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dc.contributor.authorRawal, Punam
dc.contributor.authorZhao, Liqin
dc.date.accessioned2022-01-03T19:09:05Z
dc.date.available2022-01-03T19:09:05Z
dc.date.issued2021-03-30
dc.identifier.citationRawal P and Zhao L (2021) Sialometabolism in Brain Health and Alzheimer’s Disease. Front. Neurosci. 15:648617. doi: 10.3389/fnins.2021.648617en_US
dc.identifier.urihttp://hdl.handle.net/1808/32315
dc.description.abstractSialic acids refer to a unique family of acidic sugars with a 9-carbon backbone that are mostly found as terminal residues in glycan structures of glycoconjugates including both glycoproteins and glycolipids. The highest levels of sialic acids are expressed in the brain where they regulate neuronal sprouting and plasticity, axon myelination and myelin stability, as well as remodeling of mature neuronal connections. Moreover, sialic acids are the sole ligands for microglial Siglecs (sialic acid-binding immunoglobulin-type lectins), and sialic acid-Siglec interactions have been indicated to play a critical role in the regulation of microglial homeostasis in a healthy brain. The recent discovery of CD33, a microglial Siglec, as a novel genetic risk factor for late-onset Alzheimer’s disease (AD), highlights the potential role of sialic acids in the development of microglial dysfunction and neuroinflammation in AD. Apart from microglia, sialic acids have been found to be involved in several other major changes associated with AD. Elevated levels of serum sialic acids have been reported in AD patients. Alterations in ganglioside (major sialic acid carrier) metabolism have been demonstrated as an aggravating factor in the formation of amyloid pathology in AD. Polysialic acids are linear homopolymers of sialic acids and have been implicated to be an important regulator of neurogenesis that contributes to neuronal repair and recovery from neurodegeneration such as in AD. In summary, this article reviews current understanding of neural functions of sialic acids and alterations of sialometabolism in aging and AD brains. Furthermore, we discuss the possibility of looking at sialic acids as a promising novel therapeutic target for AD intervention.en_US
dc.publisherNature Researchen_US
dc.rights© 2021 Rawal and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.subjectSialic aciden_US
dc.subjectSialylationen_US
dc.subjectGangliosideen_US
dc.subjectNeural cell adhesion moleculeen_US
dc.subjectPSA-NCAMen_US
dc.subjectSiglecen_US
dc.subjectCD33en_US
dc.subjectLate-onset Alzheimer’s diseaseen_US
dc.titleSialometabolism in Brain Health and Alzheimer’s Diseaseen_US
dc.typeArticleen_US
kusw.kuauthorRawal, Punam
kusw.kuauthorZhao, Liqin
kusw.kudepartmentPharmacology and Toxicologyen_US
kusw.kudepartmentPharmacyen_US
kusw.kudepartmentNeuroscience Graduate Programen_US
dc.identifier.doi10.3389/fnins.2021.648617en_US
kusw.oaversionScholarly/refereed, publisher versionen_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US
dc.identifier.pmidPMC8044809en_US
dc.rights.accessrightsopenAccessen_US


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© 2021 Rawal and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
Except where otherwise noted, this item's license is described as: © 2021 Rawal and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).