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No evidence of Alzheimer’s disease pathology in mice infected with Toxocara canis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F25%3A43921511" target="_blank" >RIV/00023752:_____/25:43921511 - isvavai.cz</a>

  • Alternative codes found

    RIV/67985823:_____/25:00619132 RIV/00216208:11110/25:10497939 RIV/00216208:11160/25:10497939 RIV/00216208:11310/25:10497939

  • Result on the web

    <a href="https://www.parasite-journal.org/articles/parasite/full_html/2025/01/parasite250018/parasite250018.html" target="_blank" >https://www.parasite-journal.org/articles/parasite/full_html/2025/01/parasite250018/parasite250018.html</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1051/parasite/2025019" target="_blank" >10.1051/parasite/2025019</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    No evidence of Alzheimer’s disease pathology in mice infected with Toxocara canis

  • Original language description

    The potential link between the infections and the development of Alzheimer’s disease (AD) has led to speculations about the role of various pathogens in triggering amyloid-β (Aβ) overproduction, possibly leading to AD onset. The globally distributed dog roundworm Toxocara canis was suggested to be a suitable candidate due to neurotropism of the larvae and infection chronicity. This study investigated whether chronic T. canis infection induces AD-like pathology in mice and whether Aβ is toxic to T. canis. BALB/c and APP/PS1 transgenic mice, which overproduce Aβ, were infected with T. canis L3 larvae and monitored for larval burden, Aβ accumulation, and behavioral changes. In vitro tests of recombinant Aβ toxicity against the larvae were also performed. Despite the presence of T. canis larvae in the central nervous system 8 and 16 weeks post-infection, no significant increase in Aβ concentration or AD-related behavioral alterations were observed. Aβ was detected on the surface and within the intestines of T. canis larvae, but in vitro exposure to recombinant Aβ did not affect larval viability or morphology. Our findings suggest that T. canis infection does not trigger AD-like pathology in mice, and Aβ does not act as an antiparasitic agent. This challenges the emerging hypothesis that chronic neurotoxocarosis infections may contribute to AD development.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30310 - Parasitology

Result continuities

  • Project

    <a href="/en/project/LM2023050" target="_blank" >LM2023050: National Infrastructure for Biological and Medical Imaging</a><br>

  • Continuities

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Others

  • Publication year

    2025

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Parasite

  • ISSN

    1252-607X

  • e-ISSN

    1776-1042

  • Volume of the periodical

    32

  • Issue of the periodical within the volume

    "Article Number 24"

  • Country of publishing house

    FR - FRANCE

  • Number of pages

    12

  • Pages from-to

    1-12

  • UT code for WoS article

    001463591000002

  • EID of the result in the Scopus database

    2-s2.0-105003080337