Zobrazeno 1 - 10
of 58
pro vyhledávání: '"Alexander M Kleschevnikov"'
Autor:
Pavel V Belichenko, Rime Madani, Lorianne Rey-Bellet, Maria Pihlgren, Ann Becker, Adeline Plassard, Stephanie Vuillermot, Valérie Giriens, Rachel L Nosheny, Alexander M Kleschevnikov, Janice S Valletta, Sara K S Bengtsson, Gordon R Linke, Michael T Maloney, David T Hickman, Pedro Reis, Anne Granet, Dorin Mlaki, Maria Pilar Lopez-Deber, Long Do, Nishant Singhal, Eliezer Masliah, Matthew L Pearn, Andrea Pfeifer, Andreas Muhs, William C Mobley
Publikováno v:
PLoS ONE, Vol 11, Iss 3, p e0152471 (2016)
In Down syndrome (DS) or trisomy of chromosome 21, the β-amyloid (Aβ) peptide product of the amyloid precursor protein (APP) is present in excess. Evidence points to increased APP gene dose and Aβ as playing a critical role in cognitive difficulti
Externí odkaz:
https://doaj.org/article/e6e5615e619c41a0ad64eafb049c71c7
Autor:
Pavel V Belichenko, Alexander M Kleschevnikov, Ann Becker, Grant E Wagner, Larisa V Lysenko, Y Eugene Yu, William C Mobley
Publikováno v:
PLoS ONE, Vol 10, Iss 7, p e0134861 (2015)
Down syndrome (DS), trisomy for chromosome 21, is the most common genetic cause of intellectual disability. The genomic regions on human chromosome 21 (HSA21) are syntenically conserved with regions on mouse chromosomes 10, 16, and 17 (Mmu10, Mmu16,
Externí odkaz:
https://doaj.org/article/d51c038fdc8148899fbd97c4cd544d85
Autor:
Larisa V Lysenko, Jeesun Kim, Cassandra Henry, Anna Tyrtyshnaia, Rebecca A Kohnz, Francisco Madamba, Gabriel M Simon, Natalia E Kleschevnikova, Daniel K Nomura, R Alan B Ezekowitz, Alexander M Kleschevnikov
Publikováno v:
PLoS ONE, Vol 9, Iss 12, p e114521 (2014)
Genetic alterations or pharmacological treatments affecting endocannabinoid signaling have profound effects on synaptic and neuronal properties and, under certain conditions, may improve higher brain functions. Down syndrome (DS), a developmental dis
Externí odkaz:
https://doaj.org/article/96f6bc490afe44a2a73fd867ed21e158
Autor:
Larisa V. Lysenko, Jeesun Kim, Francisco Madamba, Anna A. Tyrtyshnaia, Aarti Ruparelia, Alexander M. Kleschevnikov
Publikováno v:
Neurobiology of Disease, Vol 115, Iss , Pp 1-8 (2018)
Down syndrome (DS) is the most frequent genetic cause of developmental abnormalities leading to intellectual disability. One notable phenomenon affecting the formation of nascent neural circuits during late developmental periods is developmental swit
Externí odkaz:
https://doaj.org/article/7989499b4128411ca00c91bb376df0ee
Autor:
Alexander M. Kleschevnikov, Jessica Yu, Jeesun Kim, Larisa V. Lysenko, Zheng Zeng, Y. Eugene Yu, William C. Mobley
Publikováno v:
Neurobiology of Disease, Vol 103, Iss , Pp 1-10 (2017)
Down syndrome (DS), trisomy 21, is caused by increased dose of genes present on human chromosome 21 (HSA21). The gene-dose hypothesis argues that a change in the dose of individual genes or regulatory sequences on HSA21 is necessary for creating DS-r
Externí odkaz:
https://doaj.org/article/135245ad177b4389ba819272f358c4b3
Autor:
Alexander M, Kleschevnikov
Publikováno v:
Frontiers in Genetics. 13
The most distinctive feature of Down syndrome (DS) is moderate to severe cognitive impairment. Genetic, molecular, and neuronal mechanisms of this complex DS phenotype are currently under intensive investigation. It is becoming increasingly clear tha
Autor:
Isabella C. Kelly, Mehul Dhanani, John Q. Trojanowski, Kimberly Zhou, Sonia Podvin, Steve L. Wagner, Atsushi Miyanohara, Shanshan Wang, Piyush M. Patel, Tong Zhang, Vivian Hook, Alexander M. Kleschevnikov, Phuong Nguyen, Joseph Leem, Natalia Kleschevnikov, Brian P. Head, David M. Roth, Hemal H. Patel, Paul Savchenko
Publikováno v:
Molecular Therapy. Methods & Clinical Development
Molecular Therapy: Methods & Clinical Development, Vol 21, Iss, Pp 434-450 (2021)
Molecular Therapy: Methods & Clinical Development, Vol 21, Iss, Pp 434-450 (2021)
Alzheimer’s disease (AD) is the most common form of neurodegeneration and cognitive dysfunction in the elderly. Identifying molecular signals that mitigate and reverse neurodegeneration in AD may be exploited therapeutically. Transgenic AD mice (PS
Autor:
Alexander M. Kleschevnikov, Pavel V. Belichenko, Jessica Gall, Lizzy George, Rachel Nosheny, Michael T. Maloney, Ahmad Salehi, William C. Mobley
Publikováno v:
Neurobiology of Disease, Vol 45, Iss 2, Pp 683-691 (2012)
Cognitive impairment in Down syndrome (DS) involves the hippocampus. In the Ts65Dn mouse model of DS, deficits in hippocampus-dependent learning and synaptic plasticity were linked to enhanced inhibition. However, the mechanistic basis of changes in
Externí odkaz:
https://doaj.org/article/93792ac3bc0f4369b25a6d8cbb880d2c
Autor:
Xu-Qiao Chen, Phuong Nguyen, William C. Mobley, Maria Maccecchini, Alexander M. Kleschevnikov, Matthew L. Pearn, Ahmad Salehi, Cassia R. Overk
Publikováno v:
Alzheimer's & dementia : the journal of the Alzheimer's Association, vol 17, iss 2
Alzheimer's & Dementia
Alzheimer's & Dementia
Objective Recent clinical trials targeting amyloid beta (Aβ) and tau in Alzheimer's disease (AD) have yet to demonstrate efficacy. Reviewing the hypotheses for AD pathogenesis and defining possible links between them may enhance insights into both u
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::691143f65dfced6635b43343f8af2cf7
https://escholarship.org/uc/item/4d04n1ns
https://escholarship.org/uc/item/4d04n1ns
Autor:
John Q. Trojanowski, Brian P. Head, Atsushi Miyanohara, Mehul Dhanani, Tong Zhang, Paul Savchenko, Isabella C. Kelly, Sonia Podvin, Steve L. Wagner, Vivian Hook, Alexander M. Kleschevnikov, Natalia Kleschevnikov, Shanshan Wang, Kimberly Zhou, David M. Roth, Joseph Leem, Hemal H. Patel, Piyush M. Patel
AD presents with severe neurodegeneration which leads to cognitive deficits and dementia. Identifying the molecular signals that attenuate neurodegeneration in AD may be exploited as therapeutic targets. This study revealed that transgenic AD mice (P
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5cd4e440291b2ab8dce87aa0e8bc2f05
https://doi.org/10.1101/2020.07.24.220129
https://doi.org/10.1101/2020.07.24.220129