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Unlike familial AD, the factors that drive the onset of sporadic AD are poorly understood, although aging and stress play a role. The early onset\/severity of neuropathology observed in most genetic mouse models of AD hampers the study of the role of aging and environmental factors; thus alternate strategies are necessary to understand the contributions of these factors to sporadic AD. We demonstrate that mice acquiring a low social status (subordinate) in a lifelong chronic psychosocial stress (CPS) model, accrue widespread proteomic changes in the frontal\/temporal cortex during aging. To better understand the significance of these stress\u2010induced changes, we compared the differentially expressed proteins (DEPs) of subordinate mice to those of patients at varying stages of dementia. Sixteen and fifteen DEPs upregulated in subordinate mice were also upregulated in patients with mild cognitive impairment (MCI) and AD, respectively. Six of those upregulated proteins (CPE, ERC2, GRIN2B, SLC6A1, SYN1, WFS1) were shared by subordinate mice and patients with MCI or AD. Finally, comparison with a spatially detailed transcriptomic database revealed that the superior frontal gyrus and hippocampus had the greatest overlap between mice subjected to lifelong CPS and AD patients. Overall, most of the overlapping proteins were functionally associated with enhanced NMDA receptor mediated glutamatergic signaling, an excitotoxicity mechanism known to affect neurodegeneration. These findings support the association between stress and AD progression and provide valuable insight into potential early biomarkers and protein mediators of this relationship.<\/jats:p>","DOI":"10.1111\/ejn.15329","type":"journal-article","created":{"date-parts":[[2021,5,28]],"date-time":"2021-05-28T10:21:01Z","timestamp":1622197261000},"page":"2971-2985","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Lifelong chronic psychosocial stress induces a proteomic signature of Alzheimer's disease in wildtype mice"],"prefix":"10.1111","volume":"55","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9858-5021","authenticated-orcid":false,"given":"Carey E.","family":"Lyons","sequence":"first","affiliation":[{"name":"Department of Integrative Physiology and Biology University of Minnesota  Minneapolis MN USA"},{"name":"Graduate Program in Neuroscience University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xianxiao","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic Sciences Icahn School of Medicine at Mount Sinai  New York NY USA"},{"name":"Mount Sinai Center for Transformative Disease Modeling Icahn School of Medicine at Mount Sinai  New York NY USA"},{"name":"Icahn Institute for Data Science and Genomic Technology Icahn School of Medicine at Mount Sinai  New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Razzoli","sequence":"additional","affiliation":[{"name":"Department of Integrative Physiology and Biology University of Minnesota  Minneapolis MN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei","family":"Chen","sequence":"additional","affiliation":[{"name":"Geriatric Research Education Clinical Center Bedford VA Healthcare System  Bedford MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiming","family":"Xia","sequence":"additional","affiliation":[{"name":"Geriatric Research Education Clinical Center Bedford VA Healthcare System  Bedford MA USA"},{"name":"Department of Pharmacology and Experimental Therapeutics Boston University School of Medicine  Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Ashe","sequence":"additional","affiliation":[{"name":"Department of Neurology and N. 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