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4. Concerns about the use of polygenic embryo screening for psychiatric and cognitive traits

Author

Lencz, T, Sabatello, M, Docherty, A, Peterson, RE, Soda, T, Austin, J, Bierut, L, Crepaz-Keay, D, Curtis, D, Degenhardt, F, Huckins, L, Lazaro-Munoz, G, Mattheisen, M, Meiser, B ; https://orcid.org/0000-0002-5086-0784, Peay, H, Rietschel, M, Walss-Bass, C, Davis, LK, Lencz, T, Sabatello, M, Docherty, A, Peterson, RE, Soda, T, Austin, J, Bierut, L, Crepaz-Keay, D, Curtis, D, Degenhardt, F, Huckins, L, Lazaro-Munoz, G, Mattheisen, M, Meiser, B ; https://orcid.org/0000-0002-5086-0784, Peay, H, Rietschel, M, Walss-Bass, C, and Davis, LK

Abstract

Private companies have begun offering services to allow parents undergoing in-vitro fertilisation to screen embryos for genetic risk of complex diseases, including psychiatric disorders. This procedure, called polygenic embryo screening, raises several difficult scientific and ethical issues, as discussed in this Personal View. Polygenic embryo screening depends on the statistical properties of polygenic risk scores, which are complex and not well studied in the context of this proposed clinical application. The clinical, social, and ethical implications of polygenic embryo screening have barely been discussed among relevant stakeholders. To our knowledge, the International Society of Psychiatric Genetics is the first professional biomedical organisation to issue a statement regarding polygenic embryo screening. For the reasons discussed in this Personal View, the Society urges caution and calls for additional research and oversight on the use of polygenic embryo screening.

Published
2022

12. Glutamate triggers intracellular Ca 2+ oscillations and nitric oxide release by inducing NAADP- and InsP 3 -dependent Ca 2+ release in mouse brain endothelial cells

Author

Zuccolo, E, Kheder, DA, Lim, D, Perna, A, Di Nezza, F, Botta, L, Scarpellino, G, Negri, S, Martinotti, S, Soda, T, Forcaia, G, Riboni, L, Ranzato, E, Sancini, G, Ambrosone, L, D'Angelo, E, Guerra, G, Moccia, F, Zuccolo, E, Kheder, D, Lim, D, Perna, A, Di Nezza, F, Botta, L, Scarpellino, G, Negri, S, Martinotti, S, Soda, T, Forcaia, G, Riboni, L, Ranzato, E, Sancini, G, Ambrosone, L, D'Angelo, E, Guerra, G, and Moccia, F

Subjects
Ca, nitric oxide, oscillations, 2+, endothelial cell, glutamate, Ca2+ oscillation, neurovascular coupling (NVC)
Abstract

The neurotransmitter glutamate increases cerebral blood flow by activating postsynaptic neurons and presynaptic glial cells within the neurovascular unit. Glutamate does so by causing an increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) in the target cells, which activates the Ca 2+ /Calmodulin-dependent nitric oxide (NO) synthase to release NO. It is unclear whether brain endothelial cells also sense glutamate through an elevation in [Ca 2+ ] i and NO production. The current study assessed whether and how glutamate drives Ca 2+ -dependent NO release in bEND5 cells, an established model of brain endothelial cells. We found that glutamate induced a dose-dependent oscillatory increase in [Ca 2+ ] i , which was maximally activated at 200 μM and inhibited by α-methyl-4-carboxyphenylglycine, a selective blocker of Group 1 metabotropic glutamate receptors. Glutamate-induced intracellular Ca 2+ oscillations were triggered by rhythmic endogenous Ca 2+ mobilization and maintained over time by extracellular Ca 2+ entry. Pharmacological manipulation revealed that glutamate-induced endogenous Ca 2+ release was mediated by InsP 3 -sensitive receptors and nicotinic acid adenine dinucleotide phosphate (NAADP) gated two-pore channel 1. Constitutive store-operated Ca 2+ entry mediated Ca 2+ entry during ongoing Ca 2+ oscillations. Finally, glutamate evoked a robust, although delayed increase in NO levels, which was blocked by pharmacologically inhibition of the accompanying intracellular Ca 2+ signals. Of note, glutamate induced Ca 2+ -dependent NO release also in hCMEC/D3 cells, an established model of human brain microvascular endothelial cells. This investigation demonstrates for the first time that metabotropic glutamate-induced intracellular Ca 2+ oscillations and NO release have the potential to impact on neurovascular coupling in the brain.

Published
2019

14. Sex differences associated with corpus callosum development in human infants: A longitudinal multimodal imaging study

Author

Piven, J., Pruett, J.R., Jr., Dager, S.R., IBIS Network, Soda, T., Hazlett, H.C., Estes, A.M., Elison, J.T., Gerig, G., Shen, M.D., Schmied, A., Wolff, J.J., Schultz, R.T., McKinstry, R.C., Botteron, K.N., Styner, M., and Swanson, M.R.

Abstract

The corpus callosum (CC) is the largest connective pathway in the human brain, linking cerebral hemispheres. There is longstanding debate in the scientific literature whether sex differences are evident in this structure, with many studies indicating the structure is larger in females. However, there are few data pertaining to this issue in infancy, during which time the most rapid developmental changes to the CC occur. In this study, we examined longitudinal brain imaging data collected from 104 infants at ages 6, 12, and 24 months. We identified sex differences in brain-size adjusted CC area and thickness characterized by a steeper rate of growth in males versus females from ages 6–24 months. In contrast to studies of older children and adults, CC size was larger for male compared to female infants. Based on diffusion tensor imaging data, we found that CC thickness is significantly associated with underlying microstructural organization. However, we observed no sex differences in the association between microstructure and thickness, suggesting that the role of factors such as axon density and/or myelination in determining CC size is generally equivalent between sexes. Finally, we found that CC length was negatively associated with nonverbal ability among females.

Published
2020
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16. International Consortium on the Genetics of Electroconvulsive Therapy and Severe Depressive Disorders (Gen-ECT-ic)

Author

Soda, T, McLoughlin, DM, Clark, SR, Oltedal, L, Kessler, U, Haavik, J, Bousman, C, Smith, DJ, Bioque, M, Clements, CC, Loo, C ; https://orcid.org/0000-0003-3267-0554, Vila-Rodriguez, F, Minelli, A, Mickey, BJ, Milev, R, Docherty, AR, Langan Martin, J, Achtyes, ED, Arolt, V, Redlich, R, Dannlowski, U, Cardoner, N, Clare, E, Craddock, N, Di Florio, A, Dmitrzak-Weglarz, M, Forty, L, Gordon-Smith, K, Husain, M, Ingram, WM, Jones, L, Jones, I, Juruena, M, Kirov, G, Landén, M, Müller, DJ, Nordensköld, A, Pålsson, E, Paul, M, Permoda, A, Pliszka, B, Rea, J, Schubert, KO, Sonnen, JA, Soria, V, Stageman, W, Takamiya, A, Urretavizacaya, M, Watson, S, Zavorotny, M, Young, AH, Vieta, E, Rybakowski, JK, Gennarelli, M, Zandi, PP, Sullivan, PF, Baune, BT, Soda, T, McLoughlin, DM, Clark, SR, Oltedal, L, Kessler, U, Haavik, J, Bousman, C, Smith, DJ, Bioque, M, Clements, CC, Loo, C ; https://orcid.org/0000-0003-3267-0554, Vila-Rodriguez, F, Minelli, A, Mickey, BJ, Milev, R, Docherty, AR, Langan Martin, J, Achtyes, ED, Arolt, V, Redlich, R, Dannlowski, U, Cardoner, N, Clare, E, Craddock, N, Di Florio, A, Dmitrzak-Weglarz, M, Forty, L, Gordon-Smith, K, Husain, M, Ingram, WM, Jones, L, Jones, I, Juruena, M, Kirov, G, Landén, M, Müller, DJ, Nordensköld, A, Pålsson, E, Paul, M, Permoda, A, Pliszka, B, Rea, J, Schubert, KO, Sonnen, JA, Soria, V, Stageman, W, Takamiya, A, Urretavizacaya, M, Watson, S, Zavorotny, M, Young, AH, Vieta, E, Rybakowski, JK, Gennarelli, M, Zandi, PP, Sullivan, PF, and Baune, BT

Abstract

Recent genome-wide association studies have demonstrated that the genetic burden associated with depression correlates with depression severity. Therefore, conducting genetic studies of patients at the most severe end of the depressive disorder spectrum, those with treatment-resistant depression and who are prescribed electroconvulsive therapy (ECT), could lead to a better understanding of the genetic underpinnings of depression. Despite ECT being one of the most effective forms of treatment for severe depressive disorders, it is usually placed at the end of treatment algorithms of current guidelines. This is perhaps because ECT has controlled risk and logistical demands including use of general anaesthesia and muscle relaxants and side-effects such as short-term memory impairment. Better understanding of the genetics and biology of ECT response and of cognitive side-effects could lead to more personalized treatment decisions. To enhance the understanding of the genomics of severe depression and ECT response, researchers and ECT providers from around the world and from various depression or ECT networks, but not limited to, such as the Psychiatric Genomics Consortium, the Clinical Alliance and Research in ECT, and the National Network of Depression Centers have formed the Genetics of ECT International Consortium (Gen-ECT-ic). Gen-ECT-ic will organize the largest clinical and genetic collection to date to study the genomics of severe depressive disorders and response to ECT, aiming for 30,000 patients worldwide using a GWAS approach. At this stage it will be the largest genomic study on treatment response in depression. Retrospective data abstraction and prospective data collection will be facilitated by a uniform data collection approach that is flexible and will incorporate data from many clinical practices. Gen-ECT-ic invites all ECT providers and researchers to join its efforts.

Published
2020

17. Glutamate triggers intracellular Ca 2+ oscillations and nitric oxide release by inducing NAADP- and InsP 3 -dependent Ca 2+ release in mouse brain endothelial cells

Author

Guerra, G., Zuccolo, E., Kheder, DA., Lim, D., Perna, A., Di Nezza, F., Lucariello, A., Tafuri, D., Soda, T., De Luca, A., Ambrosone, L., D’Angelo, E., and Moccia, F.

Subjects
Ca, nitric oxide, oscillations, 2+, glutamate, neurovascular coupling (NVC), endothelial cells
Abstract

The neurotransmitter glutamate increases cerebral blood flow by activating postsynaptic neurons and presynaptic glial cells within the neurovascular unit. Glutamate does so by causing an increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) in the target cells, which activates the Ca 2+ /Calmodulin-dependent nitric oxide (NO) synthase to release NO. It is unclear whether brain endothelial cells also sense glutamate through an elevation in [Ca 2+ ] i and NO production. The current study assessed whether and how glutamate drives Ca 2+ -dependent NO release in bEND5 cells, an established model of brain endothelial cells. We found that glutamate induced a dose-dependent oscillatory increase in [Ca 2+ ] i , which was maximally activated at 200 μM and inhibited by α-methyl-4-carboxyphenylglycine, a selective blocker of Group 1 metabotropic glutamate receptors. Glutamate-induced intracellular Ca 2+ oscillations were triggered by rhythmic endogenous Ca 2+ mobilization and maintained over time by extracellular Ca 2+ entry. Pharmacological manipulation revealed that glutamate-induced endogenous Ca 2+ release was mediated by InsP 3 -sensitive receptors and nicotinic acid adenine dinucleotide phosphate (NAADP) gated two-pore channel 1. Constitutive store-operated Ca 2+ entry mediated Ca 2+ entry during ongoing Ca 2+ oscillations. Finally, glutamate evoked a robust, although delayed increase in NO levels, which was blocked by pharmacologically inhibition of the accompanying intracellular Ca 2+ signals. Of note, glutamate induced Ca 2+ -dependent NO release also in hCMEC/D3 cells, an established model of human brain microvascular endothelial cells. This investigation demonstrates for the first time that metabotropic glutamate-induced intracellular Ca 2+ oscillations and NO release have the potential to impact on neurovascular coupling in the brain.

Published
2019

19. The efficacy and safety of lenvatinib in patients who did not meet the inclusion criteria of the phase III trial (REFLECT trial) and those with BCLC Stage B hepatocellular carcinoma: A nationwide multicenter study in Japan

Author

Sakamoto, A., primary, Kurosaki, M., additional, Tsuchiya, K., additional, Abe, T., additional, Ogawa, C., additional, Soda, T., additional, Kimura, H., additional, Kondo, M., additional, Tsuji, K., additional, Koichiro, F., additional, Shigeno, M., additional, Jyoko, K., additional, Narita, R., additional, Uchida, Y., additional, Yoshida, H., additional, Akahane, T., additional, Kobashi, H., additional, Mitsuda, A., additional, Marusawa, H., additional, and Izumi, N., additional

Published
2019
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21. International Society of Psychiatric Genetics Ethics Committee: Issues facing us

Author

Lázaro-Muñoz, G, Sabatello, M, Huckins, L, Peay, H, Degenhardt, F, Meiser, B ; https://orcid.org/0000-0002-5086-0784, Lencz, T, Soda, T, Docherty, A, Crepaz-Keay, D, Austin, J, Peterson, RE, Davis, LK, Lázaro-Muñoz, G, Sabatello, M, Huckins, L, Peay, H, Degenhardt, F, Meiser, B ; https://orcid.org/0000-0002-5086-0784, Lencz, T, Soda, T, Docherty, A, Crepaz-Keay, D, Austin, J, Peterson, RE, and Davis, LK

Abstract

Psychiatric genetics research is improving our understanding of the biological underpinnings of neurodiversity and mental illness. Using psychiatric genetics in ways that maximize benefits and minimize harms to individuals and society depends largely on how the ethical, legal, and social implications (ELSI) of psychiatric genetics are managed. The International Society of Psychiatric Genetics (ISPG) is the largest international organization dedicated to psychiatric genetics. Given its history, membership, and international reach, we believe the ISPG is well-equipped to contribute to the resolution of these ELSI challenges. As such, we recently created the ISPG Ethics Committee, an interdisciplinary group comprised of psychiatric genetics researchers, clinical geneticists, genetic counselors, mental health professionals, patients, patient advocates, bioethicists, and lawyers. This article highlights key ELSI challenges identified by the ISPG Ethics Committee to be of paramount importance for the ethical translation of psychiatric research into society in three contexts: research settings, clinical settings, and legal proceedings. For each of these arenas, we identify and discuss pressing psychiatric genetics ELSI dilemmas that merit attention and require action. The goal is to increase awareness about psychiatric genetics ELSI issues and encourage dialogue and action among stakeholders.

Published
2019

25. Stim and Orai proteins as novel actors in neuronal Ca2+ signalling and excitability

Author

Moccia, F, Zuccolo, E, Soda, T, Tanzi, F, Guerra, G, Mapelli, L, Lodola, F, D’Angelo, E, Moccia F, Zuccolo E, Soda T, Tanzi F, Guerra G, Mapelli L, Lodola F, D’Angelo E, Moccia, F, Zuccolo, E, Soda, T, Tanzi, F, Guerra, G, Mapelli, L, Lodola, F, D’Angelo, E, Moccia F, Zuccolo E, Soda T, Tanzi F, Guerra G, Mapelli L, Lodola F, and D’Angelo E

Abstract

Stimi and Orail are ubiquitous proteins that have long been known to mediate Ca2+ release-activated Ca2+ (CRAC) current (Icrac) and store-operated Ca2+ entry (SOCE) only in non-excitable cells. SOCE is activated following the depletion of the endogenous Ca2+ stores, which are mainly located within the endoplasmic reticulum (ER), to replete the intracellular Ca2+ reservoir and engage specific Ca2+-dependent processes, such as proliferation, migration, cytoskeletal remodeling, and gene expression. Their paralogs, Stim2, Orai2 and Orai3, support SOCE in heterologous expression systems, but their physiological role is still obscure. Ca2 + inflow in neurons has long been exclusively ascribed to voltage-operated and receptor-operated channels. Nevertheless, recent work has unveiled that Stim1-2 and Orai1-2, but not Orai3, proteins are also expressed and mediate SOCE in neurons. Herein, we survey current knowledge about the neuronal distribution of Stim and Orai proteins in rodent and human brains; we further discuss that Orai2 is the main pore-forming subunit of CRAC channels in central neurons, in which it may be activated by either Stim1 or Stim2 depending on species, brain region and physiological stimuli. We examine the functions regulated by SOCE in neurons, where this pathway is activated under resting conditions to refill the ER, control spinogenesis and regulate gene transcription. Besides, we highlighted the possibility that SOCE also controls neuronal excitation and regulate synaptic plasticity. Finally, we evaluate the involvement of Stim and Orai proteins in severe neurodegenerative and neurological disorders, such as Alzheimer's disease and epilepsy.

Published
2015

26. Stim and Orai proteins as novel actors in neuronal Ca2+ signalling and excitability

Author

Moccia F, Zuccolo E, Soda T, Tanzi F, Guerra G, Mapelli L, Lodola F, D’Angelo E, Moccia, F, Zuccolo, E, Soda, T, Tanzi, F, Guerra, G, Mapelli, L, Lodola, F, and D’Angelo, E

Subjects
Ion channels, SOCE
Abstract

Stimi and Orail are ubiquitous proteins that have long been known to mediate Ca2+ release-activated Ca2+ (CRAC) current (Icrac) and store-operated Ca2+ entry (SOCE) only in non-excitable cells. SOCE is activated following the depletion of the endogenous Ca2+ stores, which are mainly located within the endoplasmic reticulum (ER), to replete the intracellular Ca2+ reservoir and engage specific Ca2+-dependent processes, such as proliferation, migration, cytoskeletal remodeling, and gene expression. Their paralogs, Stim2, Orai2 and Orai3, support SOCE in heterologous expression systems, but their physiological role is still obscure. Ca2 + inflow in neurons has long been exclusively ascribed to voltage-operated and receptor-operated channels. Nevertheless, recent work has unveiled that Stim1-2 and Orai1-2, but not Orai3, proteins are also expressed and mediate SOCE in neurons. Herein, we survey current knowledge about the neuronal distribution of Stim and Orai proteins in rodent and human brains; we further discuss that Orai2 is the main pore-forming subunit of CRAC channels in central neurons, in which it may be activated by either Stim1 or Stim2 depending on species, brain region and physiological stimuli. We examine the functions regulated by SOCE in neurons, where this pathway is activated under resting conditions to refill the ER, control spinogenesis and regulate gene transcription. Besides, we highlighted the possibility that SOCE also controls neuronal excitation and regulate synaptic plasticity. Finally, we evaluate the involvement of Stim and Orai proteins in severe neurodegenerative and neurological disorders, such as Alzheimer's disease and epilepsy.

Published
2015

30. 752P - The efficacy and safety of lenvatinib in patients who did not meet the inclusion criteria of the phase III trial (REFLECT trial) and those with BCLC Stage B hepatocellular carcinoma: A nationwide multicenter study in Japan

Author

Sakamoto, A., Kurosaki, M., Tsuchiya, K., Abe, T., Ogawa, C., Soda, T., Kimura, H., Kondo, M., Tsuji, K., Koichiro, F., Shigeno, M., Jyoko, K., Narita, R., Uchida, Y., Yoshida, H., Akahane, T., Kobashi, H., Mitsuda, A., Marusawa, H., and Izumi, N.

Published
2019
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44. Progression & risk factors CKD 1-5 (2)

Author

Bouba, I., primary, Bountouri, C., additional, Dounousi, E., additional, Kiatou, V., additional, Georgiou, I., additional, Chatzidakis, S., additional, Kotzadamis, N., additional, Tsakiris, D., additional, Siamopoulos, K., additional, Dimas, G., additional, Iliadis, F., additional, Tegos, T., additional, Makedou, K., additional, Didangelos, T., additional, Pitsalidis, C., additional, Chatziapostolou, A., additional, Makedou, A., additional, Baloyannis, S., additional, Grekas, D., additional, Li, O., additional, Bobkova, I., additional, Tchebotareva, N., additional, Kozlovskaya, L., additional, Varshavskiy, V., additional, Mydlik, M., additional, Derzsiova, K., additional, Bohu , B., additional, Clapp, E., additional, Kosmadakis, G., additional, Smith, A., additional, Viana, J., additional, Shirreffs, S., additional, Maughan, R., additional, Feehally, J., additional, Bevington, A., additional, Ando, M., additional, Yanagisawa, N., additional, Hara, M., additional, Tsuchiya, K., additional, Nitta, K., additional, Chen, C.-H., additional, Wang, C.-L., additional, Huang, J.-W., additional, Hung, K.-Y., additional, Tsai, T.-J., additional, Gadalean, F., additional, Gluhovschi, G., additional, Kaycsa, A., additional, Trandafirescu, V., additional, Petrica, L., additional, Velciov, S., additional, Bozdog, G., additional, Gluhovschi, C., additional, Bob, F., additional, Solberg Eikrem, O., additional, Hope Jaeger-Hoie, E., additional, Hausken, T., additional, Svarstad, E., additional, de Goeij, M., additional, Liem, M., additional, de Jager, D., additional, Voormolen, N., additional, Sijpkens, Y., additional, Boeschoten, E., additional, Dekker, F., additional, Grootendorst, D., additional, Halbesma, N., additional, Moran, A.-M., additional, Kenny, E., additional, Ward, F., additional, Dunne, O. M., additional, Holian, J., additional, Watson, A. J., additional, Saginova, E., additional, Gallyamov, M., additional, Severova, M., additional, Surkova, O., additional, Fomin, V., additional, Topchii, I., additional, Kirienko, A., additional, Schenyavskaya, E., additional, Efimova, N., additional, Bondar, T., additional, Lesovaja, A., additional, Gama Axelsson, T., additional, Barany, P., additional, Heimburger, O., additional, Lindholm, B., additional, Stenvinkel, P., additional, Qureshi, A. R., additional, Bal, Z., additional, Erkmen Uyar, M., additional, Ahmed, N., additional, Tutal, E., additional, Sezer, S., additional, Labrador, P. J., additional, Gonzalez Castillo, P. M., additional, Silva Junior, G. B., additional, Liborio, A. B., additional, Lopes Filho, A. S., additional, Figueiredo Filho, A. C., additional, Vieira, A. P. F., additional, Couto Bem, A. X., additional, Guedes, A. L. M. O., additional, Costa, C. M. B. E., additional, Holanda de Souza, J., additional, Daher, E. F., additional, Donadio, C., additional, Kanaki, A., additional, Tognotti, D., additional, Donadio, E., additional, Reznik, E., additional, Guschina, V., additional, Volinkina, V., additional, Gendlin, G., additional, Storozhakov, G., additional, Capusa, C., additional, Stancu, S., additional, Badulescu, M., additional, Ilyes, A., additional, Anghel, C., additional, Mircescu, G., additional, Yonemoto, S., additional, Fujii, N., additional, Hamano, T., additional, Okuno, A., additional, Soda, T., additional, Yamanaka, K., additional, Hirai, T., additional, Nishimura, K., additional, Ichikawa, Y., additional, Boudville, N., additional, Kemp, A., additional, Champion de Crespigny, P., additional, Fassett, R., additional, Healy, H., additional, Mangos, G., additional, Moody, H., additional, Pedagogos, E., additional, Waugh, D., additional, Kirkland, G., additional, Kay, T., additional, Hoffman, D., additional, Abaterusso, C., additional, Branco, C., additional, Thomaseth, K., additional, Graziani, M. S., additional, Lupo, A., additional, Chaudhry, M., additional, Lok, C., additional, Kudo, K., additional, Konta, T., additional, Takasaki, S., additional, Degawa, N., additional, Kubota, I., additional, Nykula, T., additional, Moyseyenko, V., additional, Topchii, A., additional, Nanami, K., additional, Yoshiharu, T., additional, Hiroshi, Y., additional, Miyuki, M., additional, Masayuki, N., additional, Sotila, G. G., additional, Rugina, S., additional, Tuta, L., additional, Dumitru, I., additional, Cernat, R., additional, Rugina, C., additional, Kim, I. Y., additional, Lee, S. B., additional, Choi, B. K., additional, Son, J., additional, Lee, H. S., additional, Lee, N., additional, Rhee, H., additional, Song, S. H., additional, Seong, E. Y., additional, and Kwak, I. S., additional

Published
2011
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