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14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2

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14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2. / Woo, Marcel S; Nilsson, Johanna; Therriault, Joseph; Rahmouni, Nesrine; Brinkmalm, Ann; Benedet, Andrea L; Ashton, Nicholas J; Macedo, Arthur C; Servaes, Stijn; Wang, Yi-Ting; Tissot, Cécile; Arias, Jaime Fernandez; Hosseini, Seyyed Ali; Chamoun, Mira; Lussier, Firoza Z; Karikari, Thomas K; Stevenson, Jenna; Mayer, Christina; Ferrari-Souza, João Pedro; Kobayashi, Eliane; Massarweh, Gassan; Friese, Manuel A; Pascoal, Tharick A; Gauthier, Serge; Zetterberg, Henrik; Blennow, Kaj; Rosa-Neto, Pedro.

in: J NEUROINFLAMM, Jahrgang 20, Nr. 1, 24.11.2023, S. 278.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Woo, MS, Nilsson, J, Therriault, J, Rahmouni, N, Brinkmalm, A, Benedet, AL, Ashton, NJ, Macedo, AC, Servaes, S, Wang, Y-T, Tissot, C, Arias, JF, Hosseini, SA, Chamoun, M, Lussier, FZ, Karikari, TK, Stevenson, J, Mayer, C, Ferrari-Souza, JP, Kobayashi, E, Massarweh, G, Friese, MA, Pascoal, TA, Gauthier, S, Zetterberg, H, Blennow, K & Rosa-Neto, P 2023, '14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2', J NEUROINFLAMM, Jg. 20, Nr. 1, S. 278. https://doi.org/10.1186/s12974-023-02962-z

APA

Woo, M. S., Nilsson, J., Therriault, J., Rahmouni, N., Brinkmalm, A., Benedet, A. L., Ashton, N. J., Macedo, A. C., Servaes, S., Wang, Y-T., Tissot, C., Arias, J. F., Hosseini, S. A., Chamoun, M., Lussier, F. Z., Karikari, T. K., Stevenson, J., Mayer, C., Ferrari-Souza, J. P., ... Rosa-Neto, P. (2023). 14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2. J NEUROINFLAMM, 20(1), 278. https://doi.org/10.1186/s12974-023-02962-z

Vancouver

Woo MS, Nilsson J, Therriault J, Rahmouni N, Brinkmalm A, Benedet AL et al. 14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2. J NEUROINFLAMM. 2023 Nov 24;20(1):278. https://doi.org/10.1186/s12974-023-02962-z

Bibtex

@article{1e6e626772b942f7a8b7e82b2bfc3d34,
title = "14-3-3 ζ/δ-reported early synaptic injury in Alzheimer{\textquoteright}s disease is independently mediated by sTREM2",
abstract = "INTRODUCTION: Synaptic loss is closely associated with tau aggregation and microglia activation in later stages of Alzheimer's disease (AD). However, synaptic damage happens early in AD at the very early stages of tau accumulation. It remains unclear whether microglia activation independently causes synaptic cleavage before tau aggregation appears.METHODS: We investigated 104 participants across the AD continuum by measuring 14-3-3 zeta/delta ([Formula: see text]) as a cerebrospinal fluid biomarker for synaptic degradation, and fluid and imaging biomarkers of tau, amyloidosis, astrogliosis, neurodegeneration, and inflammation. We performed correlation analyses in cognitively unimpaired and impaired participants and used structural equation models to estimate the impact of microglia activation on synaptic injury in different disease stages.RESULTS: 14-3-3 [Formula: see text] was increased in participants with amyloid pathology at the early stages of tau aggregation before hippocampal volume loss was detectable. 14-3-3 [Formula: see text] correlated with amyloidosis and tau load in all participants but only with biomarkers of neurodegeneration and memory deficits in cognitively unimpaired participants. This early synaptic damage was independently mediated by sTREM2. At later disease stages, tau and astrogliosis additionally mediated synaptic loss.CONCLUSIONS: Our results advertise that sTREM2 is mediating synaptic injury at the early stages of tau accumulation, underlining the importance of microglia activation for AD disease propagation.",
keywords = "Humans, Alzheimer Disease/pathology, Amyloid beta-Peptides/cerebrospinal fluid, Amyloidosis, Biomarkers/cerebrospinal fluid, Gliosis, tau Proteins/metabolism, 14-3-3 Proteins",
author = "Woo, {Marcel S} and Johanna Nilsson and Joseph Therriault and Nesrine Rahmouni and Ann Brinkmalm and Benedet, {Andrea L} and Ashton, {Nicholas J} and Macedo, {Arthur C} and Stijn Servaes and Yi-Ting Wang and C{\'e}cile Tissot and Arias, {Jaime Fernandez} and Hosseini, {Seyyed Ali} and Mira Chamoun and Lussier, {Firoza Z} and Karikari, {Thomas K} and Jenna Stevenson and Christina Mayer and Ferrari-Souza, {Jo{\~a}o Pedro} and Eliane Kobayashi and Gassan Massarweh and Friese, {Manuel A} and Pascoal, {Tharick A} and Serge Gauthier and Henrik Zetterberg and Kaj Blennow and Pedro Rosa-Neto",
note = "{\textcopyright} 2023. The Author(s).",
year = "2023",
month = nov,
day = "24",
doi = "10.1186/s12974-023-02962-z",
language = "English",
volume = "20",
pages = "278",
journal = "J NEUROINFLAMM",
issn = "1742-2094",
publisher = "BioMed Central Ltd.",
number = "1",

}

RIS

TY - JOUR

T1 - 14-3-3 ζ/δ-reported early synaptic injury in Alzheimer’s disease is independently mediated by sTREM2

AU - Woo, Marcel S

AU - Nilsson, Johanna

AU - Therriault, Joseph

AU - Rahmouni, Nesrine

AU - Brinkmalm, Ann

AU - Benedet, Andrea L

AU - Ashton, Nicholas J

AU - Macedo, Arthur C

AU - Servaes, Stijn

AU - Wang, Yi-Ting

AU - Tissot, Cécile

AU - Arias, Jaime Fernandez

AU - Hosseini, Seyyed Ali

AU - Chamoun, Mira

AU - Lussier, Firoza Z

AU - Karikari, Thomas K

AU - Stevenson, Jenna

AU - Mayer, Christina

AU - Ferrari-Souza, João Pedro

AU - Kobayashi, Eliane

AU - Massarweh, Gassan

AU - Friese, Manuel A

AU - Pascoal, Tharick A

AU - Gauthier, Serge

AU - Zetterberg, Henrik

AU - Blennow, Kaj

AU - Rosa-Neto, Pedro

N1 - © 2023. The Author(s).

PY - 2023/11/24

Y1 - 2023/11/24

N2 - INTRODUCTION: Synaptic loss is closely associated with tau aggregation and microglia activation in later stages of Alzheimer's disease (AD). However, synaptic damage happens early in AD at the very early stages of tau accumulation. It remains unclear whether microglia activation independently causes synaptic cleavage before tau aggregation appears.METHODS: We investigated 104 participants across the AD continuum by measuring 14-3-3 zeta/delta ([Formula: see text]) as a cerebrospinal fluid biomarker for synaptic degradation, and fluid and imaging biomarkers of tau, amyloidosis, astrogliosis, neurodegeneration, and inflammation. We performed correlation analyses in cognitively unimpaired and impaired participants and used structural equation models to estimate the impact of microglia activation on synaptic injury in different disease stages.RESULTS: 14-3-3 [Formula: see text] was increased in participants with amyloid pathology at the early stages of tau aggregation before hippocampal volume loss was detectable. 14-3-3 [Formula: see text] correlated with amyloidosis and tau load in all participants but only with biomarkers of neurodegeneration and memory deficits in cognitively unimpaired participants. This early synaptic damage was independently mediated by sTREM2. At later disease stages, tau and astrogliosis additionally mediated synaptic loss.CONCLUSIONS: Our results advertise that sTREM2 is mediating synaptic injury at the early stages of tau accumulation, underlining the importance of microglia activation for AD disease propagation.

AB - INTRODUCTION: Synaptic loss is closely associated with tau aggregation and microglia activation in later stages of Alzheimer's disease (AD). However, synaptic damage happens early in AD at the very early stages of tau accumulation. It remains unclear whether microglia activation independently causes synaptic cleavage before tau aggregation appears.METHODS: We investigated 104 participants across the AD continuum by measuring 14-3-3 zeta/delta ([Formula: see text]) as a cerebrospinal fluid biomarker for synaptic degradation, and fluid and imaging biomarkers of tau, amyloidosis, astrogliosis, neurodegeneration, and inflammation. We performed correlation analyses in cognitively unimpaired and impaired participants and used structural equation models to estimate the impact of microglia activation on synaptic injury in different disease stages.RESULTS: 14-3-3 [Formula: see text] was increased in participants with amyloid pathology at the early stages of tau aggregation before hippocampal volume loss was detectable. 14-3-3 [Formula: see text] correlated with amyloidosis and tau load in all participants but only with biomarkers of neurodegeneration and memory deficits in cognitively unimpaired participants. This early synaptic damage was independently mediated by sTREM2. At later disease stages, tau and astrogliosis additionally mediated synaptic loss.CONCLUSIONS: Our results advertise that sTREM2 is mediating synaptic injury at the early stages of tau accumulation, underlining the importance of microglia activation for AD disease propagation.

KW - Humans

KW - Alzheimer Disease/pathology

KW - Amyloid beta-Peptides/cerebrospinal fluid

KW - Amyloidosis

KW - Biomarkers/cerebrospinal fluid

KW - Gliosis

KW - tau Proteins/metabolism

KW - 14-3-3 Proteins

U2 - 10.1186/s12974-023-02962-z

DO - 10.1186/s12974-023-02962-z

M3 - SCORING: Journal article

C2 - 38001539

VL - 20

SP - 278

JO - J NEUROINFLAMM

JF - J NEUROINFLAMM

SN - 1742-2094

IS - 1

ER -