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000283080 037__ $$aDZNE-2025-01487
000283080 041__ $$aEnglish
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000283080 1001_ $$aLalia, Manvir$$b0
000283080 1112_ $$aAlzheimer’s Association International Conference$$cToronto$$d2025-07-27 - 2025-07-31$$gAAIC 25$$wCanada
000283080 245__ $$aCell-Type Specific Contributions to Metabolic Connectivity in an Alzheimer’s Disease Mouse Model
000283080 260__ $$c2025
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000283080 520__ $$aThe integration of molecular imaging and multivariate connectivity approaches has emerged as a novel approach to gain insights into the underlying pathophysiology in neurodegenerative diseases. Metabolic connectivity, in particular, has already demonstrated disease-related pattern changes in both human and mammalian brains. However, the cellular sources of disconnected brain regions have not been investigated in detail. This study aimed to elucidate the driving cellular sources of metabolic connectivity in an Alzheimer's disease (AD) mouse model and wild-type mice (WT).After intravenous injection of 45MBq F-18-FDG, a static PET/MRI was performed on APPNL-G-F and age- and sex-matched WT controls to obtain maps of regional FDG uptake and metabolic connectivity. To calculate the inter-regional correlations for metabolic connectivity, 26 delineated brain regions were used, resulting in a 26 × 26 matrix of Pearson's correlation coefficient pairs. Subsequently, the brain was extracted and separated into fore- and hindbrain to achieve region-specific isolation of microglia, astrocytes, oligodendrocytes, and neurons. The radioactivity of each cell fraction was measured to quantify the cell-specific FDG-uptake (Figure 1D).APPNL-G-F mice demonstrated higher FDG uptake compared to WT, along with a significantly increased metabolic connectivity between fore- and hindbrain (Figure 1A-C). Among all cell types, microglial exhibited the highest single-cell FDG uptake, in both mouse models (Figure 1E). In APPNL-G-F mice, microglia, astrocytes, and oligodendrocytes displayed increased FDG uptake, while neurons exhibited reduced uptake compared to WT. The correlation between forebrain and hindbrain cellular FDG uptake was significant across all cell types in the APPNL-G-F model (microglia r=0.89, p = 0.0006; astrocytes r=0.65, p = 0.042; oligodendrocytes r=0.77, p = 0.025 and neurons r=0.51, p = 0.005). In contrast, WT mice did not exhibit any significant correlation in single-cell uptake between forebrain and hindbrain. Notably, region-specific microglial FDG uptake correlated significantly with respective FDG-PET signals in APPNL-G-F mice (forebrain r=0.89, p = 0.007; hindbrain r=0.8, p = 0.014), whereas no significant correlation was observed for other cell types.These findings suggest that microglia are the primary drivers of the increased forebrain-hindbrain metabolic connectivity observed in the AD mouse model. Further RNA expression analyses could provide valuable insights into the molecular mechanisms underlying microglial metabolic coupling in neurodegeneration.
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000283080 650_7 $$00Z5B2CJX4D$$2NLM Chemicals$$aFluorodeoxyglucose F18
000283080 650_7 $$2NLM Chemicals$$aRadiopharmaceuticals
000283080 650_2 $$2MeSH$$aAnimals
000283080 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000283080 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000283080 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000283080 650_2 $$2MeSH$$aPositron-Emission Tomography
000283080 650_2 $$2MeSH$$aMice
000283080 650_2 $$2MeSH$$aBrain: diagnostic imaging
000283080 650_2 $$2MeSH$$aBrain: metabolism
000283080 650_2 $$2MeSH$$aBrain: pathology
000283080 650_2 $$2MeSH$$aDisease Models, Animal
000283080 650_2 $$2MeSH$$aFluorodeoxyglucose F18
000283080 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000283080 650_2 $$2MeSH$$aMice, Transgenic
000283080 650_2 $$2MeSH$$aMale
000283080 650_2 $$2MeSH$$aFemale
000283080 650_2 $$2MeSH$$aMicroglia: metabolism
000283080 650_2 $$2MeSH$$aNeurons: metabolism
000283080 650_2 $$2MeSH$$aAstrocytes: metabolism
000283080 650_2 $$2MeSH$$aRadiopharmaceuticals
000283080 7001_ $$aWagner, Stephan$$b1
000283080 7001_ $$0P:(DE-2719)9002483$$aHummel, Selina$$b2$$udzne
000283080 7001_ $$aThevis, Justus$$b3
000283080 7001_ $$0P:(DE-2719)9002550$$aPrtvar, Danilo$$b4$$udzne
000283080 7001_ $$0P:(DE-2719)9001654$$aZatcepin, Artem$$b5$$udzne
000283080 7001_ $$0P:(DE-2719)9002392$$aZenatti, Valerio$$b6$$udzne
000283080 7001_ $$aBartos, Laura$$b7
000283080 7001_ $$0P:(DE-2719)2442036$$aTahirovic, Sabina$$b8$$udzne
000283080 7001_ $$0P:(DE-2719)9001539$$aBrendel, Matthias$$b9$$udzne
000283080 7001_ $$0P:(DE-2719)9001652$$aGnörich, Johannes$$b10$$eLast author$$udzne
000283080 773__ $$0PERI:(DE-600)2201940-6$$a10.1002/alz70862_109909$$gVol. 21 Suppl 8, no. Suppl 8, p. e109909$$nSuppl 8$$pe109909$$tAlzheimer's and dementia$$v21$$x1552-5260$$y2025
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