@article {323284,
	title = {The APOE gene cluster responds to air pollution factors in mice with coordinated expression of genes that differs by age in humans.},
	journal = {Alzheimers Dement},
	year = {2020},
	month = {2020 Nov 20},
	abstract = {<p>Little is known of gene-environment interactions for Alzheimer{\textquoteright}s disease (AD) risk factors. Apolipoprotein E (APOE) and neighbors on chromosome 19q13.3 have variants associated with risks of AD, but with unknown mechanism. This study describes novel links among the APOE network, air pollution, and age-related diseases. Mice exposed to air pollution nano-sized particulate matter (nPM) had coordinate responses of Apoe-Apoc1-Tomm40 in the cerebral cortex. In humans, the AD vulnerable hippocampus and amygdala had stronger age decline in APOE cluster expression than the AD-resistant cerebellum and hypothalamus. Using consensus weighted gene co-expression network, we showed that APOE has a conserved co-expressed network in rodent and primate brains. SOX1, which has AD-associated single nucleotide polymorphisms, was among the co-expressed genes in the human hippocampus. Humans and mice shared 87\% of potential binding sites for transcription factors in APOE cluster promoter, suggesting similar inducibility and a novel link among environment, APOE cluster, and risk of AD.</p>
},
	issn = {1552-5279},
	doi = {10.1002/alz.12230},
	author = {Haghani, Amin and Thorwald, Max and Morgan, Todd E and Finch, Caleb E}
}
