Dietary interventions that reduce mTOR activity rescue autistic-like behavioral deficits in mice

Wu, Jackie; Theije, Caroline G. M. de; Silva, Sofia Lopes da; Abbring, Suzanne; Horst, Hilma van der; Broersen, Laus M.; Willemsen, Linette E. M.; Kas, Martien; Garssen, Johan; Kraneveld, Aletta D.

doi:10.1016/j.bbi.2016.09.016

Cited by 29 publications

(35 citation statements)

References 82 publications

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“…For instance, a high‐fat, low‐carbohydrate ketogenic diet has also been shown to improve deficits in social behaviors and repetitive behaviors in the BTBR mice as well as in the environmental models of autism, maternal immune activation, and valproate in utero exposure . Moreover, a modified amino acid diet (containing high concentrations of histidine, lysine, and threonine, with low concentrations of leucine, isoleucine, and valine) was shown to improve repetitive self‐grooming behavior in BTBR mice while also attenuating mammalian target of rapamycin (mTOR) signaling in the prefrontal cortex . Currently, there is little information available as to whether the ketogenic diet or other diets may improve behavioral symptoms in autistic individuals.…”

Section: The Diet–microbiota–gut–brain Axis: Toward Nutritional Psychmentioning

confidence: 99%

Recent developments in understanding the role of the gut microbiota in brain health and disease

Sherwin

Dinan

Cryan

2017

Annals of the New York Academy of Sciences

273

164

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There is a growing appreciation of the role of the gut microbiota in all aspects of health and disease, including brain health. Indeed, roles for the bacterial commensals in various psychiatric and neurological conditions, such as depression, autism, stroke, Parkinson's disease, and Alzheimer's disease, are emerging. Microbiota dysregulation has been documented in all of these conditions or in animal models thereof. Moreover, depletion or modulation of the gut microbiota can affect the severity of the central pathology or behavioral deficits observed in a variety of brain disorders. However, the mechanisms underlying such effects are only slowly being unraveled. Additionally, recent preclinical and clinical evidence suggest that targeting the microbiota through prebiotic, probiotic, or dietary interventions may be an effective "psychobiotic" strategy for treating symptoms in mood, neurodevelopmental disorders, and neurodegenerative diseases.

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Section: The Diet–microbiota–gut–brain Axis: Toward Nutritional Psychmentioning

confidence: 99%

Recent developments in understanding the role of the gut microbiota in brain health and disease

Sherwin

Dinan

Cryan

2017

Annals of the New York Academy of Sciences

273

164

View full text Add to dashboard Cite

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“…In BTBR mice it was reported capable of reversing social behavior deficits (Burket et al 2014). Similar, histidine, lysine and threonine rich diet, reportedly inhibiting mTOR1 pathway in the prefrontal and somatosensory cortices but not amygdala of the BTBR mice, reduced their excessive selfgrooming while leaving social approach unaltered (Wu et al 2016). …”

Section: Molecular Mechanismsmentioning

confidence: 99%

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Meyza

Blanchard

2017

Neuroscience & Biobehavioral Reviews

136

109

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Autism spectrum disorder (ASD) is the most commonly diagnosed neurodevelopmental disorder, with current estimates of more than 1% of affected children across nations. The patients form a highly heterogeneous group with only the behavioral phenotype in common. The genetic heterogeneity is reflected in a plethora of animal models representing multiple mutations found in families of affected children. Despite many years of scientific effort, for the majority of cases the genetic cause remains elusive. It is therefore crucial to include well-validated models of idiopathic autism in studies searching for potential therapeutic agents. One of these models is the BTBR T+Itpr3tf/J mouse. The current review summarizes data gathered in recent research on potential molecular mechanisms responsible for the autism-like behavioral phenotype of this strain.

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“…Therefore, our study is the first showing that chronic PUFA interventions with n-3 supplementation leads to developmental delay on the basis of all three measures (body weight, body length and puberty onset) that were all measured at four different time points during development. In addition, we did confirm that the developmental delay was not a consequence of affected locomotor or repetitive behavior in studies with similar and different intervention durations and ratios ( Fortunato et al, 2016;Fountain et al, 2008;Pietropaolo et al, 2014;Wu et al, 2016 ) and literature suggests that changed behavior seems to be more affected by PUFA ratio than individual lev-els ( Korotkova et al, 2005 ). Several studies indicated pathways through which this developmental delay may be established.…”

Section: Tablementioning

confidence: 48%

Chronic dietary changes in n-6/n-3 polyunsaturated fatty acid ratios cause developmental delay and reduce social interest in mice

Elst

Brouwers

Merkens

et al. 2019

European Neuropsychopharmacology

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Dietary interventions that reduce mTOR activity rescue autistic-like behavioral deficits in mice

Cited by 29 publications

References 82 publications

Recent developments in understanding the role of the gut microbiota in brain health and disease

Recent developments in understanding the role of the gut microbiota in brain health and disease

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Chronic dietary changes in n-6/n-3 polyunsaturated fatty acid ratios cause developmental delay and reduce social interest in mice

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