Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection
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 prefere...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2020
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/28469
- Acceso en línea:
- https://doi.org/10.3390/brainsci10060369
https://repository.urosario.edu.co/handle/10336/28469
- Palabra clave:
- Toxoplasma gondii
Alzheimer’s disease
Amyloid-beta
Dementia
Cognitive impairment
- Rights
- License
- Abierto (Texto Completo)
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e4467c05-0b89-4715-8ca7-84e02cd667457994277260051701355600461187bf-529a-47b0-8295-6d922dafbb99802165716002020-08-28T15:48:16Z2020-08-28T15:48:16Z2020-06-12Toxoplasma 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 a ect 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- (A ) peptide accumulation, neurofibrillary tangles, and neuroinflammation. Di erent authors have found that toxoplasmosis may a ect A production in brain areas linked with memory functioning, and can induce a central immune response and neurotransmitter imbalance, which in turn, a ect the nervous system microenvironment. In contrast, other studies have revealed a reduction of A plaques and hyperphosphorylated tau protein formation in animal models, which might cause some protective e ects. The aim of this article is to summarize and review the newest data in regard to di erent 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.application/pdfhttps://doi.org/10.3390/brainsci10060369EISSN: 2076-3425https://repository.urosario.edu.co/handle/10336/28469engMDPI AGNo. 6Brain SciencesVol. 10Brain Sciences, EISSN: 2076-3425, Vol. 10, No. 6 (2020); 19 pp.https://www.mdpi.com/2076-3425/10/6/369Abierto (Texto Completo)http://purl.org/coar/access_right/c_abf2Brain Sciencesinstname:Universidad del Rosarioreponame:Repositorio Institucional EdocURToxoplasma gondiiAlzheimer’s diseaseAmyloid-betaDementiaCognitive impairmentPathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infectionMecanismos fisiopatológicos del deterioro cognitivo y la neurodegeneración por infección por Toxoplasma gondiiarticleArtículohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501Ortiz-Guerrero, GloriaGonzález Reyes, Rodrigo Estebande-la-Torre, AlejandraMedina-Rincón, GermanNava Mesa, Mauricio Orlando10336/28469oai:repository.urosario.edu.co:10336/284692021-09-14 06:59:18.982https://repository.urosario.edu.coRepositorio institucional EdocURedocur@urosario.edu.co |
dc.title.spa.fl_str_mv |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
dc.title.TranslatedTitle.spa.fl_str_mv |
Mecanismos fisiopatológicos del deterioro cognitivo y la neurodegeneración por infección por Toxoplasma gondii |
title |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
spellingShingle |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection Toxoplasma gondii Alzheimer’s disease Amyloid-beta Dementia Cognitive impairment |
title_short |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
title_full |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
title_fullStr |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
title_full_unstemmed |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
title_sort |
Pathophysiological mechanisms of cognitive impairment and neurodegeneration bt Toxoplasma gondii infection |
dc.subject.keyword.spa.fl_str_mv |
Toxoplasma gondii Alzheimer’s disease Amyloid-beta Dementia Cognitive impairment |
topic |
Toxoplasma gondii Alzheimer’s disease Amyloid-beta Dementia Cognitive impairment |
description |
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 a ect 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- (A ) peptide accumulation, neurofibrillary tangles, and neuroinflammation. Di erent authors have found that toxoplasmosis may a ect A production in brain areas linked with memory functioning, and can induce a central immune response and neurotransmitter imbalance, which in turn, a ect the nervous system microenvironment. In contrast, other studies have revealed a reduction of A plaques and hyperphosphorylated tau protein formation in animal models, which might cause some protective e ects. The aim of this article is to summarize and review the newest data in regard to di erent 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. |
publishDate |
2020 |
dc.date.accessioned.none.fl_str_mv |
2020-08-28T15:48:16Z |
dc.date.available.none.fl_str_mv |
2020-08-28T15:48:16Z |
dc.date.created.spa.fl_str_mv |
2020-06-12 |
dc.type.eng.fl_str_mv |
article |
dc.type.coarversion.fl_str_mv |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
dc.type.coar.fl_str_mv |
http://purl.org/coar/resource_type/c_6501 |
dc.type.spa.spa.fl_str_mv |
Artículo |
dc.identifier.doi.none.fl_str_mv |
https://doi.org/10.3390/brainsci10060369 |
dc.identifier.issn.none.fl_str_mv |
EISSN: 2076-3425 |
dc.identifier.uri.none.fl_str_mv |
https://repository.urosario.edu.co/handle/10336/28469 |
url |
https://doi.org/10.3390/brainsci10060369 https://repository.urosario.edu.co/handle/10336/28469 |
identifier_str_mv |
EISSN: 2076-3425 |
dc.language.iso.spa.fl_str_mv |
eng |
language |
eng |
dc.relation.citationIssue.none.fl_str_mv |
No. 6 |
dc.relation.citationTitle.none.fl_str_mv |
Brain Sciences |
dc.relation.citationVolume.none.fl_str_mv |
Vol. 10 |
dc.relation.ispartof.spa.fl_str_mv |
Brain Sciences, EISSN: 2076-3425, Vol. 10, No. 6 (2020); 19 pp. |
dc.relation.uri.spa.fl_str_mv |
https://www.mdpi.com/2076-3425/10/6/369 |
dc.rights.coar.fl_str_mv |
http://purl.org/coar/access_right/c_abf2 |
dc.rights.acceso.spa.fl_str_mv |
Abierto (Texto Completo) |
rights_invalid_str_mv |
Abierto (Texto Completo) http://purl.org/coar/access_right/c_abf2 |
dc.format.mimetype.none.fl_str_mv |
application/pdf |
dc.publisher.spa.fl_str_mv |
MDPI AG |
dc.source.spa.fl_str_mv |
Brain Sciences |
institution |
Universidad del Rosario |
dc.source.instname.none.fl_str_mv |
instname:Universidad del Rosario |
dc.source.reponame.none.fl_str_mv |
reponame:Repositorio Institucional EdocUR |
repository.name.fl_str_mv |
Repositorio institucional EdocUR |
repository.mail.fl_str_mv |
edocur@urosario.edu.co |
_version_ |
1814167425062535168 |