Abstract
BackgroundAlzheimer’s disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and complete loss of basic functions. The ubiquitous apicomplexan parasite Toxoplasma gondii (T. gondii) infects up to one third of the world’s population and is implicated in AD.MethodsWe infected C57BL/6 wild-type male and female mice with 10 T. gondii ME49 cysts and assessed whether infection led to behavioral and anatomical effects using immunohistochemistry, immunofluorescence, Western blotting, cell culture assays, as well as an array of mouse behavior tests.ResultsWe show that T. gondii infection induced two major hallmarks of AD in the brains of C57BL/6 male and female mice: beta-amyloid (Aβ) immunoreactivity and hyperphosphorylated Tau. Infected mice showed significant neuronal death, loss of N-methyl-d-aspartate receptor (NMDAR) expression, and loss of olfactory sensory neurons. T. gondii infection also caused anxiety-like behavior, altered recognition of social novelty, altered spatial memory, and reduced olfactory sensitivity. This last finding was exclusive to male mice, as infected females showed intact olfactory sensitivity.ConclusionsThese results demonstrate that T. gondii can induce advanced signs of AD in wild-type mice and that it may induce AD in some individuals with underlying health problems.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and complete loss of basic functions
We demonstrate that as infection progresses, T. gondii induces loss of N-methyl-D-aspartate receptor (NMDAR) signal with concomitant induction of AD pathology including production of hyperphosphorylated Tau and amyloid β (Aβ) immunoreactivity in the brain
T. gondii associated with neurons and showed preference for infecting the olfactory bulb and the prefrontal cortex The high prevalence of T. gondii-infected individuals and its association with neurodegenerative diseases led us to investigate whether the parasite had the capability to induce any of the major pathological signs of AD such as Aβ deposition or pTau in C57BL/6 wild-type mice
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and complete loss of basic functions. The ubiquitous apicomplexan parasite Toxoplasma gondii (T. gondii) infects up to one third of the world’s population and is implicated in AD. Alzheimer’s disease (AD) is a progressive neurodegenerative disease associated with decline in cognitive function [1, 2]. There are 5.1 million cases of AD in the USA and almost 2 million people suffering from dementia and cognitive decline [2]. Viruses (herpes simplex virus 1), bacteria (Chlamydia pneumoniae), and parasites such as Toxoplasma gondii (T. gondii) are implicated in neurodegenerative diseases including Parkinson’s and AD [3, 4]
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