TY - JOUR
T1 - Galectins in the brain
T2 - advances in neuroinflammation, neuroprotection and therapeutic opportunities
AU - Barake, Francisca
AU - Soza, Andrea
AU - González, Alfonso
N1 - Publisher Copyright:
© 2020 Lippincott Williams and Wilkins. All rights reserved.
PY - 2020/6/1
Y1 - 2020/6/1
N2 - Purpose of reviewGalectin 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 findingsGal-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.SummaryGalectins modulate neuroinflammation and neurodegenerative processes contributing to microglia polarization, immunosurveillance and neuroprotection through extracellular and intracellular interactions with particular and dynamic patterns of glycans, suggesting potential therapeutic targets.
AB - Purpose of reviewGalectin 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 findingsGal-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.SummaryGalectins modulate neuroinflammation and neurodegenerative processes contributing to microglia polarization, immunosurveillance and neuroprotection through extracellular and intracellular interactions with particular and dynamic patterns of glycans, suggesting potential therapeutic targets.
KW - galectin
KW - glycosylation
KW - neurodegeneration
KW - neuroinflammation
KW - neuroprotection
UR - http://www.scopus.com/inward/record.url?scp=85084273221&partnerID=8YFLogxK
U2 - 10.1097/WCO.0000000000000812
DO - 10.1097/WCO.0000000000000812
M3 - Review article
C2 - 32304438
AN - SCOPUS:85084273221
SN - 1350-7540
VL - 33
SP - 381
EP - 390
JO - Current Opinion in Neurology
JF - Current Opinion in Neurology
IS - 3
ER -