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000165105 1001_ $$0P:(DE-2719)2810486$$aKaczmarczyk, Lech$$b0$$eFirst author
000165105 245__ $$aDistinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.
000165105 260__ $$aLawrence, Kan.$$bPLoS$$c2022
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000165105 520__ $$aSelective vulnerability is an enigmatic feature of neurodegenerative diseases (NDs), whereby a widely expressed protein causes lesions in specific cell types and brain regions. Using the RiboTag method in mice, translational responses of five neural subtypes to acquired prion disease (PrD) were measured. Pre-onset and disease onset timepoints were chosen based on longitudinal electroencephalography (EEG) that revealed a gradual increase in theta power between 10- and 18-weeks after prion injection, resembling a clinical feature of human PrD. At disease onset, marked by significantly increased theta power and histopathological lesions, mice had pronounced translatome changes in all five cell types despite appearing normal. Remarkably, at a pre-onset stage, prior to EEG and neuropathological changes, we found that 1) translatomes of astrocytes indicated reduced synthesis of ribosomal and mitochondrial components, 2) glutamatergic neurons showed increased expression of cytoskeletal genes, and 3) GABAergic neurons revealed reduced expression of circadian rhythm genes. These data demonstrate that early translatome responses to neurodegeneration emerge prior to conventional markers of disease and are cell type-specific. Therapeutic strategies may need to target multiple pathways in specific populations of cells, early in disease.
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000165105 650_7 $$2NLM Chemicals$$aPrions
000165105 650_2 $$2MeSH$$aAnimals
000165105 650_2 $$2MeSH$$aBrain: pathology
000165105 650_2 $$2MeSH$$aElectroencephalography
000165105 650_2 $$2MeSH$$aHumans
000165105 650_2 $$2MeSH$$aMice
000165105 650_2 $$2MeSH$$aNeurons: metabolism
000165105 650_2 $$2MeSH$$aPrion Diseases: pathology
000165105 650_2 $$2MeSH$$aPrions: metabolism
000165105 7001_ $$0P:(DE-2719)2810344$$aSchleif, Melvin$$b1
000165105 7001_ $$0P:(DE-2719)2811120$$aDittrich, Lars$$b2
000165105 7001_ $$aWilliams, Rhiannan H$$b3
000165105 7001_ $$aKoderman, Maruša$$b4
000165105 7001_ $$0P:(DE-2719)2812055$$aBansal, Vikas$$b5
000165105 7001_ $$0P:(DE-2719)2811012$$aRajput, Ashish$$b6
000165105 7001_ $$0P:(DE-2719)2810775$$aSchulte, Theresa$$b7
000165105 7001_ $$aJonson, Maria$$b8
000165105 7001_ $$0P:(DE-2719)2810527$$aKrost, Clemens$$b9
000165105 7001_ $$0P:(DE-2719)9002378$$aTestaquadra, Fabio J$$b10$$udzne
000165105 7001_ $$0P:(DE-2719)2810547$$aBonn, Stefan$$b11
000165105 7001_ $$0P:(DE-2719)2810253$$aJackson, Walker Scot$$b12$$eLast author
000165105 773__ $$0PERI:(DE-600)2205412-1$$a10.1371/journal.ppat.1010747$$gVol. 18, no. 8, p. e1010747 -$$n8$$pe1010747$$tPLoS pathogens$$v18$$x1553-7366$$y2022
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