broad spectrum of intermediate warm-blood animal hosts, including human beings ( Flegr,

2007 ; 2013 ). Since T. gondii must reach its de fi nitive host to reproduce sexually, it changes

the behavior of infected rats by reversing the innate aversion to cat odor into an attraction

toward it, increasing the odds of being eaten by a cat ( Berdoy, Webster & Macdonald,

2000 ). Similar changes have also been described for infected chimpanzees ( Poirotte et al.,

2016 ), infected hyenas ( Gering et al., 2021 ), and infected humans ( Flegr et al., 2011 ).

Although the neurobiological mechanisms by which this parasite modify the behavior of

its intermediate hosts are not completely known, previous evidence suggests that T. gondii

infection may suppress the neural activity of limbic areas that modulate the innate

defensive behavior whereas increases activity in nearby limbic areas that modulate sexual

attraction in response to cat odors ( House, Vyas & Sapolsky, 2011 ). Moreover, studies with

rodents have proposed that these effects may be mediated by brain neurotransmitters

and sex and stress hormones and their impact on the brain and behavior. For example,

it has been shown that T. gondii can directly enhance brain serotoninergic and

dopaminergic activity in its host through alterations in gene expression ( Prandovszky

et al., 2011 ; Xiao et al., 2014 ). Other studies have also associated Toxoplasma infection

with dysregulation in gamma-aminobutyric acid (GABA), glutamate, and serotonin

levels in rodents ( Fuks et al., 2012 ; David et al., 2016 ; Mahmoud, Fereig & Nishikawa,

2017 ). The areas of the brain that are particularly susceptible to changes in these

neurotransmitters are the nucleus accumbens and ventral tegmental area, which receive

projections of the limbic system, including the amygdala ( Haber & Fudge, 1997 ). Thus,

altered neurotransmitter activity in these areas may be responsible for the emotional,

motivational, cognitive, and behavioral changes observed in Toxoplasma -infected

individuals (see Tyebji et al., 2019 ). Alternative hypotheses suggest that the behavioral and

psychological alterations observed in Toxoplasma -infected individuals could be either a

side-effect of lesions in certain brain areas produced by random allocation of the

Toxoplasma cysts, or the result of the body ’ s reaction to the parasite infection ( e.g ., a

prolonged release of cytokines and chronic in fl ammation) rather than by the parasite

itself ( Del Giudice, 2019 ; Flegr & Horá č ek, 2019 ). However, given that the behavioral

changes of Toxoplasma -infected organisms can increase the risk of being caught by felines

( e.g ., lower reaction times, attraction to cat urine) ( Flegr, 2013 ; Flegr & Horá č ek, 2019 ),

the neurobiological and behavioral alterations produced by T. gondii in its intermediate

hosts have been mainly interpreted as an evolutionary adaptation of the parasite to

complete its life-cycle within its de fi nite hosts and/or to spread to new bodies ( Poirotte

et al., 2016 ; Brüne, 2019 ; Borráz-León et al., 2021a ).

Even though humans are no longer common prey of big felines, it is possible that

T. gondii manipulated hominid behavior in the past, thus making our ancestors easier

targets for big cats ( Webster, 2001 ; Flegr, 2013 ). Some previous studies have suggested that

some of the phenotypic changes associated with T. gondii infection might, at the same

time, offer some indirect advantages to its hosts ( Dass et al., 2011 ; Borráz-León et al.,

2021a ) and represent transmission-related bene fi ts for T. gondii ( Brüne, 2019 ; Del Giudice,

2019 ). For example, in one study, Toxoplasma -infected male rats were perceived as

more sexually attractive and were preferred as sexual partners by non-infected females