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

Kód výsledku v 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>

Nalezeny alternativní kódy

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

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30310 - Parasitology

Projekt

<a href="/cs/project/LM2023050" target="_blank" >LM2023050: Národní infrastruktura pro biologické a medicínské zobrazování</a><br>

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2025

Kód důvěrnosti údajů

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

Název periodika

Parasite

ISSN

1252-607X

e-ISSN

1776-1042

Svazek periodika

32

Číslo periodika v rámci svazku

"Article Number 24"

Stát vydavatele periodika

FR - Francouzská republika

Počet stran výsledku

12

Strana od-do

1-12

Kód UT WoS článku

001463591000002

EID výsledku v databázi Scopus

2-s2.0-105003080337