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The globally distributed dog roundworm <jats:italic>Toxocara canis<\/jats:italic> was suggested to be a suitable candidate due to neurotropism of the larvae and infection chronicity. This study investigated whether chronic <jats:italic>T. canis<\/jats:italic> infection induces AD-like pathology in mice and whether A\u03b2 is toxic to <jats:italic>T. canis<\/jats:italic>. BALB\/c and APP\/PS1 transgenic mice, which overproduce A\u03b2, were infected with <jats:italic>T. canis<\/jats:italic> L3 larvae and monitored for larval burden, A\u03b2 accumulation, and behavioral changes. <jats:italic>In vitro<\/jats:italic> tests of recombinant A\u03b2 toxicity against the larvae were also performed. Despite the presence of <jats:italic>T. canis<\/jats:italic> larvae in the central nervous system 8 and 16 weeks post-infection, no significant increase in A\u03b2 concentration or AD-related behavioral alterations were observed. A\u03b2 was detected on the surface and within the intestines of <jats:italic>T. canis<\/jats:italic> larvae, but <jats:italic>in vitro<\/jats:italic> exposure to recombinant A\u03b2 did not affect larval viability or morphology. Our findings suggest that <jats:italic>T. canis<\/jats:italic> infection does not trigger AD-like pathology in mice, and A\u03b2 does not act as an antiparasitic agent. This challenges the emerging hypothesis that chronic neurotoxocarosis infections may contribute to AD development.<\/jats:p>","DOI":"10.1051\/parasite\/2025019","type":"journal-article","created":{"date-parts":[[2025,4,11]],"date-time":"2025-04-11T07:52:08Z","timestamp":1744357928000},"page":"24","source":"Crossref","is-referenced-by-count":4,"title":["No evidence of Alzheimer\u2019s disease pathology in mice infected with <i>Toxocara 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