Can Toxoplasma gondii Pave the Road for Dementia?

Dementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence of Toxoplasma gondii (T. gondii). The long-term sequels of anti-Toxoplasma premunition, chiefly dominated by TNF-α, on the neurons and their receptors as the insulin-like growth factor-1 r...

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Main Authors: Enas A. El Saftawy, Noha M. Amin, Rania M. Sabry, Noha El-Anwar, Rania Y. Shash, Eman H. Elsebaie, Rita M. Wassef
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Journal of Parasitology Research
Online Access:http://dx.doi.org/10.1155/2020/8859857
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author Enas A. El Saftawy
Noha M. Amin
Rania M. Sabry
Noha El-Anwar
Rania Y. Shash
Eman H. Elsebaie
Rita M. Wassef
author_facet Enas A. El Saftawy
Noha M. Amin
Rania M. Sabry
Noha El-Anwar
Rania Y. Shash
Eman H. Elsebaie
Rita M. Wassef
author_sort Enas A. El Saftawy
collection DOAJ
description Dementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence of Toxoplasma gondii (T. gondii). The long-term sequels of anti-Toxoplasma premunition, chiefly dominated by TNF-α, on the neurons and their receptors as the insulin-like growth factor-1 receptor (IGF-1R), which is tangled in cognition and synaptic plasticity, are still not clear. IGF-1R mediates its action via IGF-1, and its depletion is incorporated in the pathogenesis of dementia. The activated TNF-α signaling pathway induces NF-κβ that may induce or inhibit neurogenesis. This study speculates the potential impact of anti-Toxoplasma immune response on the expression of IGF-1R in chronic cerebral toxoplasmosis. The distributive pattern of T. gondii cysts was studied in association with TNF-α serum levels, the in situ expression of NF-κβ, and IGF-1R in mice using the low virulent ME-49 T. gondii strain. There was an elevation of the TNF-α serum level (p value ≤ 0.004) and significant upsurge in NF-κβ whereas IGF-1R was of low abundance (p value < 0.05) compared to the controls. TNF-α had a strong positive correlation with the intracerebral expression of NF-κβ (r value ≈ 0.943, p value ≈ 0.005) and a strong negative correlation to IGF-1R (r value -0.584 and -0.725 for area% and O.D., respectively). This activated TNF-α/NF-κβ keeps T. gondii under control at the expense of IGF-1R expression, depriving neurons of the effect of IGF-1, the receptor’s ligand. We therefore deduce that T. gondii immunopathological reaction may be a road paver for developing dementia.
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spelling doaj-art-390c66b5f08f46e2b7b30d20f571e91a2025-08-20T03:55:11ZengWileyJournal of Parasitology Research2090-00232090-00312020-01-01202010.1155/2020/88598578859857Can Toxoplasma gondii Pave the Road for Dementia?Enas A. El Saftawy0Noha M. Amin1Rania M. Sabry2Noha El-Anwar3Rania Y. Shash4Eman H. Elsebaie5Rita M. Wassef6Medical Parasitology Department, Faculty of Medicine, Cairo University, Cairo, EgyptMedical Parasitology Department, Faculty of Medicine, Cairo University, Cairo, EgyptPathology Department, Faculty of Medicine, Cairo University, Cairo, EgyptArmed Forces College of Medicine, Cairo, EgyptMedical Microbiology and Immunology Department, Faculty of Medicine, Cairo University, Cairo, EgyptPublic Health and Community Medicine, Faculty of Medicine, Cairo University, Cairo, EgyptMedical Parasitology Department, Faculty of Medicine, Helwan University, Cairo, EgyptDementia is an ominous neurological disease. Scientists proposed a link between its occurrence and the presence of Toxoplasma gondii (T. gondii). The long-term sequels of anti-Toxoplasma premunition, chiefly dominated by TNF-α, on the neurons and their receptors as the insulin-like growth factor-1 receptor (IGF-1R), which is tangled in cognition and synaptic plasticity, are still not clear. IGF-1R mediates its action via IGF-1, and its depletion is incorporated in the pathogenesis of dementia. The activated TNF-α signaling pathway induces NF-κβ that may induce or inhibit neurogenesis. This study speculates the potential impact of anti-Toxoplasma immune response on the expression of IGF-1R in chronic cerebral toxoplasmosis. The distributive pattern of T. gondii cysts was studied in association with TNF-α serum levels, the in situ expression of NF-κβ, and IGF-1R in mice using the low virulent ME-49 T. gondii strain. There was an elevation of the TNF-α serum level (p value ≤ 0.004) and significant upsurge in NF-κβ whereas IGF-1R was of low abundance (p value < 0.05) compared to the controls. TNF-α had a strong positive correlation with the intracerebral expression of NF-κβ (r value ≈ 0.943, p value ≈ 0.005) and a strong negative correlation to IGF-1R (r value -0.584 and -0.725 for area% and O.D., respectively). This activated TNF-α/NF-κβ keeps T. gondii under control at the expense of IGF-1R expression, depriving neurons of the effect of IGF-1, the receptor’s ligand. We therefore deduce that T. gondii immunopathological reaction may be a road paver for developing dementia.http://dx.doi.org/10.1155/2020/8859857
spellingShingle Enas A. El Saftawy
Noha M. Amin
Rania M. Sabry
Noha El-Anwar
Rania Y. Shash
Eman H. Elsebaie
Rita M. Wassef
Can Toxoplasma gondii Pave the Road for Dementia?
Journal of Parasitology Research
title Can Toxoplasma gondii Pave the Road for Dementia?
title_full Can Toxoplasma gondii Pave the Road for Dementia?
title_fullStr Can Toxoplasma gondii Pave the Road for Dementia?
title_full_unstemmed Can Toxoplasma gondii Pave the Road for Dementia?
title_short Can Toxoplasma gondii Pave the Road for Dementia?
title_sort can toxoplasma gondii pave the road for dementia
url http://dx.doi.org/10.1155/2020/8859857
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