Abstract
Toxoplasma gondii is an obligate intracellular parasite considered one of the most successful pathogens in the world, owing to its ability to produce long-lasting infections and to persist in the central nervous system (CNS) in most warm-blooded animals, including humans. This parasite has a preference to invade neurons and affect the functioning of glial cells. This could lead to neurological and behavioral changes associated with cognitive impairment. Although several studies in humans and animal models have reported controversial results about the relationship between toxoplasmosis and the onset of dementia as a causal factor, two recent meta-analyses have shown a relative association with Alzheimer’s disease (AD). AD is characterized by amyloid-β (Aβ) peptide accumulation, neurofibrillary tangles, and neuroinflammation. Different authors have found that toxoplasmosis may affect Aβ production in brain areas linked with memory functioning, and can induce a central immune response and neurotransmitter imbalance, which in turn, affect the nervous system microenvironment. In contrast, other studies have revealed a reduction of Aβ plaques and hyperphosphorylated tau protein formation in animal models, which might cause some protective effects. The aim of this article is to summarize and review the newest data in regard to different pathophysiological mechanisms of cerebral toxoplasmosis and their relationship with the development of AD and cognitive impairment. All these associations should be investigated further through clinical and experimental studies.
Highlights
Cognitive deficits are prevalent in the elderly population, with a broad spectrum of neurological disorders, ranging from mild cognitive impairment (MCI) to severe forms such as dementia.Alzheimer’s disease (AD) is the most common type of dementia, and is a neurodegenerative condition characterized by memory loss and the weakening of other neurological functions such as orientation, language, executive function, sensory perception, and attention [1,2]
Considering the clinical relationship between toxoplasmosis, cognitive impairment and neurodegenerative disorders, the aim of this article is to review the pathological effects of Toxoplasma gondii infection in the nervous system and discuss its role in the pathophysiology of AD
Astrocytes expressing ApoE ε4 were shown to decrease ApoE production compared with ApoE ε3-expressing astrocytes; this finding is related to an increase in cholesterol biosynthesis from ApoE ε4 astrocytes, which suggests that the ApoE ε4 allele hinders astrocyte lipid metabolism
Summary
Cognitive deficits are prevalent in the elderly population, with a broad spectrum of neurological disorders, ranging from mild cognitive impairment (MCI) to severe forms such as dementia. Research evidence has suggested an association between infectious pathogens such as Chlamydia pneumonia, Helicobacter pylori, Borrelia burgdorferi, spirochetes, cytomegalovirus (CMV) and herpes simplex virus (HSV) type I, in the appearance of late-onset AD [8,9] In recent years, another pathogen, Toxoplasma gondii, has been proposed as a risk factor in the pathophysiology of AD, as well as in other neuropsychiatric disorders, such as schizophrenia [10], bipolar disorder type I [11], migraine [12], and obsessive-compulsive disorder [13]. In a recent case-control study (n = 344 patients), Toxoplasma infection (assessed by anti-T. gondii IgM and IgG antibodies) and neurological disorders were not related [20], and neither was it associated with dementia in older adults in Africa [21]. Considering the clinical relationship between toxoplasmosis, cognitive impairment and neurodegenerative disorders, the aim of this article is to review the pathological effects of Toxoplasma gondii infection in the nervous system and discuss its role in the pathophysiology of AD and cognitive impairment from a neurobiological perspective
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