Joana D. Amaral

TL;DR: It is suggested that the finely tuned, complex control of p53 by Mdm-2 (mouse double minute-2, an oncoprotein) is a key step in UDCA modulation of p52-triggered apoptosis, with particular emphasis on potential benefits of UDCA.

TL;DR: The role of bile acids in modulating the apoptosis process is reviewed, emphasizing the anti-apoptotic effects of UDCA and TUDCA, as well as their potential use as novel and alternate therapeutic agents for the treatment of apoptosis-related diseases.

TL;DR: It is reported that feeding APP/PS1 double-transgenic mice with diet containing 0.4 % TUDCA for 6 months reduced accumulation of Aβ deposits in the brain, markedly ameliorating memory deficits, suggesting that chronic feeding of TUD CA interferes with Aβ production, possibly through the regulation of lipid-metabolic mediators associated with APP processing.

TL;DR: In this paper, the main physiological characteristics responsible for the higher susceptibility of the nigrostriatal circuit to mitochondrial dysfunction and oxidative stress, as hinted by the acting mechanisms of the PD-causing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), were discussed.

TL;DR: Increased RIP3 expression and mixed lineage kinase domain-like protein (MLKL) phosphorylation in liver samples of human PBC patients, coincident with thioflavin T labeling, suggests activation of necroptosis, which may represent a therapeutic strategy for acute cholestasis.