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000266481 1001_ $$aEndepols, Heike$$b0
000266481 245__ $$aFragmentation of functional resting state brain networks in a transgenic mouse model of tau pathology: A metabolic connectivity study using [18F]FDG-PET
000266481 260__ $$aOrlando, Fla.$$bAcademic Press$$c2024
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000266481 520__ $$aIn a previous study, regional reductions in cerebral glucose metabolism have been demonstrated in the tauopathy mouse model rTg4510 (Endepols et al., 2022). Notably, glucose hypometabolism was present in some brain regions without co-localized synaptic degeneration measured with [18F]UCB-H. We hypothesized that in those regions hypometabolism may reflect reduced functional connectivity rather than synaptic damage. To test this hypothesis, we performed seed-based metabolic connectivity analyses using [18F]FDG-PET data in this mouse model. Eight rTg4510 mice at the age of seven months and 8 non-transgenic littermates were injected intraperitoneally with 11.1 ± 0.8 MBq [18F]FDG and spent a 35-min uptake period awake in single cages. Subsequently, they were anesthetized and measured in a small animal PET scanner for 30 min. Three seed-based connectivity analyses were performed per group. Seeds were selected for apparent mismatch between [18F]FDG and [18F]UCB-H. A seed was placed either in the medial orbitofrontal cortex, dorsal hippocampus or dorsal thalamus, and correlated with all other voxels of the brain across animals. In the control group, the emerging correlative pattern was strongly overlapping for all three seed locations, indicating a uniform fronto-thalamo-hippocampal resting state network. In contrast, rTg4510 mice showed three distinct networks with minimal overlap. Frontal and thalamic networks were greatly diminished. The hippocampus, however, formed a new network with the whole parietal cortex. We conclude that resting-state functional networks are fragmented in the brain of rTg4510 mice. Thus, hypometabolism can be explained by reduced functional connectivity of brain areas devoid of tau-related pathology, such as the thalamus.
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000266481 650_7 $$2Other$$aMetabolic connectivity
000266481 650_7 $$2Other$$aSmall animal PET
000266481 650_7 $$2Other$$aTauopathy mouse model
000266481 650_7 $$00Z5B2CJX4D$$2NLM Chemicals$$aFluorodeoxyglucose F18
000266481 650_2 $$2MeSH$$aAnimals
000266481 650_2 $$2MeSH$$aMice
000266481 650_2 $$2MeSH$$aFluorodeoxyglucose F18: metabolism
000266481 650_2 $$2MeSH$$aMice, Transgenic
000266481 650_2 $$2MeSH$$aPositron-Emission Tomography
000266481 650_2 $$2MeSH$$aBrain: metabolism
000266481 650_2 $$2MeSH$$aBrain Mapping
000266481 650_2 $$2MeSH$$aDisease Models, Animal
000266481 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000266481 7001_ $$0P:(DE-2719)9000008$$aAnglada-Huguet, Marta$$b1$$udzne
000266481 7001_ $$0P:(DE-2719)2541671$$aMandelkow, Eckhard$$b2$$udzne
000266481 7001_ $$aNeumaier, Bernd$$b3
000266481 7001_ $$0P:(DE-2719)2541658$$aMandelkow, Eva Maria$$b4
000266481 7001_ $$0P:(DE-2719)2811239$$aDrzezga, Alexander$$b5$$eLast author$$udzne
000266481 773__ $$0PERI:(DE-600)1466932-8$$a10.1016/j.expneurol.2023.114632$$gVol. 372, p. 114632 -$$p114632$$tExperimental neurology$$v372$$x0014-4886$$y2024
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