Cited by 140Trypanosoma species research and implicationsSleep and Wakefulness ResearchTryptophan and brain disorders

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African trypanosome infections of the nervous system: Parasite entry and effects on sleep and synaptic functions

Kristensson, Krister, Nygård, Mikael, Bertini, Giuseppe, Bentivoglio, Marina·2010·Progress in Neurobiology

DOI 10.1016/j.pneurobio.2009.12.001

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Abstract

The extracellular parasite Trypanosoma brucei causes human African trypanosomiasis (HAT), also known as sleeping sickness. Trypanosomes are transmitted by tsetse flies and HAT occurs in foci in sub-Saharan Africa. The disease, which is invariably lethal if untreated, evolves in a first hemo-lymphatic stage, progressing to a second meningo-encephalitic stage when the parasites cross the blood-brain barrier. At first, trypanosomes are restricted to circumventricular organs and choroid plexus in the brain outside the blood-brain barrier, and to dorsal root ganglia. Later, parasites cross the blood-brain barrier at post-capillary venules, through a multi-step process similar to that of lymphocytes. Accumulation of parasites in the brain is regulated by cytokines and chemokines. Trypanosomes can alter neuronal function and the most prominent manifestation is represented by sleep alterations. These are characterized, in HAT and experimental rodent infections, by disruption of the sleep-wake 24h cycle and internal sleep structure. Trypanosome infections alter also some, but not all, other endogenous biological rhythms. A number of neural pathways and molecules may be involved in such effects. Trypanosomes secrete prostaglandins including the somnogenic PGD2, and they interact with the host's immune system to cause release of pro-inflammatory cytokines. From the sites of early localization of parasites in the brain and meninges, such molecules could affect adjacent brain areas implicated in sleep-wakefulness regulation, including the suprachiasmatic nucleus and its downstream targets, to cause the changes characteristic of the disease. This raises challenging issues on the effects of cytokines on synaptic functions potentially involved in sleep-wakefulness alterations.

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Authors: Kristensson, K., Nygård, M., Bertini, G., & Bentivoglio, M.
Affiliations: Karolinska Institutet (SE)
University of Verona (IT)
Corresponding author: Kristensson, Krister
ORCID: Bertini, Giuseppe
Bentivoglio, Marina
Venue: Progress in Neurobiology
Publisher: Elsevier BV
Published: 2010-06
Volume: 91
Issue: 2
Pages: 152-171
ISSN: 0301-0082 (ISSN-L)
DOI: 10.1016/j.pneurobio.2009.12.001
OpenAlex: W2024288031
Cited by: 140
References: 208
Citations by year: 2026: 4 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 10 · 2021: 6 · 2020: 8 · 2019: 11 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 13 · 2013: 17 · 2012: 13
FWCI: 6.71
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Progress in Neurobiology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Epidemiology › Trypanosoma species research and implications
Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: Trypanosoma brucei, sleeping sickness, blood-brain barrier penetration, sleep-wake cycle disruption, sleep disorders, prostaglandin D2, inflammatory cytokines, chemokines, suprachiasmatic nucleus, circadian rhythm, synaptic function, dorsal root ganglia, choroid plexus, circumventricular organs
MeSH terms: Animals, Brain, Humans, Synaptic Transmission, Sleep, Sleep Wake Disorders, Trypanosomiasis, African, Central Nervous System Protozoal Infections

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African trypanosome infections of the nervous system: Parasite entry and effects on sleep and synaptic functions

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