54% vs. 3%). Seventy‐nine per cent of the mutations were located in the distal part of the tyrosine kinase domain of CSF1R (102 cases). There were no apparent phenotype−genotype correlations. Conclusions: The characteristics of ALSP were clarified. The phenotype of ALSP caused by CSF1R mutations is affected by sex.
Published: 2016

28. Chromosomal instability syndrome of total PCS with mosaic variegated aneuploidy: Genetic homogeneity of the two Japanese infants

Author: Matsuura, S., Ito, E., Ikeuchi, T., Kajii, T., and Komatsu, K.
Subjects: Human genetics -- Research, Chromosome abnormalities -- Research, Genetic disorders -- Research, Aneuploidy -- Research, Mosaicism -- Research, Lymphocytes -- Abnormalities, Cell death -- Abnormalities, Biological sciences
Published: 2001

29. Diagnostic Value of Brain Calcifications in Adult-Onset Leukoencephalopathy with Axonal Spheroids and Pigmented Glia

Author: Konno, T., primary, Broderick, D.F., additional, Mezaki, N., additional, Isami, A., additional, Kaneda, D., additional, Tashiro, Y., additional, Tokutake, T., additional, Keegan, B.M., additional, Woodruff, B.K., additional, Miura, T., additional, Nozaki, H., additional, Nishizawa, M., additional, Onodera, O., additional, Wszolek, Z.K., additional, and Ikeuchi, T., additional
Published: 2016
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30. RANDOM BIOPSY AND RECURRENCE RISK IN PATIENTS WITH BLADDER CANCER

Author: Hideki Watanabe, Ikeuchi T, IwaiY, Andou H, Kenjiro Kohri, Yutaro Hayashi, HoriH, Yasuyuki Yamada, T. Kawai, Hirao N, Terao E, Asaka H, Toshiyasu Tawada, Kato K, and Ito T
Subjects: Male, Risk, medicine.medical_specialty, Multivariate analysis, Biopsy, Urology, Urinary Bladder, Random biopsy, Recurrence risk, medicine, Humans, In patient, Risk factor, Aged, Retrospective Studies, Prostatectomy, Bladder cancer, medicine.diagnostic_test, business.industry, Significant difference, Middle Aged, medicine.disease, Urinary Bladder Neoplasms, Female, Neoplasm Recurrence, Local, business
Abstract: BACKGROUND We studied the relationship between the recurrence rate of primary superficial bladder cancer and random biopsy. METHODS We performed transurethral resection of primary superficial bladder cancer in 144 patients, and in 55 of those cases a random biopsy was also performed. The non-recurrence rate was examined in many recurrence facters. RESULTS The non-recurrence rate in the group with random biopsy was not significantly different from that observed in the group (100 patients) without random biopsy (chi 2 test, Generalized Wilcoxon test and multivariate analysis). Because the intravesical instillation therapy is an important inhibition factor in the recurrence rate of the primary superficial bladder cancer, we further analysed the recurrence rate in two non treated groups with or without random biopsy (13 and 35 patients respectively). No significant difference in the rate of recurrence between the two groups was observed. However, we noted recurrence of bladder cancer at biopsy positions in 8/13 patients. CONCLUSION It appears that random biopsy may have an effect on the recurrence or the implantation of tumor cells. Further studies are needed to clarify whether random biopsy is a risk factor in the recurrence rate of primary superficial bladder cancer.
Published: 1996

31. Clinical studies of efficacy of imipenem/cilastatin sodium against urinary tract infections with ureterocutaneostomy

Author: Yogi, S., Yoshikawa, H., Ikeuchi, T., and Kai, Y.
Subjects: UTI, IPM/CS, Ureterocutaneostomy, 494.9
Abstract: 尿路感染症に対するIPM/CSの臨床効果を尿管皮膚瘻造設術を受けた19例の悪性腫瘍患者(膀胱腫瘍15例, 前立腺癌3例, 子宮癌1例)について観察した.IPM/CSの投与法は1回0.5 gを1日2回点滴静注し, 薬効評価は投与後5日目にUTI判定基準に従って行った.その結果, 総合臨床効果は著効4例(20.0%), 有効9例(45.0%), 無効7例(35.0%)で総合有効率は65.0%となった.疾患病態群別にみた効果は, G-3群(単独菌感染・上部尿路感染)が3例で有効率は33.0%, G-6群(複数菌感染・カテーテル非留置)が17例で有効率は70.6%であった.細菌学的効果としては, 分離菌38株中34株が本剤投与後に消失し, 消失率は89.5%であった, Clinical efficacy of IPM/CS against urinary tract infections (UTI) was evaluated on 19 patients with malignancies (bladder tumor: 15, prostate cancer: 3, uterus cancer: 1) and 1 patient with a benign disorder (ureter stenosis) who had undergone ureterocutaneostomy between January, 1988 and December, 1990. Their ages ranged from 42 to 79 years. Postoperatively, they had UTI with pyuria of greater than or equal to 5/hpf and bacteriuria of greater than or equal to 10(4)/ml. IPM/CS was administered at a dose of 0.5 g (0.25g/0.25 g) twice a day through intravenous drip infusion. Its efficacy was evaluated according to the UTI criteria for clinical evaluation as ruled by the Japanese Society of Chemotherapy. Overall clinical value was rated "excellent" in 4 (20%), "moderate" in 9 (45%) and "poor" in 7 (35%) cases for a total of 65%. The efficacy by types of infection was 33% and 70.6% in the group of single infection and in the group of mixed infection, respectively. As to bacteriological efficacy 34 of the 38 strains (89.5%) isolated were eradicated following its administration. The eradication rate was 84.6% for P. aeruginosa, and 84.6% for E. faecalis. Microbes which appeared after its dosing amounted to 6 classes of 17 strains, 6 NFB strains of which were identified. As a side effect, elevation of serum GPT (5%) was noted. Regardless of the underlying conditions (malignant diseases and ureterocutaneostomy), clinical efficacy of IPM/CS was appreciable. In addition, the MIC for (P. aeruginosa, E. faecalis) of IPM/CS was lower than that of PIPC.
Published: 1992

32. Multiple γ-secretase product peptides are coordinately increased in concentration in the cerebrospinal fluid of a subpopulation of sporadic Alzheimer’s disease subjects

Author: Hata, S., Taniguchi, M., Piao, Y., Ikeuchi, T., Fagan, A.M., Holtzman, D.M., Bateman, R., Sohrabi, H.R., Martins, R.N., Gandy, S., Urakami, K., Suzuki, T., Hata, S., Taniguchi, M., Piao, Y., Ikeuchi, T., Fagan, A.M., Holtzman, D.M., Bateman, R., Sohrabi, H.R., Martins, R.N., Gandy, S., Urakami, K., and Suzuki, T.
Abstract: Background Alcadeinα (Alcα) is a neuronal membrane protein that colocalizes with the Alzheimer's amyloid-β precursor protein (APP). Successive cleavage of APP by β- and γ-secretases generates the aggregatable amyloid-β peptide (Aβ), while cleavage of APP or Alcα by α- and γ-secretases generates non-aggregatable p3 or p3-Alcα peptides. Aβ and p3-Alcα can be recovered from human cerebrospinal fluid (CSF). We have previously reported alternative processing of APP and Alcα in the CSF of some patients with sporadic mild cognitive impairment (MCI) and AD (SAD). Results Using the sandwich enzyme-linked immunosorbent assay (ELISA) system that detects total p3-Alcα, we determined levels of total p3-Alcα in CSF from subjects in one of four diagnostic categories (elderly controls, MCI, SAD, or other neurological disease) derived from three independent cohorts. Levels of Aβ40 correlated with levels of total p3-Alcα in all cohorts. Conclusions We confirm that Aβ40 is the most abundant Aβ species, and we propose a model in which CSF p3-Alcα can serve as a either (1) a nonaggregatable surrogate marker for γ-secretase activity; (2) as a marker for clearance of transmembrane domain peptides derived from integral protein catabolism; or (3) both. We propose the specification of an MCI/SAD endophenotype characterized by co-elevation of levels of both CSF p3-Alcα and Aβ40, and we propose that subjects in this category might be especially responsive to therapeutics aimed at modulation of γ-secretase function and/or transmembrane domain peptide clearance. These peptides may also be used to monitor the efficacy of therapeutics that target these steps in Aβ metabolis
Published: 2012

33. Spastic paraplegia, ataxia, mental retardation (SPAR) : A novel genetic disorder

Author: Hedera, P., Rainier, S., Zhao, X. P., Schalling, M., Lindblad, Kerstin, Yuan, Q-P., Ikeuchi, T., Trobe, J., Wald, J. J., Eldevik, O. P., Kluin, K., Fink, J. K., Hedera, P., Rainier, S., Zhao, X. P., Schalling, M., Lindblad, Kerstin, Yuan, Q-P., Ikeuchi, T., Trobe, J., Wald, J. J., Eldevik, O. P., Kluin, K., and Fink, J. K.
Abstract: Objective: To describe a kindred with a dominantly inherited neurologic disorder manifested either as uncomplicated spastic paraplegia or ataxia, spastic paraplegia, and mental retardation. Methods: Neurologic examinations and molecular genetic analysis (exclusion of known SCA and HSP genes and loci; and trinucleotide repeat expansion detection [RED]) were performed in six affected and four unaffected subjects in this family. MRI, electromyography (EMG), and nerve conduction studies were performed in three affected subjects. Results: The phenotype of this dominantly inherited syndrome varied in succeeding generations. Pure spastic paraplegia was present in the earliest generation; subsequent generations had ataxia and mental retardation. MRI showed marked atrophy of the spinal cord in all patients and cerebellar atrophy in those with ataxia. Laboratory analysis showed that the disorder was not caused by mutations in genes that cause SCA-1, SCA-2, SCA-3, SCA-6, SCA-7, SCA-8, and SCA-12; not linked to other known loci for autosomal dominant ataxia (SCA-4, SCA-5, SCA-10, SCA-11, SCA-13, SCA-14, and SCA-16); and not linked to known loci for autosomal dominant hereditary spastic paraplegia (HSP) (SPG-3, SPG-4, SPG-6, SPG-8, SPG-9, SPG-10, SPG-12, and SPG-13) or autosomal recessive HSP SPG-7. Analysis of intergenerational differences in age at onset of symptoms suggests genetic anticipation. Using RED, the authors did not detect expanded CAG, CCT, TGG, or CGT repeats that segregate with the disease. Conclusions: The authors describe an unusual, dominantly inherited neurologic disorder in which the phenotype (pure spastic paraplegia or spastic ataxia with variable mental retardation) differed in subsequent generations. The molecular explanation for apparent genetic anticipation does not appear to involve trinucleotide repeat expansion. The spinocerebellar ataxias (SCA) and hereditary spastic paraplegias (HSP), although clinically heterogeneous, typically are discerned as d
Published: 2002
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34. Enhanced Accumulation of Phosphorylated -Synuclein and Elevated -Amyloid 42/40 Ratio Caused by Expression of the Presenilin-1 T440 Mutant Associated with Familial Lewy Body Disease and Variant Alzheimer's Disease

Author: Kaneko, H., primary, Kakita, A., additional, Kasuga, K., additional, Nozaki, H., additional, Ishikawa, A., additional, Miyashita, A., additional, Kuwano, R., additional, Ito, G., additional, Iwatsubo, T., additional, Takahashi, H., additional, Nishizawa, M., additional, Onodera, O., additional, Sisodia, S. S., additional, and Ikeuchi, T., additional
Published: 2007
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35. Separation of metals with thiobenzoylphenyl-hydroxylamine by precipitation chromatography on circular filter paper

Author: Honjo, T., Ikeuchi, T., and Terada, K.
Published: 1987
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36. This title is unavailable for guests, please login to see more information.

Author: Yogi, S., Yoshikawa, H., Ikeuchi, T., Kai, Y., Yogi, S., Yoshikawa, H., Ikeuchi, T., and Kai, Y.
Abstract: Clinical efficacy of IPM/CS against urinary tract infections (UTI) was evaluated on 19 patients with malignancies (bladder tumor: 15, prostate cancer: 3, uterus cancer: 1) and 1 patient with a benign disorder (ureter stenosis) who had undergone ureterocutaneostomy between January, 1988 and December, 1990. Their ages ranged from 42 to 79 years. Postoperatively, they had UTI with pyuria of greater than or equal to 5/hpf and bacteriuria of greater than or equal to 10(4)/ml. IPM/CS was administered at a dose of 0.5 g (0.25g/0.25 g) twice a day through intravenous drip infusion. Its efficacy was evaluated according to the UTI criteria for clinical evaluation as ruled by the Japanese Society of Chemotherapy. Overall clinical value was rated "excellent" in 4 (20%), "moderate" in 9 (45%) and "poor" in 7 (35%) cases for a total of 65%. The efficacy by types of infection was 33% and 70.6% in the group of single infection and in the group of mixed infection, respectively. As to bacteriological efficacy 34 of the 38 strains (89.5%) isolated were eradicated following its administration. The eradication rate was 84.6% for P. aeruginosa, and 84.6% for E. faecalis. Microbes which appeared after its dosing amounted to 6 classes of 17 strains, 6 NFB strains of which were identified. As a side effect, elevation of serum GPT (5%) was noted. Regardless of the underlying conditions (malignant diseases and ureterocutaneostomy), clinical efficacy of IPM/CS was appreciable. In addition, the MIC for (P. aeruginosa, E. faecalis) of IPM/CS was lower than that of PIPC.
Published: 1992

37. Layer stackings and physical properties of mixed-layer structure phases III: preparation of mixed-layer structure phases of ReXNb1−XSe2 and OsXNb1−XSe2 and some electrical and magnetic properties

Author: Hayashi, K., primary, Chijimatsu, Y., additional, Maeda, N., additional, Ikeuchi, T., additional, and Onuma, E., additional
Published: 1998
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38. Numerical simulation on damage to pipe piers in Hyogoken-Nanbu earthquake

Author: Nishimura, N., primary, Ikeuchi, T., additional, and Taniguchi, N., additional
Published: 1998
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39. Japanese Families with Autosomal Dominant Pure Cerebellar Ataxia Map to Chromosome 19p13.1-p13.2 and Are Strongly Associated with Mild CAG Expansions in the Spinocerebellar Ataxia Type 6 Gene in Chromosome 19p13.1

Author: Ishikawa, K., primary, Tanaka, H., additional, Saito, M., additional, Ohkoshi, N., additional, Fujita, T., additional, Yoshizawa, K., additional, Ikeuchi, T., additional, Watanabe, M., additional, Hayashi, A., additional, Takiyama, Y., additional, Nishizawa, M., additional, Nakano, I., additional, Matsubayashi, K., additional, Miwa, M., additional, Shoji, S., additional, Kanazawa, I., additional, Tsuji, S., additional, and Mizusawa, H., additional
Published: 1997
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40. Potent and selective inhibition of human immunodeficiency virus type 1 transcription by piperazinyloxoquinoline derivatives

Author: Baba, M, primary, Okamoto, M, additional, Makino, M, additional, Kimura, Y, additional, Ikeuchi, T, additional, Sakaguchi, T, additional, and Okamoto, T, additional
Published: 1997
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41. Calcineurin-dependent nuclear translocation of a murine transcription factor NFATx: molecular cloning and functional characterization.

Author: Liu, J, primary, Koyano-Nakagawa, N, additional, Amasaki, Y, additional, Saito-Ohara, F, additional, Ikeuchi, T, additional, Imai, S, additional, Takano, T, additional, Arai, N, additional, Yokota, T, additional, and Arai, K, additional
Published: 1997
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42. Mixed layers in M Ta1−Se2 (M = Re, Os; 0 < x < 1)

Author: Hayashi, K., primary, Ikeuchi, T., additional, Takeuchi, H., additional, and Shimakawa, M., additional
Published: 1995
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43. Cloning, characterization, and chromosomal mapping of human aquaporin of collecting duct.

Author: Sasaki, S, primary, Fushimi, K, additional, Saito, H, additional, Saito, F, additional, Uchida, S, additional, Ishibashi, K, additional, Kuwahara, M, additional, Ikeuchi, T, additional, Inui, K, additional, and Nakajima, K, additional
Published: 1994
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44. Genotype-phenotype correlations in early onset ataxia with ocular motor apraxia and hypoalbuminaemia.

Author: Yokoseki A, Ishihara T, Koyama A, Shiga A, Yamada M, Suzuki C, Sekijima Y, Maruta K, Tsuchiya M, Date H, Sato T, Tada M, Ikeuchi T, Tsuji S, Nishizawa M, and Onodera O
Published: 2011
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45. Relationship between endotoxaemia and protein concentration of ascites in cirrhotic patients.

Author: Tarao, K, Moroi, T, Nagakura, Y, Ikeuchi, T, Suyama, T, Endo, O, and Fukushima, K
Abstract: Endotoxaemia was investigated by the Limulus assay in 42 cirrhotic patients with ascites and in 33 without ascites. The incidence of endotoxaemia in the former group (59.5%) was significantly (P less than 0.05) higher than in the latter (36.4%). Correlation between endotoxaemia and specific gravity and concentrations of total protein, albumin, and globulin in ascitic fluid was studied in the group with ascites. The specific gravity of ascites in 25 patients with endotoxaemia was significantly greater than that in 17 patients without endotoxaemia (P less than 0.01). The concentration of total protein in patients with endotoxaemia (13.95 +/- 7.18 milligram, mean +/- SD) was nearly twice as high (P less than 0.01) as in patients without endotoxaemia (7.49 +/- 3.60 milligram). The protein content of those who showed reactions greater or equal to 2(+) in the Limulus assay (16.78 +/- 7.14 milligram) was a significantly (P less than 0.05) higher than in those with 1(+) reaction (11.26 +/- 6.33 milligram). Moreover, the concentration of albumin in patients with endotoxaemia (7.68 +/- 4.60 milligram) was more than twice that of the patients without endotoxaemia (3.39 +/- 1.58 milligram, P less than 0.01). On the other hand, globulin concentration in patients with endotoxaemia was 1.6 times that of patients without endotoxaemia (P less than 0.01). Similar differences were noted between endotoxaemic and non-endotoxaemic patients in the ascites-to-serum ratio in protein, albumin, and globulin. These results suggest that in liver cirrhosis endotoxaemia may cause an increase in protein concentrations in ascitic fluid, and that it may be a precipitating factor in the formation of ascites. [ABSTRACT FROM PUBLISHER]
Published: 1979

46. Relationship between endotoxaemia and protein concentration of ascites in cirrhotic patients

Author: T Suyama, Kazuo Tarao, K. Fukushima, Y. Nagakura, Ikeuchi T, Moroi T, and Endo O
Subjects: Adult, Liver Cirrhosis, Male, medicine.medical_specialty, Cirrhosis, Globulin, Gastroenterology, Albumins, Internal medicine, Ascites, medicine, Ascitic Fluid, Humans, In patient, Specific Gravity, Limulus Test, Aged, Ascitic fluid, biology, Albumin, Fibrinogen, Proteins, Globulins, Blood Proteins, Middle Aged, biology.organism_classification, medicine.disease, Endotoxins, Limulus, Immunology, biology.protein, Female, medicine.symptom, Protein concentration, Research Article
Abstract: Endotoxaemia was investigated by the Limulus assay in 42 cirrhotic patients with ascites and in 33 without ascites. The incidence of endotoxaemia in the former group (59.5%) was significantly (P less than 0.05) higher than in the latter (36.4%). Correlation between endotoxaemia and specific gravity and concentrations of total protein, albumin, and globulin in ascitic fluid was studied in the group with ascites. The specific gravity of ascites in 25 patients with endotoxaemia was significantly greater than that in 17 patients without endotoxaemia (P less than 0.01). The concentration of total protein in patients with endotoxaemia (13.95 +/- 7.18 milligram, mean +/- SD) was nearly twice as high (P less than 0.01) as in patients without endotoxaemia (7.49 +/- 3.60 milligram). The protein content of those who showed reactions greater or equal to 2(+) in the Limulus assay (16.78 +/- 7.14 milligram) was a significantly (P less than 0.05) higher than in those with 1(+) reaction (11.26 +/- 6.33 milligram). Moreover, the concentration of albumin in patients with endotoxaemia (7.68 +/- 4.60 milligram) was more than twice that of the patients without endotoxaemia (3.39 +/- 1.58 milligram, P less than 0.01). On the other hand, globulin concentration in patients with endotoxaemia was 1.6 times that of patients without endotoxaemia (P less than 0.01). Similar differences were noted between endotoxaemic and non-endotoxaemic patients in the ascites-to-serum ratio in protein, albumin, and globulin. These results suggest that in liver cirrhosis endotoxaemia may cause an increase in protein concentrations in ascitic fluid, and that it may be a precipitating factor in the formation of ascites.
Published: 1979

47. Effects of simulated microgravity on mammalian fertilization and preimplantation embryonic development in vitro

Author: Kojima, Y., Sasaki, S., Kubota, Y., Ikeuchi, T., Hayashi, Y., and Kohri, K.
Published: 2000
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48. Characterization of a testicular 17@a,20@b-dihydroxy-4-pregnen-3-one (a spermiation-inducing steroid in fish) receptor from a teleost, Japanese eel (Anguilla japonica)^1

Author: Todo, T., Ikeuchi, T., Kobayashi, T., Kajiura-Kobayashi, H., Suzuki, K., Yoshikuni, M., Yamauchi, K., and Nagahama, Y.
Published: 2000
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49. cDNA cloning of a novel androgen receptor subtype.

Author: Ikeuchi, T, Todo, T, Kobayashi, T, and Nagahama, Y
Abstract: There has been general acceptance that only one type of androgen receptor (AR) exists in an individual. This contrasts with other members of the nuclear receptor superfamily where multiple forms have been reported (e.g. estrogen receptor alpha/beta, thyroid hormone receptor alpha/beta, etc.). We have previously identified 11-ketotestosterone (a potent androgen in teleosts) as the spermatogenesis-inducing hormone of the Japanese eel and have cloned its receptor (eAR1) cDNA from eel testis. Here we report on the cloning of a cDNA encoding a second type of AR (eAR2) from the eel testis and the functional characterization of the encoded protein. This cDNA contains a complete open reading frame encoding 797 amino acid residues. The amino acid sequence of eAR2 shows high homology with other ARs, including eAR1, in the DNA-binding (98-88%) and ligand-binding (59-85%) domains, whereas the other domains show low homology (<35%). In transient transfection assays of mammalian cells, the eAR2 protein displayed androgen-dependent activation of transcription from the androgen-responsive murine mammary tumor virus promoter. Tissue distribution of its mRNA was different from that of eAR1. We conclude that eAR2 is a novel AR in the eel, which we suggest should be named eel ARbeta to distinguish it from eAR1 (eARalpha).
Published: 1999

50. Mixed layers in MxTa1−xSe2(M = Re, Os; 0 < x< 1)

Author: Hayashi, K., Ikeuchi, T., Takeuchi, H., and Shimakawa, M.
Abstract: The layer stackings of the transition metal dichalcogenides were investigated in terms of the number of valence electrons per chemical formula. It is known that the isoelectronic compounds Re12Ta12Se2, Os13Ta23Se2, and WSe2crystallize into the 2Hb-MoS2structure, and TaSe2crystallizes into the 2Ha-NbS2structure or 1T-TaS2structure, depending on the temperature. The compounds outside these critical valence electron counts crystallize into so-called mixed-layer structures. The mixed-layer structures were simulated by stacking 300 random layers of 2Hb layers, 3R layers and 1T layers. The randomness and the mixing ratio of the prototype layers depend on the number of valence electron per chemical formula. There exists a two-phase region between the 1T-TaSe2phase and the mixed-layer phase. Hence there is no two-phase region between the mixed-layer phase and the MxTa1−xSe2critical phase. Therefore the mixed-layer phases of these systems are equilibrium phases and the 2Hb structure is the special structure of the MxTa1−xSe2mixed-layer structures. The Fermi level of the compounds is tuned by mixing the prototype layers to produce compounds with different numbers of valence electrons per chemical formula.
Published: 1995
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