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Göteborgs universitets publikationer

Gene Expression of Quaking in Sporadic Alzheimer's Disease Patients is Both Upregulated and Related to Expression Levels of Genes Involved in Amyloid Plaque and Neurofibrillary Tangle Formation

Författare och institution:
B. Farnsworth (-); C. Peuckert (-); B. Zimmermann (-); E. Jazin (-); Petronella Kettunen (Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi); L. S. Emilsson (-)
Publicerad i:
Journal of Alzheimers Disease, 53 ( 1 ) s. 209-219
ISSN:
1387-2877
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2016
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
Quaking (QKI) is a gene exclusively expressed within glial cells. QKI has previously been implicated in various neurological disorders and diseases, including Alzheimer's disease (AD), a condition for which increasing evidence suggests a central role of glia cells. The objective of the present study was to investigate the expression levels of QKI and three QKI isoforms (QKI5, QKI6, and QKI7) in AD. Genes that have previously been related to the ontogeny and progression of AD, specifically APP, PSEN1, PSEN2, and MAPT, were also investigated. A real-time PCR assay of 123 samples from human postmortem sporadic AD patients and control brains was performed. The expression values were analyzed with an analysis of covariance model and subsequent multiple regressions to explore the possibility of related expression values between QKI, QKI isoforms, and AD-related genes. Further, the sequences of AD-related genes were analyzed for the presence of QKI binding domains. QKI and all measured QKI isoforms were found to be significantly upregulated in AD samples, relative to control samples. However, APP, PSEN1, PSEN2, and MAPT were not found to be significantly different. QKI and QKI isoforms were found to be predictive for the variance of APP, PSEN1, PSEN2, and MAPT, and putative QKI binding sites suggests an interaction with QKI. Overall, these results implicate a possible role of QKI in AD, although the exact mechanism by which this occurs remains to be uncovered.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Medicinska grundvetenskaper ->
Neurovetenskaper
Nyckelord:
Amyloid-beta, APP, gene expression, glia, MAPT, neurodegenerative diseases, real-time polymerase, rna-binding protein, myelin basic-protein, presenilin-1 messenger-rna, astrocytic gliosis, oxidative stress, candidate gene, senile plaques, mutant mice, cell-death, human qki, Neurosciences & Neurology
Postens nummer:
240243
Posten skapad:
2016-08-15 13:06
Posten ändrad:
2016-08-15 13:07

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