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Involvement of the choroid plexus in Alzheimer's disease pathophysiology : findings from mouse and human proteomic studies

Aurore Delvenne, Charysse Vandendriessche (UGent) , Johan Gobom, Marlies Burgelman (UGent) , Pieter Dujardin (UGent) , Clint De Nolf (UGent) , Betty M. Tijms, Charlotte E. Teunissen, Suzanne E. Schindler, Frans Verhey, et al.
(2024) FLUIDS AND BARRIERS OF THE CNS. 21(1).
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Abstract
BackgroundStructural and functional changes of the choroid plexus (ChP) have been reported in Alzheimer's disease (AD). Nonetheless, the role of the ChP in the pathogenesis of AD remains largely unknown. We aim to unravel the relation between ChP functioning and core AD pathogenesis using a unique proteomic approach in mice and humans.MethodsWe used an APP knock-in mouse model, APPNL-G-F, exhibiting amyloid pathology, to study the association between AD brain pathology and protein changes in mouse ChP tissue and CSF using liquid chromatography mass spectrometry. Mouse proteomes were investigated at the age of 7 weeks (n = 5) and 40 weeks (n = 5). Results were compared with previously published human AD CSF proteomic data (n = 496) to identify key proteins and pathways associated with ChP changes in AD.ResultsChP tissue proteome was dysregulated in APPNL-G-F mice relative to wild-type mice at both 7 and 40 weeks. At both ages, ChP tissue proteomic changes were associated with epithelial cells, mitochondria, protein modification, extracellular matrix and lipids. Nonetheless, some ChP tissue proteomic changes were different across the disease trajectory; pathways related to lysosomal function, endocytosis, protein formation, actin and complement were uniquely dysregulated at 7 weeks, while pathways associated with nervous system, immune system, protein degradation and vascular system were uniquely dysregulated at 40 weeks. CSF proteomics in both mice and humans showed similar ChP-related dysregulated pathways.ConclusionsTogether, our findings support the hypothesis of ChP dysfunction in AD. These ChP changes were related to amyloid pathology. Therefore, the ChP could become a novel promising therapeutic target for AD.
Keywords
Alzheimer's disease, Choroid plexus, Cerebrospinal fluid, Proteomics, APP knock-in mice, Amyloid-beta (A beta), CEREBROSPINAL-FLUID PRODUCTION, MODEL, EXPRESSION, TRANSPORT, VESSELS, BARRIER, ADULT

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MLA
Delvenne, Aurore, et al. “Involvement of the Choroid Plexus in Alzheimer’s Disease Pathophysiology : Findings from Mouse and Human Proteomic Studies.” FLUIDS AND BARRIERS OF THE CNS, vol. 21, no. 1, 2024, doi:10.1186/s12987-024-00555-3.
APA
Delvenne, A., Vandendriessche, C., Gobom, J., Burgelman, M., Dujardin, P., De Nolf, C., … Vos, S. J. B. (2024). Involvement of the choroid plexus in Alzheimer’s disease pathophysiology : findings from mouse and human proteomic studies. FLUIDS AND BARRIERS OF THE CNS, 21(1). https://doi.org/10.1186/s12987-024-00555-3
Chicago author-date
Delvenne, Aurore, Charysse Vandendriessche, Johan Gobom, Marlies Burgelman, Pieter Dujardin, Clint De Nolf, Betty M. Tijms, et al. 2024. “Involvement of the Choroid Plexus in Alzheimer’s Disease Pathophysiology : Findings from Mouse and Human Proteomic Studies.” FLUIDS AND BARRIERS OF THE CNS 21 (1). https://doi.org/10.1186/s12987-024-00555-3.
Chicago author-date (all authors)
Delvenne, Aurore, Charysse Vandendriessche, Johan Gobom, Marlies Burgelman, Pieter Dujardin, Clint De Nolf, Betty M. Tijms, Charlotte E. Teunissen, Suzanne E. Schindler, Frans Verhey, Inez Ramakers, Pablo Martinez-Lage, Mikel Tainta, Rik Vandenberghe, Jolien Schaeverbeke, Sebastiaan Engelborghs, Ellen De Roeck, Julius Popp, Gwendoline Peyratout, Magda Tsolaki, Yvonne Freund-Levi, Simon Lovestone, Johannes Streffer, Lars Bertram, Kaj Blennow, Henrik Zetterberg, Pieter Jelle Visser, Roosmarijn Vandenbroucke, and Stephanie J. B. Vos. 2024. “Involvement of the Choroid Plexus in Alzheimer’s Disease Pathophysiology : Findings from Mouse and Human Proteomic Studies.” FLUIDS AND BARRIERS OF THE CNS 21 (1). doi:10.1186/s12987-024-00555-3.
Vancouver
1.
Delvenne A, Vandendriessche C, Gobom J, Burgelman M, Dujardin P, De Nolf C, et al. Involvement of the choroid plexus in Alzheimer’s disease pathophysiology : findings from mouse and human proteomic studies. FLUIDS AND BARRIERS OF THE CNS. 2024;21(1).
IEEE
[1]
A. Delvenne et al., “Involvement of the choroid plexus in Alzheimer’s disease pathophysiology : findings from mouse and human proteomic studies,” FLUIDS AND BARRIERS OF THE CNS, vol. 21, no. 1, 2024.
@article{01J73Q3F0X36FE71EVFSQ5Q591,
  abstract     = {{BackgroundStructural and functional changes of the choroid plexus (ChP) have been reported in Alzheimer's disease (AD). Nonetheless, the role of the ChP in the pathogenesis of AD remains largely unknown. We aim to unravel the relation between ChP functioning and core AD pathogenesis using a unique proteomic approach in mice and humans.MethodsWe used an APP knock-in mouse model, APPNL-G-F, exhibiting amyloid pathology, to study the association between AD brain pathology and protein changes in mouse ChP tissue and CSF using liquid chromatography mass spectrometry. Mouse proteomes were investigated at the age of 7 weeks (n = 5) and 40 weeks (n = 5). Results were compared with previously published human AD CSF proteomic data (n = 496) to identify key proteins and pathways associated with ChP changes in AD.ResultsChP tissue proteome was dysregulated in APPNL-G-F mice relative to wild-type mice at both 7 and 40 weeks. At both ages, ChP tissue proteomic changes were associated with epithelial cells, mitochondria, protein modification, extracellular matrix and lipids. Nonetheless, some ChP tissue proteomic changes were different across the disease trajectory; pathways related to lysosomal function, endocytosis, protein formation, actin and complement were uniquely dysregulated at 7 weeks, while pathways associated with nervous system, immune system, protein degradation and vascular system were uniquely dysregulated at 40 weeks. CSF proteomics in both mice and humans showed similar ChP-related dysregulated pathways.ConclusionsTogether, our findings support the hypothesis of ChP dysfunction in AD. These ChP changes were related to amyloid pathology. Therefore, the ChP could become a novel promising therapeutic target for AD.}},
  articleno    = {{58}},
  author       = {{Delvenne, Aurore and Vandendriessche, Charysse and  Gobom, Johan and Burgelman, Marlies and Dujardin, Pieter and De Nolf, Clint and  Tijms, Betty M. and  Teunissen, Charlotte E. and  Schindler, Suzanne E. and  Verhey, Frans and  Ramakers, Inez and  Martinez-Lage, Pablo and  Tainta, Mikel and  Vandenberghe, Rik and  Schaeverbeke, Jolien and  Engelborghs, Sebastiaan and  De Roeck, Ellen and  Popp, Julius and  Peyratout, Gwendoline and  Tsolaki, Magda and  Freund-Levi, Yvonne and  Lovestone, Simon and  Streffer, Johannes and  Bertram, Lars and  Blennow, Kaj and  Zetterberg, Henrik and  Visser, Pieter Jelle and Vandenbroucke, Roosmarijn and  Vos, Stephanie J. B.}},
  issn         = {{2045-8118}},
  journal      = {{FLUIDS AND BARRIERS OF THE CNS}},
  keywords     = {{Alzheimer's disease,Choroid plexus,Cerebrospinal fluid,Proteomics,APP knock-in mice,Amyloid-beta (A beta),CEREBROSPINAL-FLUID PRODUCTION,MODEL,EXPRESSION,TRANSPORT,VESSELS,BARRIER,ADULT}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{17}},
  title        = {{Involvement of the choroid plexus in Alzheimer's disease pathophysiology : findings from mouse and human proteomic studies}},
  url          = {{http://doi.org/10.1186/s12987-024-00555-3}},
  volume       = {{21}},
  year         = {{2024}},
}
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