Early paracetamol exposure decreases brain-derived neurotrophic factor (BDNF) in striatum and affects social behaviour and exploration in rats

Blecharz-Klin, Kamilla; Wawer, Adriana; Jawna-Zboińska, Katarzyna; Pyrzanowska, Justyna; Piechal, Agnieszka; Mirowska‐Guzel, Dagmara; Widy-Tyszkiewicz, Ewa

doi:10.1016/j.pbb.2018.03.004

Cited by 39 publications

(34 citation statements)

References 46 publications

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“…Indeed, in our current study, APAP treatment had a mild opposite effect on the WT microglia, neuronal dendritic spines, and mEPSCs in comparison to Dp(16) mice and consistently decreased cognitive performance in WT mice. In line with our results, administration of APAP to WT rats can cause a significant decrease in cognitive behavior (Blecharz-Klin et al, 2018;Ishida et al, 2007).…”

Section: Ll Open Accesssupporting

confidence: 92%

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome

Pinto

Morelli

Rastogi

et al. 2020

Neuron

103

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Section: Ll Open Accesssupporting

confidence: 92%

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome

Pinto

Morelli

Rastogi

et al. 2020

Neuron

103

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“…In mice, exposure to large doses of acetaminophen early in life has been found to impair behavior and cognitive function in later life [13,14]. In rats, exposure to large doses of acetaminophen early in life has been found to degrade neurotransmission, motor function, spatial memory, and social behavior in later life [15,16]. In humans, ASD is often associated with poor motor function [17], deficits in spatial working memory [18], and deficits in social behavior [19].…”

Section: Introductionmentioning

confidence: 99%

Postnatal Acetaminophen and Potential Risk of Autism Spectrum Disorder among Males

Bittker

Bell²

2020

Behavioral Sciences

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Some evidence from the literature suggests that postnatal acetaminophen exposure may be associated with increased risk of autism spectrum disorder (ASD). Using a data set obtained from a previous study that was derived from an Internet-based survey among parents on 1515 children from the US, an adjusted odds ratio (aOR) and gender-specific aORs for doses of postnatal acetaminophen provided before age two were calculated against the outcome of ASD. Separately, parental uncertainty on the number of doses of acetaminophen provided was analyzed. A population attributable fraction (PAF) associated with postnatal acetaminophen exposure before age two for ASD among males was also estimated. Postnatal acetaminophen exposure, measured in doses before age two, was found to be associated with ASD among male children (aOR 1.023, CI 1.005–1.043, p = 0.020*), and parental uncertainty on the number of doses of acetaminophen provided before age two was also found to be associated with ASD. Using this data set, the PAF associated with postnatal acetaminophen was estimated to be about 40% of the risk of ASD among male children in the US. These results suggest the possibility that postnatal acetaminophen may be a significant contributor to the risk of ASD among males in the US.

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“…Two additional papers were excluded after reading the full paper version (in both because paracetamol was not used in these studies, but mentioned in the abstract), and one additional paper was included following citation verification to result in 20 papers (Prisma flowchart, Figure 1). Table I provides an overview on the quality assessment (SYRCLE's risk of bias tool) results [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45]. This reflects a heterogeneous pattern with mainly issues related to blinding (for performance, for detection) procedures in a relevant portion of the studies (unclear or unreported, high risk in 16/20 for both) and allocation concealment (was the method used to conceal the allocation sequence described in sufficient detail to determine whether intervention allocation could have been foreseen before or during enrolment?).…”

Section: Resultsmentioning

confidence: 99%

“…This does not mean that these aspects were not considered during the design or study conduct, but we were not able to extract this information from the methods section description. Table II provides an overview on the characteristics of these studies [26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45]. Juvenile species reported are rat (n = 9), zebrafish larvae (n = 6), or mice/mouse (n = 5).…”

Section: Resultsmentioning

confidence: 99%

How to translate neuro-cognitive and behavioural outcome data in animals exposed to paracetamol to the human perinatal setting?

Allegaert

Anker

2020

Arch Med Sci

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IntroductionIntroduction: There are epidemiological – not necessary causal – observations that link perinatal paracetamol (acetaminophen) exposure to impaired neuro-cognition and behaviour, but animal models may assist to better understand the mechanisms.Material and methodsTo provide an overview on preclinical data and mechanisms explored, we conducted a structured literature search on animal models and neuro-cognition and behavioural outcome following perinatal paracetamol exposure.ResultsThis search resulted in 20 papers [rat (n = 9), zebrafish larvae (n = 6), mice (n = 5)], published between 2009 and 2020. Eight discussed pregnancy/fetal paracetamol exposure, 6 juvenile, 6 studies combined pregnancy and juvenile exposure. Quality assessment (SYRCLE’s bias risk) showed a heterogeneous pattern with blinding issues. Most papers (n = 16) described paracetamol exposure without indication, except for an induced fever and repetitive needle pricking (rat), brain injury (mice), and a zebrafish nociception model. Reported outcomes related to biochemistry (mono-amines, amino acids, protein expression), anatomy (teratogen, morphology, nuclear size) or behaviour (spatial memory, motor, social behaviour and exploration, sexual behaviour). On mechanisms, the cumulative data support an interesting ‘cannabinoid’ hypothesis to link paracetamol to neuro-cognitive and behavioural outcome. Besides limited species diversity, there is relevant within-species paracetamol dosing variability (dose, duration) with undocumented exposure.ConclusionsModels should further integrate clinical indications, as non-exposure is the obvious safest setting in the absence of an indication. Besides pain and fever and related to the cannabinoid hypothesis, this should include perinatal brain injury, as there is animal experimental evidence that cannabinoids are neuroprotective in newborn brain injury or asphyxia, further supported by evidence from non-perinatal models of paracetamol-related neuroprotective effects.

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Early paracetamol exposure decreases brain-derived neurotrophic factor (BDNF) in striatum and affects social behaviour and exploration in rats

Cited by 39 publications

References 46 publications

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome

Postnatal Acetaminophen and Potential Risk of Autism Spectrum Disorder among Males

How to translate neuro-cognitive and behavioural outcome data in animals exposed to paracetamol to the human perinatal setting?

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