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000164314 1001_ $$00000-0001-7046-5581$$aOuali Alami, Najwa$$b0
000164314 245__ $$aMultiplexed chemogenetics in astrocytes and motoneurons restore blood–spinal cord barrier in ALS
000164314 260__ $$aHeidelberg$$bEMBO Press$$c2020
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000164314 520__ $$aBlood-spinal cord barrier (BSCB) disruption is thought to contribute to motoneuron (MN) loss in amyotrophic lateral sclerosis (ALS). It is currently unclear whether impairment of the BSCB is the cause or consequence of MN dysfunction and whether its restoration may be directly beneficial. We revealed that SOD1 G93A , FUS ΔNLS , TDP43 G298S , and Tbk1 +/- ALS mouse models commonly shared alterations in the BSCB, unrelated to motoneuron loss. We exploit PSAM/PSEM chemogenetics in SOD1 G93A mice to demonstrate that the BSCB is rescued by increased MN firing, whereas inactivation worsens it. Moreover, we use DREADD chemogenetics, alone or in multiplexed form, to show that activation of Gi signaling in astrocytes restores BSCB integrity, independently of MN firing, with no effect on MN disease markers and dissociating them from BSCB disruption. We show that astrocytic levels of the BSCB stabilizers Wnt7a and Wnt5a are decreased in SOD1 G93A mice and strongly enhanced by Gi signaling, although further decreased by MN inactivation. Thus, we demonstrate that BSCB impairment follows MN dysfunction in ALS pathogenesis but can be reversed by Gi-induced expression of astrocytic Wnt5a/7a.
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000164314 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: blood
000164314 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: metabolism
000164314 650_2 $$2MeSH$$aAnimals
000164314 650_2 $$2MeSH$$aAstrocytes: metabolism
000164314 650_2 $$2MeSH$$aAstrocytes: physiology
000164314 650_2 $$2MeSH$$aDisease Models, Animal
000164314 650_2 $$2MeSH$$aDisease Progression
000164314 650_2 $$2MeSH$$aFemale
000164314 650_2 $$2MeSH$$aHumans
000164314 650_2 $$2MeSH$$aMale
000164314 650_2 $$2MeSH$$aMice
000164314 650_2 $$2MeSH$$aMice, Inbred C57BL
000164314 650_2 $$2MeSH$$aMice, Transgenic
000164314 650_2 $$2MeSH$$aMotor Neurons: metabolism
000164314 650_2 $$2MeSH$$aMotor Neurons: physiology
000164314 650_2 $$2MeSH$$aSpinal Cord: metabolism
000164314 650_2 $$2MeSH$$aSpine: blood supply
000164314 650_2 $$2MeSH$$aSpine: metabolism
000164314 650_2 $$2MeSH$$aSuperoxide Dismutase: metabolism
000164314 650_2 $$2MeSH$$aSuperoxide Dismutase-1: genetics
000164314 650_2 $$2MeSH$$aSuperoxide Dismutase-1: metabolism
000164314 650_2 $$2MeSH$$aWnt Proteins: metabolism
000164314 650_2 $$2MeSH$$aWnt-5a Protein: metabolism
000164314 7001_ $$aTang, Linyun$$b1
000164314 7001_ $$0P:(DE-2719)2812844$$aWiesner, Diana$$b2$$udzne
000164314 7001_ $$aCommisso, Barbara$$b3
000164314 7001_ $$aBayer, David$$b4
000164314 7001_ $$0P:(DE-2719)9000455$$aWeishaupt, Jochen H$$b5$$udzne
000164314 7001_ $$aDupuis, Luc$$b6
000164314 7001_ $$aWong, Phillip$$b7
000164314 7001_ $$aBaumann, Bernd$$b8
000164314 7001_ $$aWirth, Thomas$$b9
000164314 7001_ $$0P:(DE-2719)2812855$$aBöckers, Tobias$$b10$$udzne
000164314 7001_ $$00000-0003-1483-0286$$aYilmazer-Hanke, Deniz$$b11
000164314 7001_ $$0P:(DE-2719)2812633$$aLudolph, Albert$$b12$$udzne
000164314 7001_ $$0P:(DE-2719)2812851$$aRoselli, Francesco$$b13$$eLast author$$udzne
000164314 773__ $$0PERI:(DE-600)2948687-7$$a10.26508/lsa.201900571$$gVol. 3, no. 11, p. e201900571 -$$n11$$pe201900571$$tLife science alliance$$v3$$x2575-1077$$y2020
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