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Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death

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Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death. / Hughes, Craig; Choi, Minee L.; Yi, Jee Hyun; Kim, Seung Chan; Drews, Anna; George-Hyslop, Peter St; Bryant, Clare; Gandhi, Sonia; Cho, Kwangwook; Klenerman, David.

In: Communications Biology, Vol. 3, No. 1, 79, 01.12.2020.

Research output: Contribution to journalArticle

Harvard

Hughes, C, Choi, ML, Yi, JH, Kim, SC, Drews, A, George-Hyslop, PS, Bryant, C, Gandhi, S, Cho, K & Klenerman, D 2020, 'Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death', Communications Biology, vol. 3, no. 1, 79. https://doi.org/10.1038/s42003-020-0792-9

APA

Hughes, C., Choi, M. L., Yi, J. H., Kim, S. C., Drews, A., George-Hyslop, P. S., ... Klenerman, D. (2020). Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death. Communications Biology, 3(1), [79]. https://doi.org/10.1038/s42003-020-0792-9

Vancouver

Hughes C, Choi ML, Yi JH, Kim SC, Drews A, George-Hyslop PS et al. Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death. Communications Biology. 2020 Dec 1;3(1). 79. https://doi.org/10.1038/s42003-020-0792-9

Author

Hughes, Craig ; Choi, Minee L. ; Yi, Jee Hyun ; Kim, Seung Chan ; Drews, Anna ; George-Hyslop, Peter St ; Bryant, Clare ; Gandhi, Sonia ; Cho, Kwangwook ; Klenerman, David. / Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death. In: Communications Biology. 2020 ; Vol. 3, No. 1.

Bibtex Download

@article{455a86563f3f43b3a6cb992a2996c909,
title = "Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death",
abstract = "The molecular events causing memory loss and neuronal cell death in Alzheimer’s disease (AD) over time are still unknown. Here we found that picomolar concentrations of soluble oligomers of synthetic beta amyloid (Aβ42) aggregates incubated with BV2 cells or rat astrocytes caused a sensitised response of Toll-like receptor 4 (TLR4) with time, leading to increased production of TNF-α. Aβ aggregates caused long term potentiation (LTP) deficit in hippocampal slices and predominantly neuronal cell death in co-cultures of astrocytes and neurons, which was blocked by TLR4 antagonists. Soluble Aβ aggregates cause LTP deficit and neuronal death via an autocrine/paracrine mechanism due to TLR4 signalling. These findings suggest that the TLR4-mediated inflammatory response may be a key pathophysiological process in AD.",
author = "Craig Hughes and Choi, {Minee L.} and Yi, {Jee Hyun} and Kim, {Seung Chan} and Anna Drews and George-Hyslop, {Peter St} and Clare Bryant and Sonia Gandhi and Kwangwook Cho and David Klenerman",
year = "2020",
month = "12",
day = "1",
doi = "10.1038/s42003-020-0792-9",
language = "English",
volume = "3",
journal = "Communications Biology",
publisher = "Springer Nature",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Beta amyloid aggregates induce sensitised TLR4 signalling causing long-term potentiation deficit and rat neuronal cell death

AU - Hughes, Craig

AU - Choi, Minee L.

AU - Yi, Jee Hyun

AU - Kim, Seung Chan

AU - Drews, Anna

AU - George-Hyslop, Peter St

AU - Bryant, Clare

AU - Gandhi, Sonia

AU - Cho, Kwangwook

AU - Klenerman, David

PY - 2020/12/1

Y1 - 2020/12/1

N2 - The molecular events causing memory loss and neuronal cell death in Alzheimer’s disease (AD) over time are still unknown. Here we found that picomolar concentrations of soluble oligomers of synthetic beta amyloid (Aβ42) aggregates incubated with BV2 cells or rat astrocytes caused a sensitised response of Toll-like receptor 4 (TLR4) with time, leading to increased production of TNF-α. Aβ aggregates caused long term potentiation (LTP) deficit in hippocampal slices and predominantly neuronal cell death in co-cultures of astrocytes and neurons, which was blocked by TLR4 antagonists. Soluble Aβ aggregates cause LTP deficit and neuronal death via an autocrine/paracrine mechanism due to TLR4 signalling. These findings suggest that the TLR4-mediated inflammatory response may be a key pathophysiological process in AD.

AB - The molecular events causing memory loss and neuronal cell death in Alzheimer’s disease (AD) over time are still unknown. Here we found that picomolar concentrations of soluble oligomers of synthetic beta amyloid (Aβ42) aggregates incubated with BV2 cells or rat astrocytes caused a sensitised response of Toll-like receptor 4 (TLR4) with time, leading to increased production of TNF-α. Aβ aggregates caused long term potentiation (LTP) deficit in hippocampal slices and predominantly neuronal cell death in co-cultures of astrocytes and neurons, which was blocked by TLR4 antagonists. Soluble Aβ aggregates cause LTP deficit and neuronal death via an autocrine/paracrine mechanism due to TLR4 signalling. These findings suggest that the TLR4-mediated inflammatory response may be a key pathophysiological process in AD.

UR - http://www.scopus.com/inward/record.url?scp=85079654079&partnerID=8YFLogxK

U2 - 10.1038/s42003-020-0792-9

DO - 10.1038/s42003-020-0792-9

M3 - Article

C2 - 32071389

AN - SCOPUS:85079654079

VL - 3

JO - Communications Biology

JF - Communications Biology

IS - 1

M1 - 79

ER -

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