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Emerging work suggests that parasites may influence the central nervous system indirectly through microbiota disruption and chronic immune activation, or directly through neurotropism, ultimately converging on neuroinflammation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main body<\/jats:title>\n                    <jats:p>\n                      Here, we synthesize human and experimental evidence that protozoan and helminth infections can remodel the microbiota\u2013immune\u2013brain axis and promote neuroinflammatory states associated with behavioral dysfunction. Across neurotropic (e.g.,\n                      <jats:italic>Toxoplasma gondii<\/jats:italic>\n                      ,\n                      <jats:italic>Plasmodium<\/jats:italic>\n                      spp.,\n                      <jats:italic>Trypanosoma<\/jats:italic>\n                      spp.) and primarily intestinal parasites (e.g.,\n                      <jats:italic>Enterobius vermicularis<\/jats:italic>\n                      ,\n                      <jats:italic>Toxocara<\/jats:italic>\n                      spp., schistosomes, and\n                      <jats:italic>Taenia solium<\/jats:italic>\n                      \u2013associated neurocysticercosis), convergent pathways include: (i) sustained peripheral cytokine production and immune-cell reprogramming; (ii) gut dysbiosis with increased microbial products and reduced short-chain fatty acids; (iii) increased intestinal permeability and enhanced immune-to-brain signaling; (iv) blood\u2013brain barrier dysfunction and activation of microglia and astrocytes; and (v) downstream neurochemical and transcriptional remodeling, including perturbations in dopamine\/serotonin\/GABA-related signaling, indoleamine 2,3-dioxygenase\u2013driven tryptophan catabolism, and infection-associated epigenetic and microRNA changes. Clinically, these cascades are associated with seizures, sleep disturbance, cognitive impairment, mood and anxiety symptoms, and under specific contexts psychosis-like phenotypes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>We propose an integrative mechanistic model in which parasite-induced microbiota disturbance and chronic immune activation converge on glial activation and barrier dysfunction to shape brain circuitry and behavior. Defining shared neuroinflammatory nodes across parasitic diseases may reveal tractable biomarkers and host-directed therapeutic strategies to mitigate long-term neuropsychiatric risk.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12974-026-03804-4","type":"journal-article","created":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T05:56:19Z","timestamp":1776405379000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["From parasite-induced immune activation to neuroinflammation and behavioral dysfunction: convergent mechanisms across protozoa and helminths: a review"],"prefix":"10.1186","volume":"23","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1631-8606","authenticated-orcid":false,"given":"Al- Shaimaa Mohsen","family":"Sadek","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-2514-5587","authenticated-orcid":false,"given":"Reem Hamada","family":"Mahmoud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,17]]},"reference":[{"key":"3804_CR1","doi-asserted-by":"publisher","first-page":"1877","DOI":"10.1152\/physrev.00018.2018","volume":"99","author":"JF Cryan","year":"2019","unstructured":"Cryan JF, O\u2019Riordan KJ, Cowan CS, Sandhu KV, Bastiaanssen TF, Boehme M, et al. 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