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NOVEL ETIOLOGIES OF RAISED GGT VALUES The classic view stemming from the mid-1960s considered GGT as a marker of different types of liver disease such as hepatitis C, cholestatic syndromes, alcohol-related liver disease, porphyria cutanea tarda (which is not rarely associated with alcohol abuse), drug-induced liver injury, and nonalcoholic steatohepatitis (NASH) [19,20] which typically belongs to the alcohol-like liver disease in nonalcoholics disease spectrum [21]

Bernal W, Lee WM, Wendon J, Larsen FS, Williams R

The disconnect between preclinical efficacy and human clinical outcomes remains unexplained and represents a significant limitation for potential therapeutic applications

785 Moreover, enhanced SIRT6 activity abrogates the neurotoxic phenotype of astrocytes expressing ALS-linked mutant SOD1, thus indicating that SIRT6 could serve as a potential therapeutic target to prevent astrocyte-mediated motor neuron death in ALS

Inhibit osteoclast activation and differentiation, reduce bone resorption Block osteoclast differentiation signal RANKL/RANK/OPG pathway: AOD 9604 downregulates the expression of RANKL (a key factor in osteoclast differentiation) and upregulates the expression of OPG (a RANKL antagonist), reducing the RANKL/OPG ratio by 50-60% and blocking the differentiation of osteoclast precursors into mature osteoclasts