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O5‐10‐03: MAPPING GENOME REPAIR HOTSPOTS IN POST‐MITOTIC HUMAN NEURONS
Author(s) -
Reid Dylan A.,
Linker Sara B.,
Schlachetzki Johannes C.M.,
Glass Christopher K.,
Gage Fred H.
Publication year - 2019
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.2019.06.4890
Subject(s) - genome instability , genome , biology , dna repair , human genome , chromatin , gene , genetics , genomics , embryonic stem cell , computational biology , dna damage , dna
microglial module genes in affected brain regions from postmortem brain tissue from human AD tissue donors. In pathologically confirmed AD cases, we found preliminary evidence that microglial genes may be dysregulated in a sex-specific manner. Finally, we identified specific and significant overlap between the described microglial gene set—identified by unbiased co-expression analysis—and genes known to impart risk for AD. Conclusions: Our findings suggest that microglial genes show enriched expression in AD-vulnerable brain regions, are upregulated during aging and neurodegeneration in mice, and are selectively upregulated in pathologically affected brain regions in AD. Taken together, our data-driven findings reemphasize the importance of microglial gene expression alterations in AD and, more importantly, suggest that regional and sex-specific variation in microglial gene expression may be implicated in risk for and progression of neurodegenerative disease.