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EnglishThe concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau.
Puzzo, D., Piacentini, R., Fá, M., Gulisano, W., Li Puma, D. D., Staniszewski, A., Zhang, H., Tropea, M. R., Cocco, S., Palmeri, A., Fraser, P., D'adamio, L., Grassi, C., Arancio, O., LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent, <<ELIFE>>, 2017; 2017 (6): N/A-N/A. [doi:10.7554/eLife.26991] [http://hdl.handle.net/10807/106325]
| Autori: | ||
| Titolo: | LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent | |
| Digital Object Identifier (DOI): | http://dx.doi.org/10.7554/eLife.26991 | |
| Data di pubblicazione: | 2017 | |
| Abstract: | The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau. | |
| Lingua: | Inglese | |
| Rivista: | ||
| Citazione: | Puzzo, D., Piacentini, R., Fá, M., Gulisano, W., Li Puma, D. D., Staniszewski, A., Zhang, H., Tropea, M. R., Cocco, S., Palmeri, A., Fraser, P., D'adamio, L., Grassi, C., Arancio, O., LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent, <<ELIFE>>, 2017; 2017 (6): N/A-N/A. [doi:10.7554/eLife.26991] [http://hdl.handle.net/10807/106325] | |
| Appare nelle tipologie: | Articolo in rivista, Nota a sentenza |
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| eLife 6, e26991, 2017.pdf | Versione Editoriale (PDF) | Nessuna Nota |  | Open Access Visualizza/Apri |
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