S100B and Latent Toxoplasmosis in Alzheimer’s disease

Abstract

A lzheimer's disease (AD) is a fatal neurodegenerative disorder characterized by progressive neuronal loss and loss of cognitive function. AD is the most common type of dementia and its prevalence is approximately 10% after 90 years of age [1]. The number of cases worldwide in 2005 was 47 million and it is expected to be 131 million in the year 2050 [2]. Although neuronal loss and brain dysfunction is well known in AD, its pathogenic mechanism is not fully clear. Studies in the literature have focused on 3 pathological conditions in patients with AD: amyloid plaques, neurofibrillary tangles, and astrogliosis [3-5]. The development of amyloid plaques is related to the pathologies of astrocytes [6], and this condition may be induced by neurotoxic molecules, cytokine secretion, or the activation of the complement system [7]. Toxoplasma gondii is a protozoan parasite that infects both animals and humans. In humans it is usually transmitted through the ingestion of the oocyst, which can be found in cat feces, or undercooked meat containing tissue cysts [8]. Due to the high neurotrophic effects of the parasite, the most affected body tissue in a case of chronic infection is the brain [9]. This infection causes neurodegenerative changes related to neuronal inflammation in the central nervous system (CNS) [10]. Neural degeneration caused by neuroinflammation is known to be the basis of the pathogenesis in chronic neurodegenerative Objectives: Alzheimer's disease (AD) is a fatal, multifactorial neurodegenerative disorder characterized by progressive neuronal loss and the loss of cognitive function. The etiology has not yet been fully elucidated. It has been suggested in some studies that central nervous system infections may play a role in the development of Alzheimer's disease. The aim of the present study was to investigate a possible relationship with a latent Toxoplasma gondii (T. gondii) infection in astrocytes and S100 proteins released as a result of astrocyte damage. Methods: A total of 33 patients with AD and 32 healthy individuals were included in this study. There were 16 Toxoplasma-negative and 17 Toxoplasma-positive patients in the AD group, and 15 Toxoplasma-negative and 17 Toxoplasmapositive individuals in the control group. Results: There were no statistically significant differences between the groups in terms of mean age or gender. An inter-group comparison of the subjects revealed that the S100B level was higher in patients with AD than in the control group (p<0.05). There was no statistically significant difference between the groups in terms of the T. gondii immunoglobulin G test (p>0.05). Conclusion: In our study, although there was no relationship between T. gondii infection and AD, significantly higher levels of S100B in patients with AD suggest that this protein may be important both in diagnosis and in possible treatment processes. The authors suggest that reproduction of the current study using different genotypes of T. gondii would further contribute to knowledge of the etiology of AD.

Serum Biomarker Concentrations upon Admission in Acute Traumatic Brain Injury: Associations with TBI Severity, Toxoplasma gondii Infection, and Outcome in a Referral Hospital Setting in Cameroon

“…To the best of our knowledge, this is the first study exploring the effects of T. gondii infection on biomarkers in TBI. However, Ayyildiz et al [43] studied S100B serum levels associated with T. gondii positivity in Alzheimer disease, and found no significant variation in the levels of serum S100B between T. gondii-positive and -negative Alzheimer patients. This variation in results may be due to the fact that their sample size was small (33) or simply to a difference in the underlying pathology, e.g., chronic versus acute.…”

A Review of Immunological and Neuropsychobehavioral Effects of Latent Toxoplasmosis on Humans

“…Another study in a murine of Alzheimer's disease suggested that Toxoplasma infection of brain can inhibit neuronal degeneration and memory and learning impairments [26]. The infection may modulate the immune system and affect the balance of neurotransmitters, such as dopamine, serotonin and glutamate, which may influence the mood, behaviour and cognition of individuals with Alzheimer's disease [45, 50]. LT may increase the risk of dementia by affecting the development of the brain during foetal or early childhood stages [45].…”

CanToxoplasma gondiiPave the Road for Dementia?

“…gondii is considered to be among the most resistant intracellular parasites but is thought to remain asymptomatic in most cases. However, recent human studies have implicated toxoplasmosis as a hidden contributor to various forms of dementia [12][13][14][15][16][17].…”