Zobrazeno 1 - 10
of 23
pro vyhledávání: '"Helen Y Figueroa"'
Autor:
Hongjun Fu, S Abid Hussaini, Susanne Wegmann, Caterina Profaci, Jacob D Daniels, Mathieu Herman, Sheina Emrani, Helen Y Figueroa, Bradley T Hyman, Peter Davies, Karen E Duff
Publikováno v:
PLoS ONE, Vol 11, Iss 7, p e0159463 (2016)
3D volume imaging using iDISCO+ was applied to observe the spatial and temporal progression of tau pathology in deep structures of the brain of a mouse model that recapitulates the earliest stages of Alzheimer's disease (AD). Tau pathology was compar
Externí odkaz:
https://doaj.org/article/dd6c376d0fad48e2bc7f2456a4cdbcac
Autor:
Shan Jiang, Eric J. Sydney, Avery M. Runyan, Rossana Serpe, Malavika Srikanth, Helen Y. Figueroa, Mu Yang, Natura Myeku
Publikováno v:
Frontiers in Cellular Neuroscience, Vol 18 (2024)
BackgroundAccumulation of tau in synapses in the early stages of Alzheimer’s disease (AD) has been shown to cause synaptic damage, synaptic loss, and the spread of tau pathology through trans-synaptically connected neurons. Moreover, synaptic loss
Externí odkaz:
https://doaj.org/article/27a34eeb4b2a402ea82611858f3d7e7c
Autor:
Tal Nuriel, Sergio L. Angulo, Usman Khan, Archana Ashok, Qiuying Chen, Helen Y. Figueroa, Sheina Emrani, Li Liu, Mathieu Herman, Geoffrey Barrett, Valerie Savage, Luna Buitrago, Efrain Cepeda-Prado, Christine Fung, Eliana Goldberg, Steven S. Gross, S. Abid Hussaini, Herman Moreno, Scott A. Small, Karen E. Duff
Publikováno v:
Nature Communications, Vol 8, Iss 1, Pp 1-14 (2017)
The APOE4 allele is the leading risk factor for late-onset Alzheimer’s disease, but how it might contribute to the disease is not clear. Here the authors show that a mouse expressing the human APOE4 allele displays hyperactivity in the entorhinal c
Externí odkaz:
https://doaj.org/article/91098ce8e7d943429a161e6bc0ddcf3e
Autor:
Shan Jiang, Eric J. Sydney, Avery M. Runyan, Rossana Serpe, Helen Y. Figueroa, Mu Yang, Natura Myeku
Publikováno v:
bioRxiv
Accumulation of tau in synapses in Alzheimer’s disease (AD) has been shown to cause synaptic damage, synaptic loss, and the spread of pathology through synaptically connected neurons. Synaptic loss correlates with a decline in cognition, providing
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::61de21ca06a98604914d10f0dd07f9d3
https://doi.org/10.1101/2023.02.03.526871
https://doi.org/10.1101/2023.02.03.526871
Autor:
Tal Nuriel, Katherine Y. Peng, Archana Ashok, Allissa A. Dillman, Helen Y. Figueroa, Justin Apuzzo, Jayanth Ambat, Efrat Levy, Mark R. Cookson, Paul M. Mathews, Karen E. Duff
Publikováno v:
Frontiers in Neuroscience, Vol 11 (2017)
Possession of the ε4 allele of apolipoprotein E (APOE) is the major genetic risk factor for late-onset Alzheimer's disease (AD). Although numerous hypotheses have been proposed, the precise cause of this increased AD risk is not yet known. In order
Externí odkaz:
https://doaj.org/article/8794427b24664e6d86a8a5394eb6994b
Autor:
Rishi R. Agrawal, Kathleen Shannon, Ernest Fraenkel, Steven S. Gross, David N. Guilfoyle, Helen Y. Figueroa, Allissa Dillman, Karen Duff, Archana Ashok, Tal Nuriel, Estela Area-Gomez, Marta Pera, Hirra A. Arain, Qiuying Chen, Mark R. Cookson, Leila Pirhaji, Delfina Larrea
Publikováno v:
Scientific Reports, Vol 10, Iss 1, Pp 1-20 (2020)
Scientific Reports
Scientific Reports
The ε4 allele of apolipoprotein E (APOE) is the dominant genetic risk factor for late-onset Alzheimer’s disease (AD). However, the reason for the association between APOE4 and AD remains unclear. While much of the research has focused on the abili
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::45568ad65135cb2eadd210e151d3591f
http://link.springer.com/article/10.1038/s41598-020-61142-8
http://link.springer.com/article/10.1038/s41598-020-61142-8
Autor:
Andrea Possenti, Benjamin Lassus, Michele Vendruscolo, Hongjun Fu, Rosie Freer, Shuo Chen, Nancy C Hernandez Villegas, Gail V.W. Johnson, Yoshikazu Nakano, Helen Y. Figueroa, Maoping Tang, Stephanie L. Fowler, Edward D. Huey, Karen Duff, Paula Victoria Maglio Cauhy
Publikováno v:
Nature neuroscience
Excitatory neurons are preferentially impaired in early Alzheimer’s disease but the pathways contributing to their relative vulnerability remain largely unknown. Here we report that pathological tau accumulation takes place predominantly in excitat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a79458113d843f274540c8c0f2b1f9f2
http://europepmc.org/articles/PMC6330709
http://europepmc.org/articles/PMC6330709
Autor:
Helen Y. Figueroa, Ismael Santa-Maria, Catherine L. Clelland, Stephanie L. Fowler, Avery M. Runyan, Seiji Shioda, Karen Duff, Natura Myeku, Ari W. Schaler, Eric J. Sydney
Publikováno v:
Sci Transl Med
Accumulation of pathological tau in synapses has been identified as an early event in Alzheimer’s disease (AD) and correlates with cognitive decline in patients with AD. Tau is a cytosolic axonal protein, but under disease conditions, tau accumulat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4592613b852703aaed0fa4d06b220617
https://doi.org/10.1126/scitranslmed.aba7394
https://doi.org/10.1126/scitranslmed.aba7394
Autor:
Paul M. Mathews, Hirra A. Arain, Tal Nuriel, Mark R. Cookson, Gautam Kumar, Karen Duff, Helen Y. Figueroa
Publikováno v:
Alzheimer's & Dementia. 16
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f06f35419a772b5b6e36d9f7461900c6
https://doi.org/10.1002/alz.046192
https://doi.org/10.1002/alz.046192
Publikováno v:
Science Advances
Spread of tau pathology in a mouse model of AD assessed by MRI is associated with reduced brain tissue volume but not neuron loss.
Tau pathology in Alzheimer’s disease (AD) first develops in the entorhinal cortex (EC), then spreads to the hipp
Tau pathology in Alzheimer’s disease (AD) first develops in the entorhinal cortex (EC), then spreads to the hipp
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::72064072fc904f3ac3f0805334735390
https://doi.org/10.1126/sciadv.abc8098
https://doi.org/10.1126/sciadv.abc8098