Amyloid β protein immunotherapy neutralizes Aβ oligomers that disrupt synaptic plasticity in vivo

2005 ◽  
Vol 11 (5) ◽  
pp. 556-561 ◽  
Author(s):  
Igor Klyubin ◽  
Dominic M Walsh ◽  
Cynthia A Lemere ◽  
William K Cullen ◽  
Ganesh M Shankar ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Aβ Oligomers ◽  
Β Protein

scholarly journals Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

2008 ◽  
Vol 14 (8) ◽  
pp. 837-842 ◽  
Author(s):  
Ganesh M Shankar ◽  
Shaomin Li ◽  
Tapan H Mehta ◽  
Amaya Garcia-Munoz ◽  
Nina E Shepardson ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Protein Dimers ◽  
Β Protein

Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo

Nature ◽  
2002 ◽  
Vol 416 (6880) ◽  
pp. 535-539 ◽  
Author(s):  
Dominic M. Walsh ◽  
Igor Klyubin ◽  
Julia V. Fadeeva ◽  
William K. Cullen ◽  
Roger Anwyl ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

scholarly journals GLP-1 analogue CJC-1131 prevents amyloid β protein-induced impirments of spatial memory and synaptic plasticity in rats

2017 ◽  
Vol 326 ◽  
pp. 237-243 ◽  
Author(s):  
Sheng-Xiao Zhang ◽  
Hong-Yan Cai ◽  
Xiao-Wen Ma ◽  
Li Yuan ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Memory ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

scholarly journals Upregulation of Alzheimer’s Disease Amyloid-β Protein Precursor in Astrocytes Both in vitro and in vivo

2020 ◽  
pp. 1-12 ◽  
Author(s):  
Yingxia Liang ◽  
Frank Raven ◽  
Joseph F. Ward ◽  
Sherri Zhen ◽  
Siyi Zhang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Β Protein

scholarly journals The common inhalation anesthetic isoflurane induces caspase activation and increases amyloid β-protein level in vivo

2008 ◽  
Vol 64 (6) ◽  
pp. 618-627 ◽  
Author(s):  
Zhongcong Xie ◽  
Deborah J. Culley ◽  
Yuanlin Dong ◽  
Guohua Zhang ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Protein Level ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Caspase Activation ◽  
Inhalation Anesthetic ◽  
Β Protein ◽  
The Common

scholarly journals Effects of secreted oligomers of amyloid β-protein on hippocampal synaptic plasticity: a potent role for trimers

2006 ◽  
Vol 572 (2) ◽  
pp. 477-492 ◽  
Author(s):  
Matthew Townsend ◽  
Ganesh M. Shankar ◽  
Tapan Mehta ◽  
Dominic M. Walsh ◽  
Dennis J. Selkoe
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Hippocampal Synaptic Plasticity ◽  
Β Protein

Lixisenatide rescues spatial memory and synaptic plasticity from amyloid β protein-induced impairments in rats

Neuroscience ◽  
2014 ◽  
Vol 277 ◽  
pp. 6-13 ◽  
Author(s):  
H.-Y. Cai ◽  
C. Hölscher ◽  
X.-H. Yue ◽  
S.-X. Zhang ◽  
X.-H. Wang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Memory ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

scholarly journals Na, K-ATPase α3 is a death target of Alzheimer patient amyloid-β assembly

2015 ◽  
Vol 112 (32) ◽  
pp. E4465-E4474 ◽  
Author(s):  
Takayuki Ohnishi ◽  
Masako Yanazawa ◽  
Tomoya Sasahara ◽  
Yasuki Kitamura ◽  
Hidekazu Hiroaki ◽  
...  
Keyword(s):  
Specific Activity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Aβ Oligomers ◽  
Alzheimer Patient ◽  
Knowledge Based ◽  
Β Protein ◽  
Mature Neurons ◽  
Α3 Subunit ◽  
Target Binding

Neurodegeneration correlates with Alzheimer’s disease (AD) symptoms, but the molecular identities of pathogenic amyloid β-protein (Aβ) oligomers and their targets, leading to neurodegeneration, remain unclear. Amylospheroids (ASPD) are AD patient-derived 10- to 15-nm spherical Aβ oligomers that cause selective degeneration of mature neurons. Here, we show that the ASPD target is neuron-specific Na+/K+-ATPase α3 subunit (NAKα3). ASPD-binding to NAKα3 impaired NAKα3-specific activity, activated N-type voltage-gated calcium channels, and caused mitochondrial calcium dyshomeostasis, tau abnormalities, and neurodegeneration. NMR and molecular modeling studies suggested that spherical ASPD contain N-terminal-Aβ–derived “thorns” responsible for target binding, which are distinct from low molecular-weight oligomers and dodecamers. The fourth extracellular loop (Ex4) region of NAKα3 encompassing Asn879 and Trp880 is essential for ASPD–NAKα3 interaction, because tetrapeptides mimicking this Ex4 region bound to the ASPD surface and blocked ASPD neurotoxicity. Our findings open up new possibilities for knowledge-based design of peptidomimetics that inhibit neurodegeneration in AD by blocking aberrant ASPD–NAKα3 interaction.

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