Title |
Amyloid beta protein-induced zinc sequestration leads to synaptic loss via dysregulation of the ProSAP2/Shank3 scaffold
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Published in |
Molecular Neurodegeneration, September 2011
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DOI | 10.1186/1750-1326-6-65 |
Pubmed ID | |
Authors |
Andreas M Grabrucker, Michael J Schmeisser, Patrick T Udvardi, Magali Arons, Michael Schoen, Nathaniel S Woodling, Katrin I Andreasson, Patrick R Hof, Joseph D Buxbaum, Craig C Garner, Tobias M Boeckers |
Abstract |
Memory deficits in Alzheimer's disease (AD) manifest together with the loss of synapses caused by the disruption of the postsynaptic density (PSD), a network of scaffold proteins located in dendritic spines. However, the underlying molecular mechanisms remain elusive. Since it was shown that ProSAP2/Shank3 scaffold assembly within the PSD is Zn2+-dependent and that the amyloid beta protein (Aβ) is able to bind Zn2+, we hypothesize that sequestration of Zn2+ ions by Aβ contributes to ProSAP/Shank platform malformation. |
X Demographics
Geographical breakdown
Country | Count | As % |
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Unknown | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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United Kingdom | 2 | 2% |
Netherlands | 1 | 1% |
Unknown | 80 | 96% |
Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 19 | 23% |
Student > Ph. D. Student | 18 | 22% |
Student > Doctoral Student | 12 | 14% |
Student > Master | 9 | 11% |
Student > Bachelor | 6 | 7% |
Other | 10 | 12% |
Unknown | 9 | 11% |
Readers by discipline | Count | As % |
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Agricultural and Biological Sciences | 24 | 29% |
Neuroscience | 18 | 22% |
Biochemistry, Genetics and Molecular Biology | 10 | 12% |
Medicine and Dentistry | 9 | 11% |
Psychology | 3 | 4% |
Other | 9 | 11% |
Unknown | 10 | 12% |