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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: High-salt diet does not boost neuroinflammation and neurodegeneration in a model of α-synucleinopathy

Fig. 5

Pathophysiological features of MSA and EAE models and potential pathogenic effect of a high-salt diet. a Schematic overview of the central nervous system in healthy conditions. b In MSA, α-syn accumulates in the cytoplasm of oligodendrocytes inducing oligodendroglial dysfunction. Soluble α-syn oligomeric species spread through the brain parenchyma and trigger microglial activation and neuroinflammation. All these events lead to demyelination and neurodegeneration. High-salt diet exposure has no effect on the CNS of PLP-hαSyn mice possibly due to the absence of peripheral immune cell involvement in MSA brain pathology. c EAE mice model mimics many features of MS, such as blood-brain barrier (BBB) disruption, demyelinating lesions associated with infiltrating T cells, macrophages, and B cells, microglial activation, neuroinflammation, and neurodegeneration. In EAE mice, high-salt diet increases activation and infiltration of T cells and peripheral macrophages in the CNS accelerating disease onset, augmenting its severity and enhancing blood-brain barrier disruption and brain pathology

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