Mini review: Mitochondrial dysfunction in Alzheimer's disease: Therapeutic implications of lithium

Lithium and Stroke Recovery: A Systematic Review and Meta-Analysis of Stroke Models in Rodents and Human Data

“…These mechanisms include the inhibition of glycogen synthase kinase-3β, an important hub of signaling control in multiple cell types, with a central role in the regulation of apoptotic and neuro-regenerative processes. 21,22,56 Animal models of stroke have produced data consistent with a neuroprotective effect of lithium, as inferred by the reduced volume of infarcts, 10,53 attenuation of postischemic excitotoxicity, 25,51 and the enabling of poststroke recovery. 10 Other studies have shown that lithium treatment is associated with antiapoptotic eff ects, 15,34,43,49,51,52 decreased expression of inflammatory markers, 31,42,43,45,50 reduced oxidative stress, 35,43,45 and activation of immunomediated responses involved in the restoration of blood-brain barrier integrity.…”

“…6 These results suggest that treatment with lithium may contribute to preserving the integrity of neurons, a conclusion that is reinforced by the compelling evidence from basic science about the neuroprotective properties of lithium. 21 However, treatment with lithium cannot be seen as a panacea for neurodegenerative disorders. For example, a randomized, double-blind, placebo-controlled trial of lithium carbonate (target serum concentration of 0.4-0.8 mmol/L) for the treatment of 214 adults with amyotrophic lateral sclerosis found no evidence of increased survival among those treated with lithium for 18 months, although the medication was well tolerated by participants.…”

“…7,8,[16][17][18][19][20] Lithium exerts its effect through modification of multiple intracellular signaling systems, with emphasis on the inhibition of glycogen synthase kinase-3β and subsequent downstream effects reducing inflammation, promoting maintenance of glial and neuronal structures, and downregulating apoptosis. 21,22 In this systematic review, we first sought to examine animal models of ischemic and hemorrhagic stroke to determine if treatment with lithium decreased stroke volume and the apoptosis of neural cells and increased poststroke neurogenesis and function. Second, we reviewed observational data in humans and reported the association between exposure to lithium and the risk of stroke, and evaluated the results of clinical trials investigating the effects of treatment with lithium among adults after stroke.…”

“…7,8,16-20 Lithium exerts its effect through modification of multiple intracellular signaling systems, with emphasis on the inhibition of glycogen synthase kinase-3β and subsequent downstream effects reducing inflammation, promoting maintenance of glial and neuronal structures, and downregulating apoptosis. 21,22…”

Neuroprotection of Gastrodia elata polyphenols against H2O2-induced PC12 cell cytotoxicity by reducing oxidative stress

“…The occurrence of mitochondrial dysfunction will lead to oxidative stress, reduced cytochrome c oxidase activity and decreased energy metabolism. MMP is an electrochemical potential formed between the two sides of the inner mitochondrial membrane during the process of respiratory oxidation, and a decrease in MMP is closely related to apoptosis ( Anandatheerthavarada and Devi, 2007 ; Singulani et al, 2021 ). In this study, we used JC-1 staining to investigate the effect of H 2 O 2 damage on the membrane potential of PC12 cells, and the results showed that H 2 O 2 -induced oxidative stress significantly decreased MMP, while GPP pretreatment enhanced cellular MMP to resist oxidative stress damage.…”