English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The Plexin-A 4 ( PLXNA4 ) gene, has recently been identified in genome wide association studies (GWAS), as a novel genetic player associated with Alzheimer's disease (AD). Additionally,  PLXNA4  genetic variations were also found to increase AD risk by tau pathology  in vitro . However, the potential roles of  PLXNA4  variants in the amyloid-β (Aβ) pathology, were not evaluated. Five targeted loci capturing the top common variations in  PLXNA4 , were extracted using tagger methods. Multiple linear regression models were used to explore whether these variations can affect the cerebrospinal fluid (CSF) (Aβ 1−42 , T-tau, and P-tau) phenotypes in the Alzheimer's disease Neuroimaging Initiative (ADNI) dataset. We detected that two loci (rs6467431, rs67468325) were significantly associated with CSF Aβ 1−42  levels in the hybrid population (rs6467431:  P  = 0.01376, rs67468325:  P  = 0.006536) and the significance remained after false discovery rate (FDR) correction (rs6467431:  P c = 0.03441, rs67468325:  P c = 0.03268). In the subgroup analysis, we further confirmed the association of rs6467431 in the cognitively normal (CN) subgroup ( P  = 0.01904,  P c = 0.04761). Furthermore, rs6467431-A carriers and rs67468325-G carriers showed higher CSF Aβ 1−42  levels than non-carriers. Nevertheless, we did not detect any significant relationships between the levels of T-tau, P-tau and these  PLXNA4  loci. Our findings provided preliminary evidence that  PLXNA4  variants can confer AD risk through modulating the Aβ deposition.

Common Variants in PLXNA4 and Correlation to CSF-related Phenotypes in Alzheimer's Disease