Neuropathological changes and clinical features of autism spectrum disorder participants are similar to that reported in congenital and chronic cerebral toxoplasmosis in humans and mice

Prandota, J

doi:10.1016/j.rasd.2009.09.007

Cited by 32 publications

(17 citation statements)

References 158 publications

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“…11 Recently, it was suggested that chronic T gondii infection may be the key infectious agent responsible for triggering and development of several neurodegenerative diseases associated with an increased generation of several pro-and anti-inflammatory cytokines, including IL-1b. [12][13][14] Toxoplasmosis is one of the most frequent infections affecting both healthy and immunocompromised humans with approximately 6 billion people infected. 15,16 During its life cycle, the pathogen interacts with approximately 3000 host genes or proteins, and many of them represent an extensive Toxoplasma gondii host-pathogen interactome enrichment in several psychiatric and neurological diseases.…”

mentioning

confidence: 99%

Possible Link BetweenToxoplasma Gondiiand the Anosmia Associated With Neurodegenerative Diseases

Prandota

2014

Am J Alzheimers Dis Other Demen

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Toxoplasma gondii is an intracellular protozoan infecting 30% to 50% of global human population. Recently, it was suggested that chronic latent neuroinflammation caused by the parasite may be responsible for the development of several neurodegenerative diseases manifesting with the loss of smell. Studies in animals inoculated with the parasite revealed cysts in various regions of the brain, including olfactory bulb. Development of behavioral changes was paralleled by the preferential persistence of cysts in defined anatomic structures of the brain, depending on the host, strain of the parasite, its virulence, and route of inoculation. Olfactory dysfunction reported in Alzheimer's disease, multiple sclerosis, and schizophrenia was frequently associated with the significantly increased serum anti-T gondii immunoglobulin G antibody levels. Damage of the olfactory system may be also at least in part responsible for the development of depression because T gondii infection worsened mood in such patients, and the olfactory bulbectomized rat serves as a model of depression.

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confidence: 99%

Possible Link BetweenToxoplasma Gondiiand the Anosmia Associated With Neurodegenerative Diseases

Prandota

2014

Am J Alzheimers Dis Other Demen

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“…In vitro preincubation of tachyzoites with recombinant human prolactin resulted in a significant reduction (up to 36.15%) in replication abilities of the parasite, and the inhibition of replication was caused by a limited capacity of the parasites to penetrate host's cells as demonstrated by the reduced number of infected cells [212]. More detailed effects of chronic T. gondii infection concerning modulation of human innate immunity and metabolism were presented in other works [213][214][215][216]. Tables 9 and 10 summarized host cell-mediated evasion strategy against infection with the parasite.…”

Section: Humansmentioning

confidence: 96%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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“…Other disorders in which the IO has been implicated include autism spectrum disorders (Bailey et al 1998;Welsh et al 2005;Prandota 2010), fetal alcohol syndrome (Swayze et al 1997;Dikranian et al 2005;Jacobson et al 2008b), semantic dementia (Davies et al 2005), fatal insomnia (Montagna et al 2003;Ayuso Blanco et al 2006), as well as acute respiratory defects (Harper et al 2000;Matschke and Laas 2007) and Wolfram syndrome (Hilson et al 2009). …”

Section: Pathology Of Inferior Olivementioning

confidence: 99%

Inferior Olive: All Ins and Outs

Gruijl

Bosman

Zeeuw

et al. 2013

Handbook of the Cerebellum and Cerebellar Disorders

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The inferior olive provides all climbing fibers to the Purkinje cells in the cerebellar cortex and thereby has a strong impact on cerebellar output. As a consequence, the integration of inputs to olivary neurons as well as their intrinsic properties are critical for cerebellar function. In this chapter, all issues that are relevant for their ultimate function are addressed. This chapter starts by reviewing developmental aspects such as the origin and migratory routes of inferior olivary neurons and a description of their axonal outgrowth into climbing fibers innervating Purkinje cells. Subsequently, a detailed description of the olivary subdivisions and the ultrastructure of their neuropil is provided. This is characterized by the presence of dendro-dendritic gap junctions located in glomeruli and by the consistently combined excitatory and inhibitory innervation of their coupled spines. Furthermore, the electrophysiological behavior of olivary neurons is described and discussed. Finally, these unique properties are integrated in cellular and system models. Both type of models show that the inferior olive is very well able to control both rate

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Neuropathological changes and clinical features of autism spectrum disorder participants are similar to that reported in congenital and chronic cerebral toxoplasmosis in humans and mice

Cited by 32 publications

References 158 publications

Possible Link BetweenToxoplasma Gondiiand the Anosmia Associated With Neurodegenerative Diseases

Possible Link BetweenToxoplasma Gondiiand the Anosmia Associated With Neurodegenerative Diseases

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Inferior Olive: All Ins and Outs

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