Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models
<div><p>Many mouse models of Alzheimer’s disease (AD) exhibit impairments in hippocampal long-term-potentiation (LTP), seemingly corroborating the strong correlation between synaptic loss and cognitive decline reported in human studies. In other AD mouse models LTP is unaffected, but oth...
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| مؤلفون آخرون: | , , , |
| منشور في: |
2019
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| _version_ | 1864513515129143296 |
|---|---|
| author | Enrico Faldini (18602953) |
| author2 | Tariq Ahmed (5768081) Luc Bueé (18602956) David Blum (344593) Detlef Balschun (8096618) |
| author2_role | author author author author |
| author_facet | Enrico Faldini (18602953) Tariq Ahmed (5768081) Luc Bueé (18602956) David Blum (344593) Detlef Balschun (8096618) |
| author_role | author |
| dc.creator.none.fl_str_mv | Enrico Faldini (18602953) Tariq Ahmed (5768081) Luc Bueé (18602956) David Blum (344593) Detlef Balschun (8096618) |
| dc.date.none.fl_str_mv | 2019-12-09T03:00:00Z |
| dc.identifier.none.fl_str_mv | 10.1186/s40478-019-0813-4 |
| dc.relation.none.fl_str_mv | https://figshare.com/articles/journal_contribution/Tau-_but_not_A_-pathology_enhances_NMDAR-dependent_depotentiation_in_AD-mouse_models/25886935 |
| dc.rights.none.fl_str_mv | CC BY 4.0 info:eu-repo/semantics/openAccess |
| dc.subject.none.fl_str_mv | Biomedical and clinical sciences Neurosciences Alzheimer’s disease Synaptic plasticity Depotentiation Hippocampus CA1-region Tau Aβ Glycogen synthase kinase-3β |
| dc.title.none.fl_str_mv | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| dc.type.none.fl_str_mv | Text Journal contribution info:eu-repo/semantics/publishedVersion text contribution to journal |
| description | <div><p>Many mouse models of Alzheimer’s disease (AD) exhibit impairments in hippocampal long-term-potentiation (LTP), seemingly corroborating the strong correlation between synaptic loss and cognitive decline reported in human studies. In other AD mouse models LTP is unaffected, but other defects in synaptic plasticity may still be present. We recently reported that THY-Tau22 transgenic mice, that overexpress human Tau protein carrying P301S and G272 V mutations and show normal LTP upon high-frequency-stimulation (HFS), develop severe changes in NMDAR mediated long-term-depression (LTD), the physiological counterpart of LTP. In the present study, we focused on putative effects of AD-related pathologies on depotentiation (DP), another form of synaptic plasticity. Using a novel protocol to induce DP in the CA1-region, we found in 11–15 months old male THY-Tau22 and APPPS1–21 transgenic mice that DP was not deteriorated by Aß pathology while significantly compromised by Tau pathology. Our findings advocate DP as a complementary form of synaptic plasticity that may help in elucidating synaptic pathomechanisms associated with different types of dementia.</p><p> </p></div><h2>Other Information</h2> <p> Published in: Acta Neuropathologica Communications<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1186/s40478-019-0813-4" target="_blank">https://dx.doi.org/10.1186/s40478-019-0813-4</a></p> |
| eu_rights_str_mv | openAccess |
| id | Manara2_3a16595e9c79bacd9233323dc565384d |
| identifier_str_mv | 10.1186/s40478-019-0813-4 |
| network_acronym_str | Manara2 |
| network_name_str | Manara2 |
| oai_identifier_str | oai:figshare.com:article/25886935 |
| publishDate | 2019 |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| rights_invalid_str_mv | CC BY 4.0 |
| spelling | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse modelsEnrico Faldini (18602953)Tariq Ahmed (5768081)Luc Bueé (18602956)David Blum (344593)Detlef Balschun (8096618)Biomedical and clinical sciencesNeurosciencesAlzheimer’s diseaseSynaptic plasticityDepotentiationHippocampusCA1-regionTauAβGlycogen synthase kinase-3β<div><p>Many mouse models of Alzheimer’s disease (AD) exhibit impairments in hippocampal long-term-potentiation (LTP), seemingly corroborating the strong correlation between synaptic loss and cognitive decline reported in human studies. In other AD mouse models LTP is unaffected, but other defects in synaptic plasticity may still be present. We recently reported that THY-Tau22 transgenic mice, that overexpress human Tau protein carrying P301S and G272 V mutations and show normal LTP upon high-frequency-stimulation (HFS), develop severe changes in NMDAR mediated long-term-depression (LTD), the physiological counterpart of LTP. In the present study, we focused on putative effects of AD-related pathologies on depotentiation (DP), another form of synaptic plasticity. Using a novel protocol to induce DP in the CA1-region, we found in 11–15 months old male THY-Tau22 and APPPS1–21 transgenic mice that DP was not deteriorated by Aß pathology while significantly compromised by Tau pathology. Our findings advocate DP as a complementary form of synaptic plasticity that may help in elucidating synaptic pathomechanisms associated with different types of dementia.</p><p> </p></div><h2>Other Information</h2> <p> Published in: Acta Neuropathologica Communications<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1186/s40478-019-0813-4" target="_blank">https://dx.doi.org/10.1186/s40478-019-0813-4</a></p>2019-12-09T03:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1186/s40478-019-0813-4https://figshare.com/articles/journal_contribution/Tau-_but_not_A_-pathology_enhances_NMDAR-dependent_depotentiation_in_AD-mouse_models/25886935CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/258869352019-12-09T03:00:00Z |
| spellingShingle | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models Enrico Faldini (18602953) Biomedical and clinical sciences Neurosciences Alzheimer’s disease Synaptic plasticity Depotentiation Hippocampus CA1-region Tau Aβ Glycogen synthase kinase-3β |
| status_str | publishedVersion |
| title | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| title_full | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| title_fullStr | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| title_full_unstemmed | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| title_short | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| title_sort | Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models |
| topic | Biomedical and clinical sciences Neurosciences Alzheimer’s disease Synaptic plasticity Depotentiation Hippocampus CA1-region Tau Aβ Glycogen synthase kinase-3β |