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In vitro models of AD, PD and MS have demonstrated that SFN is efficient in counteracting cell death, neuroinflammation, oxidative stress and protein-aggregation induced by various toxins such as A plaques, LPS, 6-OHDA or hydrogen peroxide, through upregulation of the NRF2/ARE-axis (Table 2)

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Both models are susceptible to ferroptosis due to inhibition of cystine uptake, elevated iron levels, and high concentrations of polyunsaturated fatty acids (PUFAs)

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Targeting mitochondrial dysfunction and oxidative stress in activated microglia using dendrimer-based therapeutics

This was only rescued by carnitine, not by KG