Membrane Proteome Remodeling in Female APP Mice Following Muscarinic Acetylcholine Receptor M1 Modulation Revealed by Peptidisc Enabled DIA-MS.
Ashim BhattacharyaiD, Frank AntonyiD, Hiroyuki AokiiD, Mohan BabuiD, Stephen S. G. FergusoniD, Khaled S. Abd‐ElrahmaniD, Franck DuongiD
Abstract
Alzheimers disease (AD) is linked to profound dysregulation of membrane-embedded and membrane-associated proteins that govern amyloid processing, synaptic signaling, and neuronal communication. Yet most proteomic analyses prioritize soluble fractions, resulting in systematic underrepresentation of integral membrane proteins and limited access to disease-relevant membrane pathways. Here, we use a membrane-mimetic, data-independent acquisition proteomic workflow to define disease- and drug-induced remodeling of the cortical membrane proteome in an APP mouse model of Alzheimers disease. Female B6C3F1/J mice were aged to 9 months and treated for 8 weeks with or without the M1 muscarinic acetylcholine receptor positive allosteric modulator VU0486846. APP pathology drove a pronounced, genotype-specific remodeling of the membrane proteome, with enrichment of multiple membrane proteins linked to AD, including RyR2, PLD3, ITM2C, and CNTNAP2. Wild-type mice cortical membranes were instead enriched for membrane proteins involved in axon guidance and synaptic organization, such as EPHA5 and ROBO2. In contrast, activation of M1 using the VU0486846 produced minimal membrane proteome changes in wild-type mice but selectively enriched proteins involved in neuronal trafficking and synaptic plasticity in APP mice, including SORCS2, PLXND1, and CADM1. Together, these findings demonstrate that AD-associated proteomic remodeling is strongly concentrated at the membrane level and that M1 receptor activation preferentially engages disease-altered membrane networks rather than inducing widespread proteomic changes. This work establishes peptidisc-enabled membrane proteomics as a powerful approach for identifying membrane-associated biomarkers and evaluating therapeutic target engagement in AD. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=76 SRC="FIGDIR/small/707828v2_ufig1.gif" ALT="Figure 1"> View larger version (26K): org.highwire.dtl.DTLVardef@16dc5c9org.highwire.dtl.DTLVardef@1d433c1org.highwire.dtl.DTLVardef@92015dorg.highwire.dtl.DTLVardef@197871d_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstractC_FLOATNO C_FIG
02 /Specification & Classification
Click any tag to browse matching papers- Citations
- 0
- Organism
- Assay
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Unexpected Early Proteomic Changes in Alzheimer’s Disease Model Mice Synaptosomes
Kerri A. Ball, Addolorata Pisconti, … Michael H. B. Stowell·bioRxiv·Jun 15, 2017
- Amyloid accumulation drives proteome-wide alterations in mouse models of Alzheimers disease like pathology
Jeffrey N. Savas, Yizhi Wang, … John R. Yates·Cell ReportsPeer-reviewed·Nov 1, 2017
- Activation of M1 muscarinic receptors reduce pathology and slow progression of neurodegenerative disease.
Louis Dwomoh, Mario Rossi, … Andrew B. Tobin·bioRxiv·Jul 30, 2021
- Single Plaque Proteomics Reveals the Composition and Dynamics of the Amyloid Microenvironment in Alzheimer's Disease
Mengqi Chu, Ju Wang, … Junmin Peng·bioRxiv·Feb 4, 2026
- Age-dependent brain proteome remodeling links Abca7 deficiency to insulin signaling and neuroinflammation in Alzheimers disease mice
Dániel Mittli, Jens Pahnke·bioRxiv·Jul 31, 2026
- Mapping the spatial proteomic signature of dorsal and ventral hippocampus in a mouse model of early Alzheimer's disease: changes in synaptic plasticity-related proteins associated with sexual dimorphism
Ana Contreras, Raquel Jiménez‐Herrera, … Lydia Jiménez‐Díaz·bioRxiv·May 8, 2024