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O3‐04‐01: ASSOCIATIONS BETWEEN TAU, Aβ AND CORTICAL THICKNESS WITH COGNITION IN ALZHEIMER'S DISEASE
Author(s) -
Ossenkoppele Rik,
Smith Ruben,
Strandberg Olof,
Insel Philip,
Ohlsson Tomas,
Mattsson Niklas,
Palmqvist Sebastian,
Hansson Oskar
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.2788
Subject(s) - dementia , neuropsychology , neuroscience , psychology , cognition , alzheimer's disease , medicine , disease , audiology
five novel risk loci for LOAD: NICN1 (p1⁄42.2E-07), RAB43 (p1⁄42.0E-06), VKORC1 (p1⁄43.5E-09), HPR (p1⁄43.0E-07), and PARD6G (p1⁄43.6E-07). Our analysis also highlighted LIMS2 (p1⁄49.4E-12) near BIN1, IL10 (p1⁄43.7E-07) which is 700kb upstream of CR1, and two novel genes ADRA1A (p1⁄41.3E-09) and EXTL3 (p1⁄45.1E-12) at the CLU-PTK2B locus. Conclusions: Cross-tissue transcriptome-wide association analysis identified multiple novel loci for LOAD and suggested novel risk genes at known risk loci. Many of our newly identified genes have been implicated in AD pathophysiology in prior studies. Several genes, including IL10 and ADRA1A, also have therapeutic potential to improve neurodegeneration. These results provide insights into the genetic basis of LOAD and may guide functional studies in the future.