HNK-1 Carrier Glycoproteins Are Decreased in the Alzheimer's Disease Brain.

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García-Ayllón, María-Salud (author)

HNK-1 Carrier Glycoproteins Are Decreased in the Alzheimer's Disease Brain.

Article/chapterEnglish2017

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2016-01-06
Springer Science and Business Media LLC,2017

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LIBRIS-ID:oai:gup.ub.gu.se/235475
https://gup.ub.gu.se/publication/235475URI
https://doi.org/10.1007/s12035-015-9644-xDOI
http://kipublications.ki.se/Default.aspx?queryparsed=id:135038643URI

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Language:English

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Subject category:art swepub-publicationtype

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The human natural killer-1 (HNK-1), 3-sulfonated glucuronic acid, is a glycoepitope marker of cell adhesion that participates in cell-cell and cell-extracellular matrix interactions and in neurite growth. Very little is known about the regulation of the HNK-1 glycan in neurodegenerative disease, particularly in Alzheimer's disease (AD). In this study, we investigate changes in the levels of HNK-1 carrier glycoproteins in AD. We demonstrate an overall decrease in HNK-1 immunoreactivity in glycoproteins extracted from the frontal cortex of AD subjects, compared with levels from non-demented controls (NDC). Immunoblotting of ventricular post-mortem and lumbar ante-mortem cerebrospinal fluid with HNK-1 antibodies indicate similar levels of carrier glycoproteins in AD and NDC samples. Decrease in HNK-1 carrier glycoproteins were not paralleled by changes in messenger RNA (mRNA) levels of the enzymes involved in the synthesis of the glycoepitope, β-1,4-galactosyltransferase (β4GalT), glucuronyltransferases GlcAT-P and GlcAT-S, or sulfotransferase HNK-1ST. Over-expression of amyloid precursor protein in Tg2576 transgenic mice and in vitro treatment of SH-SY5Y neuroblastoma cells with the amyloidogenic Aβ42 peptide resulted in a decrease in HNK-1 immunoreactivity levels in brain and cellular extracts, whereas the levels of soluble HNK-1 glycoproteins detected in culture media were not affected by Aβ treatment. HNK-1 levels remain unaffected in the brain extracts of Tg-VLW mice, a model of mutant hyperphosphorylated tau, and in SH-SY5Y cells over-expressing hyperphosphorylated wild-type tau. These results provide evidence that cellular levels of HNK-1 carrier glycoforms are decreased in the brain of AD subjects, probably influenced by the β-amyloid protein.

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Botella-López, Arancha (author)
Cuchillo-Ibañez, Inmaculada (author)
Rábano, Alberto (author)
Andreasen, Niels (author)
Blennow, Kaj,1958Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry(Swepub:gu)xbleka (author)
Ávila, Jesús (author)
Sáez-Valero, Javier (author)
Göteborgs universitetInstitutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi (creator_code:org_t)

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In:Molecular neurobiology: Springer Science and Business Media LLC54:1, s. 188-1991559-11820893-7648

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MEDICAL AND HEALTH SCIENCES: MEDICAL AND HEAL ...; and Basic Medicine; and Neurosciences

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By the university: University of Gothenburg; Karolinska Institutet

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