is the etiologic agent of toxoplasmosis, a highly prevalent parasitosis. () transits in the brain from acute (AT) to chronic toxoplasmosis (CT), under host immune control. In immunocompromised patients, reactivation of CT is potentially life-threatening. Behavioral and neurological complications have been associated with CT. Furthermore, an effective treatment targeting CT is still lacking. We previously reported the efficacy of imiquimod against CT. Here, we demonstrate the molecular effects of imiquimod or imiquimod followed by the clinically used combination of sulfadiazine and pyrimethamine (SDZ + PYR) on CT-associated behavior in a rat model. Imiquimod decreased the number of cysts in the brains of chronically infected rats due to an induced reactivation of bradyzoites into tachyzoites. Importantly, this decrease was more pronounced in rats treated with imiquimod followed by SDZ + PYR. Rats chronically infected with exhibited an anxiety-like behavior. Notably, treatment with imiquimod reversed this behavior aberrancy, with even a more pronounced effect with imiquimod followed by SDZ/PYR. Similarly, rats chronically infected with exhibited learning deficits, and imiquimod alone or followed by SDZ/PYR reversed this behavior. Our results enhance our knowledge of the implications of CT on behavioral aberrancies and highlight the potency of imiquimod followed by SDZ + PYR on these CT-associated complications.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11202296PMC
http://dx.doi.org/10.3390/biomedicines12061295DOI Listing

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Article Synopsis
  • Toxoplasmosis is a prevalent parasite globally, and the study aims to find new, safer treatments for pregnant women and infants using nanoemulsion miltefosine (NEM).
  • NEM was formulated using triacetin, Tween 80, and ethanol, and when tested on mice and rats, it showed varying effectiveness against acute and chronic toxoplasmosis compared to other treatments like sulfadiazine (SDZ) and pyrimethamine (PYR).
  • The findings suggest that NEM effectively penetrates the blood-brain barrier, significantly reducing the number and size of tissue cysts in chronic toxoplasmosis, positioning it as a hopeful new therapeutic option.
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Department of Experimental Pathology, Immunology and Microbiology, Faculty of Medicine, American University of Beirut, Beirut 1107 2020, Lebanon.

is the etiologic agent of toxoplasmosis, a highly prevalent parasitosis. () transits in the brain from acute (AT) to chronic toxoplasmosis (CT), under host immune control. In immunocompromised patients, reactivation of CT is potentially life-threatening.

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