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HAND persists in treated patients as a result of chronic inflammation and low-level expression of viral proteins, though the mechanisms involved in synaptic damage are unclear. Here, we report that the chemokine CXCL12 recoups both cognitive performance and synaptodendritic health in a rodent model of HAND, which recapitulates the neuroinflammatory state of virally controlled individuals and the associated structural\/functional deficiencies. CXCL12 preferentially regulates plastic thin spines on layer II\/III pyramidal neurons of the medial prefrontal cortex via CXCR4-dependent stimulation of the Rac1\/PAK actin polymerization pathway, leading to increased spine density and improved flexible behavior. Our studies unveil a critical role of CXCL12\/CXCR4 signaling in spine dynamics and cognitive flexibility, suggesting that HAND - or other diseases driven by spine loss - may be reversible and upturned by targeting Rac1-dependent processes in cortical neurons.<\/jats:p>","DOI":"10.7554\/elife.49717","type":"journal-article","created":{"date-parts":[[2020,1,23]],"date-time":"2020-01-23T08:00:27Z","timestamp":1579766427000},"source":"Crossref","is-referenced-by-count":42,"title":["CXCL12-induced rescue of cortical dendritic spines and cognitive flexibility"],"prefix":"10.7554","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5419-9532","authenticated-orcid":true,"given":"Lindsay K","family":"Festa","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia, United States"},{"name":"Center of Neuroimmunology and CNS Therapeutics, Institute of Molecular Medicine and Infectious Diseases, Drexel 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