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The neuroprotective effects of s-allyl cysteine, s-ethyl cysteine, and s-propyl cysteine in d-galactose (DG)-treated mice were examined. DG treatment increased the formation of Aβ1–40and Aβ1–42, enhanced mRNA expression of β-amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1), and reduced neprilysin expression in brain (P< 0.05); however, the intake of three test compounds significantly decreased the production of Aβ1–40and Aβ1–42and suppressed the expression of APP and BACE1 (P< 0.05). DG treatments declined brain protein kinase C (PKC) activity and mRNA expression (P< 0.05). Intake of test compounds significantly retained PKC activity, and the expression of PKC-α and PKC-γ (P< 0.05). DG treatments elevated brain activity and mRNA expression of aldose reductase (AR) and sorbitol dehydrogenase as well as increased brain levels of carboxymethyllysine (CML), pentosidine, sorbitol, and fructose (P< 0.05). Test compounds significantly lowered AR activity, AR expression, and CML and pentosidine levels (P< 0.05). DG treatments also significantly increased the formation of reactive oxygen species (ROS) and protein carbonyl and decreased the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (P< 0.05); however, the intake of test compounds in DG-treated mice significantly decreased ROS and protein carbonyl levels and restored brain GPX, SOD, and catalase activities (P< 0.05). These findings support that these compounds via their anti-Aβ, antiglycative, and antioxidative effects were potent agents against the progression of neurodegenerative disorders such as Alzheimer's disease.

Mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were used to examine the neuroprotective effects of carnosine. Carnosine at 0.5, 1, and 2 g/L was directly added to the drinking water for 4 weeks. MPTP treatment significantly depleted striatal glutathione content, reduced the activity of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase, increased malondialdehyde and reactive oxygen species levels, and elevated interleukin-6, nitrite, and tumor necrosis factor-α production as well as enhanced inducible nitric oxide synthase (iNOS) activity in the striatum (P< 0.05). The preintake of carnosine significantly attenuated MPTP-induced glutathione loss, retained the activity of GPX and SOD, diminished oxidative stress, and lowered inflammatory cytokines and nitrite levels as well as suppressed iNOS activity (P< 0.05). MPTP treatment significantly suppressed GPX mRNA expression and enhanced iNOS mRNA expression (P< 0.05). Carnosine preintake significantly elevated GPX mRNA expression and declined iNOS mRNA expression (P< 0.05). Preintake of carnosine also significantly improved MPTP-induced dopamine depletion and maintained 3,4-dihydroxyphenylacetic acid and homovanillic acid levels (P< 0.05). These results suggest that carnosine could provide antioxidative and anti-inflammatory protection for the striatum against the development of Parkinson’s disease.