Gene immunotherapy regulated by astrocytic reactivity in a mouse model of amyloidosis

Wedi'i Gadw mewn:
Manylion Llyfryddiaeth
Cyhoeddwyd yn:Alzheimer's & Dementia vol. 21 (Dec 1, 2025)
Prif Awdur: Dibia, Chinaza Lilian
Awduron Eraill: Vacaresse, Nathalie, Kofoed, Rikke Han, Laurette, Brandy, Rubio‐Atonal, Luis Fernando, Yurtsever, Dildare, Aubert, Isabelle
Cyhoeddwyd:
John Wiley & Sons, Inc.
Pynciau:
Mynediad Ar-lein:Citation/Abstract
Full Text - PDF
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001 3286100885
003 UK-CbPIL
022 |a 1552-5260 
022 |a 1552-5279 
024 7 |a 10.1002/alz70855_103554  |2 doi 
035 |a 3286100885 
045 0 |b d20251201 
100 1 |a Dibia, Chinaza Lilian  |u University of Toronto, Toronto, ON, Canada, 
245 1 |a Gene immunotherapy regulated by astrocytic reactivity in a mouse model of amyloidosis 
260 |b John Wiley & Sons, Inc.  |c Dec 1, 2025 
513 |a Journal Article 
520 3 |a Background Recombinant adeno‐associated viruses (AAVs) capable of crossing the blood‐brain barrier (e.g. AAV.PHP.eB) and encoding antibodies against amyloid beta peptides (Aβ) have potential to evaluate brain‐wide gene immunotherapies in Alzheimer's disease (AD). Furthermore, leveraging astrocytic reactivity in response to Aβ pathology, the glial fibrillary acidic protein (GFAP) promoter could serve as a regulator of gene immunotherapy. Hypothesis Reactive astrocytes can regulate the expression of the recombinant anti‐Aβ antibody (rSol) under the control of a GFAP promoter in the TgCRND8 (Tg) mouse model of amyloidosis. Method To study GFAP expression in Tg mice, GFAP mRNA levels were quantified using qPCR in the hippocampal formation at 3, 5, and 6 months (n = 6 per group). Next, AAV.PHP.eB.GFAP.rSol‐myc‐tag and AAV.PHP.eB.GFAP.GFP were co‐injected intravenously in Tg mice while non‐Tg littermates and C57BL/6J mice served as controls. One‐month post‐injection, brain sections were processed for immunohistochemistry and RNAscope. Result GFAP mRNA levels doubled in 6‐month‐old compared to 3‐month‐old Tg mice. Brain‐wide GFP expression in astrocytes confirmed efficacy of the GFAP promoter. Notably, brain cell transduction varied across Tg mice, peaking in the C57BL/6J line. Ly6A, a protein previously shown to facilitate AAV.PHP.eB entry into the brain, may explain this variability in transduction levels. We are currently examining Ly6A expression in our transgenic mouse line to determine the Tg background that will deliver the most efficient viral transduction. Conclusion These results suggest that the GFAP promoter could control the production of therapeutics, such as rSol, in response to amyloid‐induced astrocytic reactivity. Long‐term studies will assess whether rSol prevents Aβ pathology progression in Tg‐Aβ mice. 
653 |a Pathology 
653 |a Reactivity 
653 |a Encoding 
653 |a Immunotherapy 
653 |a Brain 
653 |a Encoding (Cognitive process) 
653 |a Animals 
653 |a Amyloidosis 
653 |a Efficacy 
653 |a Alzheimer's disease 
653 |a Viruses 
653 |a Antibodies 
700 1 |a Vacaresse, Nathalie  |u Sunnybrook Research Institute, Toronto, ON, Canada, 
700 1 |a Kofoed, Rikke Han  |u Center for Experimental Neuroscience (CENSE), Department of Neurosurgery, Aarhus University Hospital, Aarhus N, Denmark, Aarhus N, Aarhus, Denmark, 
700 1 |a Laurette, Brandy  |u Sunnybrook Research Institute, Toronto, ON, Canada, 
700 1 |a Rubio‐Atonal, Luis Fernando  |u Sunnybrook Research Institute, Toronto, ON, Canada, 
700 1 |a Yurtsever, Dildare  |u Sunnybrook Research Institute, Toronto, ON, Canada, 
700 1 |a Aubert, Isabelle  |u Sunnybrook Research Institute, Toronto, ON, Canada, 
773 0 |t Alzheimer's & Dementia  |g vol. 21 (Dec 1, 2025) 
786 0 |d ProQuest  |t Consumer Health Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3286100885/abstract/embedded/L8HZQI7Z43R0LA5T?source=fedsrch 
856 4 0 |3 Full Text - PDF  |u https://www.proquest.com/docview/3286100885/fulltextPDF/embedded/L8HZQI7Z43R0LA5T?source=fedsrch