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These modulatory effects - which most likely involve binding with functional thiol residues - are interwoven with neurotoxic actions of both mercurials.

THIM is metabolized in the body to ethyl mercury (EtHg) and subsequently to inorganic mercury forms, which accumulate in tissues of vital organs, including the brain (22). Information about neurochemical and neurotoxic effects of THIM is still limited, but the existing data indicate that in pharmacodynamics and toxicity THIM/EtHg does not differ significantly from methyl mercury (MeHg), which has been studied more extensively, although these compounds differ somewhat in pharmacokinetics (8).

Several studies documented that the neurotoxic effects of mercurials involve glutamate-mediated excitotoxicty, due to their ability to inhibit uptake of glutamate in astrocytes, resulting in an increase of the extracellular level of this excitatory amino acid

These results suggest that early mitochondrial damage plays a key role in induction of glutamate neurotoxicity.

A number of the catabolites produced along this pathway show neurotoxic or neuroprotective activities, and their role in the generation of central nervous system inflammation is well documented.

myloid plaques and microgliosis in the brain of Alzheimer’s mice fed with GSE were also reduced by 49% and 70%, respectively

Curcumin also significantly reduced brain Aβ burden and microglia activation

polyphenol-rich GSE prevents the Aβ deposition and attenuates the inflammation in the brain of a transgenic mouse model, and this thus is promising in delaying development of AD.

It is now well recognized that the disease manifestation is reduced in pregnant women with relapsing-remitting MS

This occurs particularly during the third trimester when levels of estrogens (estradiol and estriol) and progesterone (see Table 2) are elevated up to about 20 times

This seems well correlated with a decrease in active white matter lesions detected by MRI

The activated microglia mount a complex local proinflammatory response

PPARγ plays a critical role in regulating the inflammatory responses of microglia and monocytes to β-amyloid

PPARγ agonists were shown to inhibit the β-amyloid-stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor α. Furthermore, PPARγ agonists inhibited the expression of cyclooxygenase-2.