Lithium exerts neuroprotective effects in ischemic stroke through multiple mechanisms

Lithium exerts neuroprotective effects in ischemic stroke through multiple mechanisms. GSK-3: glycogen synthase kinase 3; mTOR: mammalian target of rapamycin; MAPK: mitogen-activated protein kinase; ERK: extracellular signal- regulated kinase; MMP: matrix metalloproteinase; NMDAR: N-methyl-d-aspartate receptor; FoxO3a: forkhead box O3; NLRP3: nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3; cAMP: cyclic adenosine monophosphate; PKA: protein kinase A; PI3K: phosphatidylinositol 3-kinase; AKT: protein kinase B; CREB: cAMP-response element binding protein; BDNF: brain-derived neurotrophic factor; Trk: tropomyosin-related kinase; PSD-95: postsynaptic density protein 95; GAP-43: growth associated protein-43; BBB: blood-brain barrier. Lines with solid arrows represent stimulatory connections; lines with flattened ends represent inhibitory connections. Dashed lines represent pathways with reduced activity as a result of lithium treatment

Publication

Exploring the Neuroprotective Effects of Lithium in Ischemic Stroke: A literature review (2024) Weihua Wang, et al. Int J Med Sci. 2024;21(2). Figure: F1. Homo sapiens

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