Rowan Michael J相关文献与解析，生知库 | 链接生命科学的每一步

Ondrejcak Tomas, Hu Neng-Wei, Coode Emily, Campbell Tom, Corbett Grant T, Doykov Ivan, Mills Kevin, Walsh Dominic M, Livesey Frederick J, Rowan Michael J, Klyubin Igor

细胞生物学

发表日期：2025

文献求助收藏

Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer's disease?

海马体中 tau 蛋白突触长期抑制相互作用在阿尔茨海默病进展中是否起关键作用？

期刊:Neural Regeneration Research

影响因子:6.7

doi:10.4103/1673-5374.360166

Hu, Zhengtao; Ondrejcak, Tomas; Yu, Pengpeng; Zhang, Yangyang; Yang, Yin; Klyubin, Igor; Kennelly, Sean P; Rowan, Michael J; Hu, Neng-Wei

Pre-plaque Aß-Mediated Impairment of Synaptic Depotentiation in a Transgenic Rat Model of Alzheimer's Disease Amyloidosis

在阿尔茨海默病淀粉样变性转基因大鼠模型中，斑块前Aβ介导的突触去增强作用受损

期刊:Frontiers in Neuroscience

影响因子:3.2

doi:10.3389/fnins.2019.00861

Qi, Yingjie; Klyubin, Igor; Hu, Neng-Wei; Ondrejcak, Tomas; Rowan, Michael J

Extracellular Forms of Aβ and Tau from iPSC Models of Alzheimer's Disease Disrupt Synaptic Plasticity

来自阿尔茨海默病iPSC模型的细胞外Aβ和Tau蛋白会破坏突触可塑性

期刊:Cell Reports

影响因子:6.9

doi:10.1016/j.celrep.2018.04.040

Hu, Neng-Wei; Corbett, Grant T; Moore, Steven; Klyubin, Igor; O'Malley, Tiernan T; Walsh, Dominic M; Livesey, Frederick J; Rowan, Michael J

Physiological activation of mGlu5 receptors supports the ion channel function of NMDA receptors in hippocampal LTD induction in vivo

体内实验表明，mGlu5受体的生理激活支持NMDA受体在海马LTD诱导中的离子通道功能。

期刊:Scientific Reports

影响因子:3.9

doi:10.1038/s41598-018-22768-x

O'Riordan, Kenneth J; Hu, Neng-Wei; Rowan, Michael J

信号转导

发表日期：2018

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Peripheral administration of a humanized anti-PrP antibody blocks Alzheimer's disease Aβ synaptotoxicity

外周注射人源化抗PrP抗体可阻断阿尔茨海默病Aβ突触毒性

期刊:Journal of Neuroscience

影响因子:4

doi:10.1523/JNEUROSCI.3526-13.2014

Klyubin, Igor; Nicoll, Andrew J; Khalili-Shirazi, Azadeh; Farmer, Michael; Canning, Stephanie; Mably, Alexandra; Linehan, Jacqueline; Brown, Alexander; Wakeling, Madeleine; Brandner, Sebastian; Walsh, Dominic M; Rowan, Michael J; Collinge, John

Secreted amyloid β-proteins in a cell culture model include N-terminally extended peptides that impair synaptic plasticity

细胞培养模型中分泌的β-淀粉样蛋白包含N端延伸的肽段，这些肽段会损害突触可塑性。

期刊:Biochemistry

影响因子:3

doi:10.1021/bi5003053

Welzel, Alfred T; Maggio, John E; Shankar, Ganesh M; Walker, Donald E; Ostaszewski, Beth L; Li, Shaomin; Klyubin, Igor; Rowan, Michael J; Seubert, Peter; Walsh, Dominic M; Selkoe, Dennis J

Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo

外泌体在体内可中和Aβ聚集体破坏突触可塑性的活性。

期刊:Molecular Brain

影响因子:2.9

doi:10.1186/1756-6606-6-47

An, Kyongman; Klyubin, Igor; Kim, Youngkyu; Jung, Jung Hoon; Mably, Alexandra J; O'Dowd, Sean T; Lynch, Timothy; Kanmert, Daniel; Lemere, Cynthia A; Finan, Gina M; Park, Joon Won; Kim, Tae-Wan; Walsh, Dominic M; Rowan, Michael J; Kim, Joung-Hun

Alzheimer's disease Aβ assemblies mediating rapid disruption of synaptic plasticity and memory

阿尔茨海默病中Aβ聚集体介导突触可塑性和记忆的快速破坏

期刊:Molecular Brain

影响因子:2.9

doi:10.1186/1756-6606-5-25

Klyubin, Igor; Cullen, William K; Hu, Neng-Wei; Rowan, Michael J

Alzheimer's disease brain-derived amyloid-β-mediated inhibition of LTP in vivo is prevented by immunotargeting cellular prion protein

免疫靶向细胞朊蛋白可阻止阿尔茨海默病脑源性β-淀粉样蛋白介导的体内长时程增强（LTP）抑制。

期刊:Journal of Neuroscience

影响因子:4

doi:10.1523/JNEUROSCI.6500-10.2011

Barry, Andrew E; Klyubin, Igor; Mc Donald, Jessica M; Mably, Alexandra J; Farrell, Michael A; Scott, Michael; Walsh, Dominic M; Rowan, Michael J

Synaptotoxic effects of extracellular tau are mediated by its microtubule-binding region.

细胞外 tau 蛋白的突触毒性作用是由其微管结合区介导的

Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer's disease?

海马体中 tau 蛋白突触长期抑制相互作用在阿尔茨海默病进展中是否起关键作用？

Pre-plaque Aß-Mediated Impairment of Synaptic Depotentiation in a Transgenic Rat Model of Alzheimer's Disease Amyloidosis

在阿尔茨海默病淀粉样变性转基因大鼠模型中，斑块前Aβ介导的突触去增强作用受损

Extracellular Forms of Aβ and Tau from iPSC Models of Alzheimer's Disease Disrupt Synaptic Plasticity

来自阿尔茨海默病iPSC模型的细胞外Aβ和Tau蛋白会破坏突触可塑性

Physiological activation of mGlu5 receptors supports the ion channel function of NMDA receptors in hippocampal LTD induction in vivo

体内实验表明，mGlu5受体的生理激活支持NMDA受体在海马LTD诱导中的离子通道功能。

Peripheral administration of a humanized anti-PrP antibody blocks Alzheimer's disease Aβ synaptotoxicity

外周注射人源化抗PrP抗体可阻断阿尔茨海默病Aβ突触毒性

Secreted amyloid β-proteins in a cell culture model include N-terminally extended peptides that impair synaptic plasticity

细胞培养模型中分泌的β-淀粉样蛋白包含N端延伸的肽段，这些肽段会损害突触可塑性。

Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo

外泌体在体内可中和Aβ聚集体破坏突触可塑性的活性。

Alzheimer's disease Aβ assemblies mediating rapid disruption of synaptic plasticity and memory

阿尔茨海默病中Aβ聚集体介导突触可塑性和记忆的快速破坏

Alzheimer's disease brain-derived amyloid-β-mediated inhibition of LTP in vivo is prevented by immunotargeting cellular prion protein

免疫靶向细胞朊蛋白可阻止阿尔茨海默病脑源性β-淀粉样蛋白介导的体内长时程增强（LTP）抑制。