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000154788 1001_ $$00000-0002-9682-9811$$aPérez-Sisqués, Leticia$$b0
000154788 245__ $$aRTP801/REDD1 contributes to neuroinflammation severity and memory impairments in Alzheimer’s disease
000154788 260__ $$aLondon [u.a.]$$bNature Publishing Group$$c2021
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000154788 520__ $$aRTP801/REDD1 is a stress-regulated protein whose upregulation is necessary and sufficient to trigger neuronal death. Its downregulation in Parkinson's and Huntington's disease models ameliorates the pathological phenotypes. In the context of Alzheimer's disease (AD), the coding gene for RTP801, DDIT4, is responsive to Aβ and modulates its cytotoxicity in vitro. Also, RTP801 mRNA levels are increased in AD patients' lymphocytes. However, the involvement of RTP801 in the pathophysiology of AD has not been yet tested. Here, we demonstrate that RTP801 levels are increased in postmortem hippocampal samples from AD patients. Interestingly, RTP801 protein levels correlated with both Braak and Thal stages of the disease and with GFAP expression. RTP801 levels are also upregulated in hippocampal synaptosomal fractions obtained from murine 5xFAD and rTg4510 mice models of the disease. A local RTP801 knockdown in the 5xFAD hippocampal neurons with shRNA-containing AAV particles ameliorates cognitive deficits in 7-month-old animals. Upon RTP801 silencing in the 5xFAD mice, no major changes were detected in hippocampal synaptic markers or spine density. Importantly, we found an unanticipated recovery of several gliosis hallmarks and inflammasome key proteins upon neuronal RTP801 downregulation in the 5xFAD mice. Altogether our results suggest that RTP801 could be a potential future target for theranostic studies since it could be a biomarker of neuroinflammation and neurotoxicity severity of the disease and, at the same time, a promising therapeutic target in the treatment of AD. 
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000154788 650_2 $$2MeSH$$aAlzheimer Disease: complications
000154788 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000154788 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000154788 650_2 $$2MeSH$$aAnimals
000154788 650_2 $$2MeSH$$aCase-Control Studies
000154788 650_2 $$2MeSH$$aDisease Models, Animal
000154788 650_2 $$2MeSH$$aEncephalitis: etiology
000154788 650_2 $$2MeSH$$aEncephalitis: genetics
000154788 650_2 $$2MeSH$$aEncephalitis: pathology
000154788 650_2 $$2MeSH$$aFemale
000154788 650_2 $$2MeSH$$aHumans
000154788 650_2 $$2MeSH$$aMale
000154788 650_2 $$2MeSH$$aMemory Disorders: etiology
000154788 650_2 $$2MeSH$$aMemory Disorders: genetics
000154788 650_2 $$2MeSH$$aMemory Disorders: pathology
000154788 650_2 $$2MeSH$$aMice
000154788 650_2 $$2MeSH$$aMice, Transgenic
000154788 650_2 $$2MeSH$$aNeuroimmunomodulation: genetics
000154788 650_2 $$2MeSH$$aNeurotoxicity Syndromes: etiology
000154788 650_2 $$2MeSH$$aNeurotoxicity Syndromes: genetics
000154788 650_2 $$2MeSH$$aNeurotoxicity Syndromes: pathology
000154788 650_2 $$2MeSH$$aSeverity of Illness Index
000154788 650_2 $$2MeSH$$aTranscription Factors: physiology
000154788 7001_ $$aSancho-Balsells, Anna$$b1
000154788 7001_ $$aSolana-Balaguer, Júlia$$b2
000154788 7001_ $$aCampoy-Campos, Genís$$b3
000154788 7001_ $$aVives-Isern, Marcel$$b4
000154788 7001_ $$aSoler-Palazón, Ferran$$b5
000154788 7001_ $$0P:(DE-2719)9000008$$aAnglada-Huguet, Marta$$b6$$udzne
000154788 7001_ $$aLópez-Toledano, Miguel-Ángel$$b7
000154788 7001_ $$0P:(DE-2719)2541658$$aMandelkow, Eva-Maria$$b8$$udzne
000154788 7001_ $$00000-0002-8684-2721$$aAlberch, Jordi$$b9
000154788 7001_ $$00000-0001-5334-0963$$aGiralt, Albert$$b10
000154788 7001_ $$00000-0001-7185-436X$$aMalagelada, Cristina$$b11
000154788 773__ $$0PERI:(DE-600)2541626-1$$a10.1038/s41419-021-03899-y$$gVol. 12, no. 6, p. 616$$n6$$p616$$tCell death & disease$$v12$$x2041-4889$$y2021
000154788 8564_ $$uhttps://www.nature.com/articles/s41419-021-03899-y
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