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Zeitschriftenartikel zum Thema „Slitrya“

Autor: Grafiati

Veröffentlicht am 29. Juni 2021

Zuletzt aktualisiert am 6. Februar 2022

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1

Miranda, Débora Marques de, Marco Aurélio Romano Silva und Antônio Lúcio Teixeira. „Síndrome de Tourette“. Revista Neurociências 15, Nr. 1 (23.01.2019): 84–87. http://dx.doi.org/10.34024/rnc.2007.v15.8735.

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A Síndrome de Gilles de la Tourette (ST) é uma entidade neuropsiquiátrica caracterizada pela presença de tics e com importante componente hereditário. Muitos grupos vem estudando os aspectos genéticos da ST, mas frequentemente os achados não se sustentam em estudos subsequentes e fica clara toda a dificuldade em estabelecer os genes relacionados com a ST. Entretanto, no último ano foi publicado estudo que correlaciona mutação no gene da Slit and Trk-like family member 1 (SLITRK1) com a presença ST em um pequeno grupo de pacientes. Esse gene codifica a proteína SLITRK1 que é homóloga às proteínas SLIT e o receptor de tirosina cinase (TRK). A família das proteínas SLIT estão envolvidos no direcionamento axonal durante o cruzamento da linha média na medula vertebral. Enquanto o receptor de TRK acelera a diferenciação induzida pelo fator de crescimento neuronal. A SLITRK aparentemente está envolvida no crescimento de dendritos e axônios. Faltam estudos que avaliem a presença de mutações no gene da SLITRK1 em outras populações, assim como que avaliem a possibilidade de alteração de outros genes dessa via de sinalização. Entretanto, caso se confirmem as alterações no gene da SLITRK1, ou de genes correlacionados, o entendimento e o estudo de ST passará a envolver o direcionamento axonal e especialmente as proteínas da via SLITRK-SLIT-ROBO.

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2

Miranda, Débora Marques de, Marco Aurélio Romano Silva und Antônio Lúcio Teixeira. „Síndrome de Tourette:“. Revista Neurociências 15, Nr. 1 (31.10.1999): 84–87. http://dx.doi.org/10.34024/rnc.2007.v15.8737.

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A Síndrome de Gilles de la Tourette (ST) é uma entidade neuropsiquiátrica caracterizada pela presença de tics e com importante componente hereditário. Muitos grupos vem estudando os aspectos genéticos da ST, mas frequentemente os achados não se sustentam em estudos subsequentes e fica clara toda a dificuldade em estabelecer os genes relacionados com a ST. Entretanto, no último ano foi publicado estudo que correlaciona mutação no gene da Slit and Trk-like family member 1 (SLITRK1) com a presença ST em um pequeno grupo de pacientes. Esse gene codifica a proteína SLITRK1 que é homóloga às proteínas SLIT e o receptor de tirosina cinase (TRK). A família das proteínas SLIT estão envolvidos no direcionamento axonal durante o cruzamento da linha média na medula vertebral. Enquanto o receptor de TRK acelera a diferenciação induzida pelo fator de crescimento neuronal. A SLITRK aparentemente está envolvida no crescimento de dendritos e axônios. Faltam estudos que avaliem a presença de mutações no gene da SLITRK1 em outras populações, assim como que avaliem a possibilidade de alteração de outros genes dessa via de sinalização. Entretanto, caso se confirmem as alterações no gene da SLITRK1, ou de genes correlacionados, o entendimento e o estudo de ST passará a envolver o direcionamento axonal e especialmente as proteínas da via SLITRK-SLIT-ROBO.

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3

Katayama, Kei-ichi, Kazuyuki Yamada, Takashi Inoue, Maya Ota und Jun Aruga. „Analysis of Slitrk1- and Slitrk2-deficient mice“. Neuroscience Research 58 (Januar 2007): S47. http://dx.doi.org/10.1016/j.neures.2007.06.276.

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4

Yamazaki, Sho, Kazuki Taoka, Shunya Arai, Masashi Miyauchi, Keisuke Kataoka, Akihide Yoshimi und Mineo Kurokawa. „Patient-Derived Induced Pluripotent Stem Cells Identified SLITRK4 As a Causative Gene of Chronic Myelomonocytic Leukemia“. Blood 128, Nr. 22 (02.12.2016): 1134. http://dx.doi.org/10.1182/blood.v128.22.1134.1134.

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Abstract Chronic myelomonocytic leukemia (CMML), the most frequent disease entity of myelodysplastic syndrome/myeloproliferative neoplasm is a clonal hematopoietic malignancy that is characterized by persistent monocytosis, morphologic myeloid dysplasia, and progression to acute myeloid leukemia. The pathogenesis of CMML remains entirely elusive because of the lack of suitable mouse models and the difficulties in the establishment of CMML cell lines. We have previously reported that we established induced pluripotent stem cells (iPSC) from CMML CD34 positive leukemic cells (CMML-iPSC) as a new disease model. Co-cultured with C3H10T1/2 stromal cells in the presence of vascular endothelial growth factor, CMML-iPSC generated CD34 CD43 double-positive hematopoietic progenitor cells (CMML-HPC). CMML-HPC have recapitulated important disease features of parental CMML cells in terms of genetic abnormalities, acceleration of cell proliferation, and aberrant surface markers expression. In addition, a novel human CMML xenograft mouse model has been established through secondary transplantation of human HPCs from CMML-iPSC-derived teratomas. This model produced HPCs that mimicked the properties of CMML in vivo. To identify key molecular abnormalities that contribute to the pathophysiology of CMML, we conducted comprehensive gene expression and DNA methylation profiling analyses of normal and CMML parental CD34 positive cells, iPSC, and their hematopoietic progenies, respectively. Correlation analysis revealed that gene expression and DNA methylation status between normal and CMML iPSC-derived HPC exhibited similar pattern (R2 = 0.92 and 0.96, respectively), although normal and CMML parental CD34 positive cells were quite different (R2 = 0.72 and 0.90, respectively), indicating that reprogramming followed by re-differentiation may enable to obtain more homogenous population of normal and CMML cells that reside in almost the same differentiation stage. These results allowed us to determine the difference in the genetic and epigenetic status between normal and CMML iPSC-derived HPC, which remained through reprogramming and re-differentiation, in order to find out causative genes in the pathogenesis of CMML. Using these combined omics platforms, we identified SLIT and NTRK like family member 4 (SLITRK4) as a candidate gene involving in pathogenesis of CMML, whose expression was enhanced and whose promoters were hypo-methylated in CMML-HPC. In other CMML patients' CD34 positive leukemic cells, the expression of SLITRK4 was up-regulated compared to healthy CD34 positive bone marrow cells and other leukemia cells. In addition, we revealed SLITRK4 had pro-proliferative activity as the knockdown of SLITRK4 inhibited proliferation of leukemic cell lines OCI-AML3. To elucidate whether SLITRK4 exert any biological functions in CMML, we established CMML-iPSC clones harboring hetero-knockout (wt/-) or homo-knockout (-/-) of SLITRK4 gene by CRISPR/Cas9 system. Although SLITRK4 (wt/-) and (-/-) clones did not exhibit any morphological and proliferative difference in CMML-iPSC, the production of HPC from CMML-iPSC was dramatically attenuated in SLITRK4-dependent manner. Therefore, while little has been known about the roles of SLITRK molecules in tumorigenesis, we demonstrated SLITRK4 was indispensable for generation of CMML leukemic cells and suggested the possibility of novel molecular therapy targeting SLITRK4, based on the findings obtained from our combined omics platforms. In summary, we identified SLITRK4 as a novel candidate gene responsible for the pathogenesis of CMML through our combined omics platform using patient-derived iPSC. This platform may provide a potential to trace causative genes in a variety of diseases. Disclosures Kataoka: Kyowa Hakko Kirin: Honoraria; Boehringer Ingelheim: Honoraria; Yakult: Honoraria.

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5

Salesse, Charleen, Julien Charest, Hélène Doucet-Beaupré, Anne-Marie Castonguay, Simon Labrecque, Paul De Koninck und Martin Lévesque. „Opposite Control of Excitatory and Inhibitory Synapse Formation by Slitrk2 and Slitrk5 on Dopamine Neurons Modulates Hyperactivity Behavior“. Cell Reports 30, Nr. 7 (Februar 2020): 2374–86. http://dx.doi.org/10.1016/j.celrep.2020.01.084.

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6

Urh, Kristian, Margareta Žlajpah, Nina Zidar und Emanuela Boštjančič. „Identification and Validation of New Cancer Stem Cell-Related Genes and Their Regulatory microRNAs in Colorectal Cancerogenesis“. Biomedicines 9, Nr. 2 (11.02.2021): 179. http://dx.doi.org/10.3390/biomedicines9020179.

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Significant progress has been made in the last decade in our understanding of the pathogenetic mechanisms of colorectal cancer (CRC). Cancer stem cells (CSC) have gained much attention and are now believed to play a crucial role in the pathogenesis of various cancers, including CRC. In the current study, we validated gene expression of four genes related to CSC, L1TD1, SLITRK6, ST6GALNAC1 and TCEA3, identified in a previous bioinformatics analysis. Using bioinformatics, potential miRNA-target gene correlations were prioritized. In total, 70 formalin-fixed paraffin-embedded biopsy samples from 47 patients with adenoma, adenoma with early carcinoma and CRC without and with lymph node metastases were included. The expression of selected genes and microRNAs (miRNAs) was evaluated using quantitative PCR. Differential expression of all investigated genes and four of six prioritized miRNAs (hsa-miR-199a-3p, hsa-miR-335-5p, hsa-miR-425-5p, hsa-miR-1225-3p, hsa-miR-1233-3p and hsa-miR-1303) was found in at least one group of CRC cancerogenesis. L1TD1, SLITRK6, miR-1233-3p and miR-1225-3p were correlated to the level of malignancy. A negative correlation between miR-199a-3p and its predicted target SLITRK6 was observed, showing potential for further experimental validation in CRC. Our results provide further evidence that CSC-related genes and their regulatory miRNAs are involved in CRC development and progression and suggest that some them, particularly miR-199a-3p and its SLITRK6 target gene, are promising for further validation in CRC.

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7

Zuchner, S., M. L. Cuccaro, K. N. Tran-Viet, H. Cope, R. R. Krishnan, M. A. Pericak-Vance, H. H. Wright und A. Ashley-Koch. „SLITRK1 mutations in Trichotillomania“. Molecular Psychiatry 11, Nr. 10 (27.09.2006): 888–89. http://dx.doi.org/10.1038/sj.mp.4001865.

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8

Zuchner, S., M. L. Cuccaro, K. N. Tran-Viet, H. Cope, R. R. Krishnan, M. A. Pericak-Vance, H. H. Wright und A. Ashley-Koch. „SLITRK1 mutations in trichotillomania“. Molecular Psychiatry 11, Nr. 10 (27.09.2006): 887. http://dx.doi.org/10.1038/sj.mp.4001898.

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9

Burton, Adrian. „SLITRK1 trouble in Tourette's syndrome“. Lancet Neurology 4, Nr. 12 (Dezember 2005): 801. http://dx.doi.org/10.1016/s1474-4422(05)70242-8.

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10

Grice, D. E., Y. Kajiwara, T. Sakurai und J. D. Buxbaum. „Functional dissection of SLITRK1 signaling“. European Psychiatry 22 (März 2007): S88. http://dx.doi.org/10.1016/j.eurpsy.2007.01.1201.

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11

Larsen, Knud, Jamal Momeni, Leila Farajzadeh und Christian Bendixen. „Porcine SLITRK1: Molecular cloning and characterization“. FEBS Open Bio 4, Nr. 1 (01.01.2014): 872–78. http://dx.doi.org/10.1016/j.fob.2014.10.001.

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12

Liao, Huanan, Haruna Sato, Ryosuke Chiba, Tomoko Kawai, Kazuhiko Nakabayashi, Kenichiro Hata, Hidenori Akutsu, Shigeyoshi Fujiwara und Hiroyuki Nakamura. „Human cytomegalovirus downregulates SLITRK6 expression through IE2“. Journal of NeuroVirology 23, Nr. 1 (16.08.2016): 79–86. http://dx.doi.org/10.1007/s13365-016-0475-y.

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13

Matsumoto, Yoshifumi, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Soichi Nagao und Masaharu Kudoh. „Auditory and vestibular impairment of Slitrk6-Deficient mice“. Neuroscience Research 71 (September 2011): e150. http://dx.doi.org/10.1016/j.neures.2011.07.648.

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14

Ozomaro, Uzoezi, Guiqing Cai, Yuji Kajiwara, Seungtai Yoon, Vladimir Makarov, Richard Delorme, Catalina Betancur et al. „Characterization of SLITRK1 Variation in Obsessive-Compulsive Disorder“. PLoS ONE 8, Nr. 8 (21.08.2013): e70376. http://dx.doi.org/10.1371/journal.pone.0070376.

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15

Grice, D. E., J. D. Buxbaum, T. Sakurai und R. Vitale. „[P189]: Dissection of SLITRK1 signalling in neuronal development“. International Journal of Developmental Neuroscience 24, Nr. 8 (16.11.2006): 576–77. http://dx.doi.org/10.1016/j.ijdevneu.2006.09.249.

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16

Abelson, J. F. „Sequence Variants in SLITRK1 Are Associated with Tourette's Syndrome“. Science 310, Nr. 5746 (14.10.2005): 317–20. http://dx.doi.org/10.1126/science.1116502.

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17

Proenca, Catia C., Kate P. Gao, Sergey V. Shmelkov, Shahin Rafii und Francis S. Lee. „Slitrks as emerging candidate genes involved in neuropsychiatric disorders“. Trends in Neurosciences 34, Nr. 3 (März 2011): 143–53. http://dx.doi.org/10.1016/j.tins.2011.01.001.

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18

Geddes, MR. „A break near SLITRK1: A breakthrough in Tourette syndrome“. Clinical Genetics 69, Nr. 3 (02.03.2006): 206–8. http://dx.doi.org/10.1111/j.1399-0004.2006.0583c.x.

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19

Zhang, Kevin, Yu Feng, Karen G. Wigg, Paul Sandor und Cathy L. Barr. „Association study of the SLITRK5 gene and Tourette syndrome“. Psychiatric Genetics 25, Nr. 1 (Februar 2015): 31–34. http://dx.doi.org/10.1097/ypg.0000000000000067.

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20

Song, Minseok, Joanna Giza, Catia C. Proenca, Deqiang Jing, Mark Elliott, Iva Dincheva, Sergey V. Shmelkov et al. „Slitrk5 Mediates BDNF-Dependent TrkB Receptor Trafficking and Signaling“. Developmental Cell 33, Nr. 6 (Juni 2015): 690–702. http://dx.doi.org/10.1016/j.devcel.2015.04.009.

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21

Asadi, Shahin. „The role of mutations on gene SLITRK1, in Tourette’s Syndrome“. Gazette of Medical Sciences 1, Nr. 5 (13.10.2020): 47–51. http://dx.doi.org/10.46766/thegms.medgen.20100501.

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22

Won, Seoung Youn, Pedro Lee und Ho Min Kim. „Synaptic organizer: Slitrks and type IIa receptor protein tyrosine phosphatases“. Current Opinion in Structural Biology 54 (Februar 2019): 95–103. http://dx.doi.org/10.1016/j.sbi.2019.01.010.

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23

Tekin, Mustafa, Barry A. Chioza, Yoshifumi Matsumoto, Oscar Diaz-Horta, Harold E. Cross, Duygu Duman, Haris Kokotas et al. „SLITRK6 mutations cause myopia and deafness in humans and mice“. Journal of Clinical Investigation 123, Nr. 5 (01.04.2013): 2094–102. http://dx.doi.org/10.1172/jci65853.

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24

Abeshi, Andi, Pamela Coppola, Tommaso Beccari, Munis Dundar, Leonardo Colombo und Matteo Bertelli. „Genetic testing for Mendelian myopia“. EuroBiotech Journal 1, s1 (27.10.2017): 74–76. http://dx.doi.org/10.24190/issn2564-615x/2017/s1.23.

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Abstract We studied the scientific literature and disease guidelines in order to summarize the clinical utility of genetic testing for Mendelian myopia (MM), a large and heterogeneous group of inherited refraction disorders. Variations in the SLC39A5, SCO2 and COL2A1 genes have an autosomal dominant transmission, whereas those in the LRPAP1, P3H2, LRP2 and SLITRK6 genes have autosomal recessive transmission. The prevalence of MM is currently unknown. Clinical diagnosis is based on clinical findings, family history, ophthalmological examination and other tests depending on complications. The genetic test is useful for confirming diagnosis, and for differential diagnosis, couple risk assessment and access to clinical trials.

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25

Wright, Rogers H. „Of Slithy Toves, Rape-Trauma Syndrome, Burn-Out, etc.“ Psychotherapy in Private Practice 3, Nr. 1 (28.02.1985): 99–108. http://dx.doi.org/10.1300/j294v03n01_12.

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26

Wang, Chao-Jie. „SLITRK3 expression correlation to gastrointestinal stromal tumor risk rating and prognosis“. World Journal of Gastroenterology 21, Nr. 27 (2015): 8398. http://dx.doi.org/10.3748/wjg.v21.i27.8398.

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27

Wang, Junjie, Hao Chen, Lingling Lin, Weiming Ai und Xiao Chen. „Mitochondrial genome and phylogenetic position of the sliteye shark Loxodon macrorhinus“. Mitochondrial DNA Part A 27, Nr. 6 (24.09.2015): 4288–89. http://dx.doi.org/10.3109/19401736.2015.1082099.

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28

Deng, H., W. D. Le, W. J. Xie und J. Jankovic. „Examination of the SLITRK1 gene in Caucasian patients with Tourette syndrome“. Acta Neurologica Scandinavica 114, Nr. 6 (Dezember 2006): 400–402. http://dx.doi.org/10.1111/j.1600-0404.2006.00706.x.

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29

Katayama, K., K. Yamada, V. G. Ornthanalai, T. Inoue, M. Ota, N. P. Murphy und J. Aruga. „Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities“. Molecular Psychiatry 15, Nr. 2 (16.09.2008): 177–84. http://dx.doi.org/10.1038/mp.2008.97.

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30

O'Roak, B. J., T. M. Morgan, D. O. Fishman, E. Saus, P. Alonso, M. Gratacòs, X. Estivill et al. „Additional support for the association of SLITRK1 var321 and Tourette syndrome“. Molecular Psychiatry 15, Nr. 5 (30.03.2010): 447–50. http://dx.doi.org/10.1038/mp.2009.105.

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31

Matsumoto, Yoshifumi, Kei-ichi Katayama, Naoko Morimura, Kazuyuki Yamada, V. G. Ornthanalai, Maya Ota, Niall P. Murphy und Jun Aruga. „Slitrk5-deficient mice display elevated anxiety-like behavior and serotonergic abnormalities“. Neuroscience Research 65 (Januar 2009): S257. http://dx.doi.org/10.1016/j.neures.2009.09.1469.

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32

Matsumoto, Yoshifumi, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao und Jun Aruga. „Impaired Auditory-Vestibular Functions and Behavioral Abnormalities of Slitrk6-Deficient Mice“. PLoS ONE 6, Nr. 1 (26.01.2011): e16497. http://dx.doi.org/10.1371/journal.pone.0016497.

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33

김명미, 김진수, 문성민, 조선호, Park Bo ram, 이동설, 모신엽, 김춘성 und 최미숙. „Regulation of SLITRK1 gene by neuron restrictive silencer factor in NMB cells“. Oral Biology Research 37, Nr. 2 (Oktober 2013): 88–97. http://dx.doi.org/10.21851/obr.37.2.201310.88.

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34

Song, Minseok, Carol A. Mathews, S. Evelyn Stewart, Sergey V. Shmelkov, Jason G. Mezey, Juan L. Rodriguez-Flores, Steven A. Rasmussen et al. „Rare Synaptogenesis-Impairing Mutations in SLITRK5 Are Associated with Obsessive Compulsive Disorder“. PLOS ONE 12, Nr. 1 (13.01.2017): e0169994. http://dx.doi.org/10.1371/journal.pone.0169994.

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35

Takahashi, Hideto, Kei-ichi Katayama, Kazuhiro Sohya, Hiroyuki Miyamoto, Tuhina Prasad, Yoshifumi Matsumoto, Maya Ota et al. „Selective control of inhibitory synapse development by Slitrk3-PTPδ trans-synaptic interaction“. Nature Neuroscience 15, Nr. 3 (29.01.2012): 389–98. http://dx.doi.org/10.1038/nn.3040.

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36

Ko, Jaewon. „The leucine-rich repeat superfamily of synaptic adhesion molecules: LRRTMs and Slitrks“. Molecules and Cells 34, Nr. 4 (04.07.2012): 335–40. http://dx.doi.org/10.1007/s10059-012-0113-3.

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37

Beaubien, FranÃ§ois, und Jean-FranÃ§ois Cloutier. „Differential expression of slitrk family members in the mouse nervous system“. Developmental Dynamics 238, Nr. 12 (Dezember 2009): 3285–96. http://dx.doi.org/10.1002/dvdy.22160.

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38

Round, Jennifer, Brittany Ross, Mark Angel, Kayla Shields und Barbara Lom. „Slitrk gene duplication and expression in the developing zebrafish nervous system“. Developmental Dynamics 243, Nr. 2 (21.11.2013): 339–49. http://dx.doi.org/10.1002/dvdy.24076.

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39

Yim, Y. S., Y. Kwon, J. Nam, H. I. Yoon, K. Lee, D. G. Kim, E. Kim, C. H. Kim und J. Ko. „Slitrks control excitatory and inhibitory synapse formation with LAR receptor protein tyrosine phosphatases“. Proceedings of the National Academy of Sciences 110, Nr. 10 (23.01.2013): 4057–62. http://dx.doi.org/10.1073/pnas.1209881110.

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40

Aruga, Jun, Kei-ichi Katayama, Zine Azel und Maya Ota. „Disorganized innervation and neuronal loss in the inner ear of Slitrk6-deficient mice“. Neuroscience Research 65 (Januar 2009): S41. http://dx.doi.org/10.1016/j.neures.2009.09.044.

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41

Katayama, Kei-ichi, Azel Zine, Maya Ota, Yoshifumi Matsumoto, Takashi Inoue, Bernd Fritzsch und Jun Aruga. „Disorganized Innervation and Neuronal Loss in the Inner Ear of Slitrk6-Deficient Mice“. PLoS ONE 4, Nr. 11 (11.11.2009): e7786. http://dx.doi.org/10.1371/journal.pone.0007786.

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42

Speed, William C., Brian J. O'Roak, Zsanett Tárnok, Csaba Barta, Andrew J. Pakstis, Matthew W. State und Kenneth K. Kidd. „Haplotype evolution of SLITRK1, a candidate gene for Gilles de la Tourette Syndrome“. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 147B, Nr. 4 (2008): 463–66. http://dx.doi.org/10.1002/ajmg.b.30641.

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43

Morlet, Thierry, Mindy R. Rabinowitz, Liesl R. Looney, Tammy Riegner, L. Ashleigh Greenwood, Eric A. Sherman, Nathan Achilly et al. „A homozygous SLITRK6 nonsense mutation is associated with progressive auditory neuropathy in humans“. Laryngoscope 124, Nr. 3 (17.12.2013): E95—E103. http://dx.doi.org/10.1002/lary.24361.

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44

Mah, AK. „SLITRK5, a protein that links striatal deficits to OCD-like behaviours in mice“. Clinical Genetics 78, Nr. 4 (06.09.2010): 350–52. http://dx.doi.org/10.1111/j.1399-0004.2010.01507.x.

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Zimprich, Alexander, Katharina Hatala, Franz Riederer, Elisabeth Stogmann, Harald N. Aschauer und Mara Stamenkovic. „Sequence analysis of the complete SLITRK1 gene in Austrian patients with Touretteʼs disorder“. Psychiatric Genetics 18, Nr. 6 (Dezember 2008): 308–9. http://dx.doi.org/10.1097/ypg.0b013e3283060f6f.

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Kim, Jinhu, Kyung Ah Han, Dongseok Lim, Jaewon Ko und Ji Won Um. „Slitrk2 promotes excitatory synapse development by its C-terminal PDZ domain-binding sequence“. IBRO Reports 6 (September 2019): S528—S529. http://dx.doi.org/10.1016/j.ibror.2019.07.1647.

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Kim, Dongwook, Taekhan Yoon, Jinhu Kim, Jiwon Um und Jaewon Ko. „Functional crosstalk between Slitrk3 and neuroligin-2 in medial prefrontal cortex of mice“. IBRO Reports 6 (September 2019): S529. http://dx.doi.org/10.1016/j.ibror.2019.07.1648.

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Salime, Sara, Zied Riahi, Soukaina Elrharchi, Lamiae Elkhattabi, Hicham Charoute, Halima Nahili, Hassan Rouba et al. „A novel mutation in SLITRK6 causes deafness and myopia in a Moroccan family“. Gene 659 (Juni 2018): 89–92. http://dx.doi.org/10.1016/j.gene.2018.03.042.

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Yamashita, Daisuke, Saya Ozaki, Satoshi Suehiro, Kazuhiro Sonomura, Toru Kondo, Taka-Aki Sato, Takeharu Kunieda und Ichiro Nakano. „CBMS-01 AGE-DEPENDENT GLIOBLASTOMA PROGRESSION SUPPRESSED BY NAD+“. Neuro-Oncology Advances 1, Supplement_2 (Dezember 2019): ii5. http://dx.doi.org/10.1093/noajnl/vdz039.021.

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Abstract The rise in population aging worldwide is causing an unparalleled increase in death from many cancers, including glioblastoma (GBM). Here, we have explored the impact of aging and rejuvenation on GBM tumorigenesis. Compared with old GBM, young GBM displayed elevated neuronal/synaptic signaling via brain-derived neurotrophic factor (BDNF) and SLIT and NTRK like-family member 6 (SLITRK6), promoting favorable survival rates. These effects were attributed to the rise in nicotinamide adenine dinucleotide (NAD+) levels, as brain rejuvenation by parabiosis or administration of nicotinamide mononucleotide (NMN) in mice elicited a younger phenotype with activated neuronal/synaptic signaling and improved outcomes. Our data indicate that age-associated NAD+ loss contributes to the highly aggressive GBM in the elderly. These findings have therapeutic implications in GBM and provide mechanistic insights into the exacerbation of GBM tumorigenesis with age.

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Pallanti, Stefano, und Eric Hollander. „Pharmacological, experimental therapeutic, and transcranial magnetic stimulation treatments for compulsivity and impulsivity“. CNS Spectrums 19, Nr. 1 (01.11.2013): 50–61. http://dx.doi.org/10.1017/s1092852913000618.

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Obsessive-compulsive disorder (OCD) has been recently drawn apart from anxiety disorder by the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5) and clustered together with related disorders (eg, hoarding, hair pulling disorder, skin picking), which with it seems to share clinical and neurophysiological similarities. Recent literature has mainly explored brain circuitries (eg, orbitofrontal cortex, striatum), molecular pathways, and genes (eg, Hoxb8, Slitrk5, Sapap3) that represent the new target of the treatments; they also lead the development of new probes and compounds. In the therapeutic field, monotherapy with cognitive behavioral therapy (CBT) or selective serotonin reuptake inhibitors (SSRIs) is recommendable, but combination or augmentation with a dopaminergic or glutamatergic agent is often adopted. A promising therapy for OCD is represented by repetitive transcranial magnetic stimulation (rTMS), which is suitable to treat compulsivity and impulsivity depending on the protocol of stimulation and the brain circuitries targeted.

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