Galectins in the brain: advances in neuroinflammation, neuroprotection and therapeutic opportunities

Purpose of review Galectin interactions with glycoproteins and glycolipids modulate a variety of cellular responses that are now increasingly explored to better understand neuroinflammation processes and eventually find new therapeutic opportunities for neurological diseases. Recent findings Gal-1 confirmed its indirect neuroprotective roles through anti-inflammatory properties whereas Gal-3 remains elusive, showing anti-inflammatory or pro-inflammatory roles depending on damaging conditions and genetic background of mice models. Interestingly, microglial intracellular rather than extracellular overexpression of Gal-3 arose as contributing to the pathogenesis of Huntington disease, involving NLRP3 inflammasome activation and inhibition of autophagic removal of damaged endolysosomes. Decreasing Gal-3 expression had favorable effects upon disease symptoms. Gal-3 expanded its role in this endolysosomal surveillance system originally involving Gal-8 and Gal-9, which protect cells against neuropathogenic proteins and becomes impaired or even detrimental under neurodegenerative conditions. Also, Gal-1, Gal-3 and Gal-4, together with changes in glycan structures define the outcome of neuroinflammation and remyelination processes. Gal-8 emerged as a new neuroprotector factor, which added to its immunosuppressive role and presence in human cerebrospinal fluid (CSF) may generate a neuroprotective environment in the brain. Summary Galectins modulate neuroinflammation and neurode...
Source: Current Opinion in Neurology - Category: Neurology Tags: CNS INFLAMMATORY DISORDERS OUTSIDE MULTIPLE SCLEROSIS: Edited by Bruce T. Volpe Source Type: research