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In fact, most of the patients with TDP-43 pathology do not have mutations in their TARDP gene, and yet have protein accumulations containing phosphorylated TDP-43 13 , and mostly ubiquitinated protein aggregates 10,14,15

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Together, these mechanisms mitigate M1 microglial polarization, promote M2 transition, and prevent degeneration of tyrosine hydroxylase (TH)-positive neurons in the nigrostriatal pathway ( Emerging evidence suggests that BL may exert neuroprotective effects in PD by modulating NF-B signaling and inflammasome activity (Li et al., 2020)

Nanomaterials (2022) 12(14):2365

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