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https://www.readbyqxmd.com/read/29787855/dysbiosis-of-microbiome-and-probiotic-treatment-in-a-genetic-model-of-autism-spectrum-disorders
#1
Tabouy Laure, Getselter Dimitry, Ziv Oren, Karpuj Marcela, Tabouy Timothée, Maayouf Rasha, Werbner Nir, Ben-Amram Hila, Nuriel-Ohayon Meital, Koren Omry, Elliott Evan
Recent studies have determined that the microbiome has direct effects on behavior, and may be dysregulated in neurodevelopmental conditions. Considering that neurodevelopmental conditions, such as autism, have a strong genetic etiology, it is necessary to understand if genes associated with neurodevelopmental disorders, such as Shank3, can influence the gut microbiome, and if probiotics can be a therapeutic tool. In this study, we have identified dysregulation of several genera and species of bacteria in the gut and colon of both male and female Shank3 KO mice...
May 19, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29785777/paradoxical-effect-of-baclofen-on-social-behavior-in-the-fragile-x-syndrome-mouse-model
#2
Shimriet Zeidler, Andreea S Pop, Israa A Jaafar, Helen de Boer, Ronald A M Buijsen, Celine E F de Esch, Ingeborg Nieuwenhuizen-Bakker, Renate K Hukema, Rob Willemsen
INTRODUCTION: Fragile X syndrome (FXS) is a common monogenetic cause of intellectual disability, autism spectrum features, and a broad range of other psychiatric and medical problems. FXS is caused by the lack of the fragile X mental retardation protein (FMRP), a translational regulator of specific mRNAs at the postsynaptic compartment. The absence of FMRP leads to aberrant synaptic plasticity, which is believed to be caused by an imbalance in excitatory and inhibitory network functioning of the synapse...
April 26, 2018: Brain and Behavior
https://www.readbyqxmd.com/read/29783181/autistic-traits-in-epilepsy-models-why-when-and-how
#3
REVIEW
Jana Velíšková, Jill L Silverman, Melissa Benson, Pierre-Pascal Lenck-Santini
Autism spectrum disorder (ASD) is a common comorbidity of epilepsy and seizures and/or epileptiform activity are observed in a significant proportion of ASD patients. Current research also implies that autistic traits can be observed to a various degree in mice and rats with seizures. This suggests that there are shared mechanisms in both ASD and epilepsy syndromes. Here, we first review the standard, validated methods used to assess autistic traits in animal models as well as their limitations with regards to epilepsy models...
May 18, 2018: Epilepsy Research
https://www.readbyqxmd.com/read/29775702/abnormal-sleep-architecture-and-hippocampal-circuit-dysfunction-in-a-mouse-model-of-fragile-x-syndrome
#4
Christine E Boone, Heydar Davoudi, Jon B Harrold, David J Foster
Fragile X syndrome (FXS) is the most common heritable cause of intellectual disability and single-gene cause of autism spectrum disorder. The Fmr1 null mouse models much of the human disease including hyperarousal, sensory hypersensitivity, seizure activity, and hippocampus-dependent cognitive impairment. Sleep architecture is disorganized in FXS patients, but has not been examined in Fmr1 knockout (Fmr1-KO) mice. Hippocampal neural activity during sleep, which is implicated in memory processing, also remains uninvestigated in Fmr1-KO mice...
May 15, 2018: Neuroscience
https://www.readbyqxmd.com/read/29772261/maternal-immune-activation-with-staphylococcal-enterotoxin-a-produces-unique-behavioral-changes-in-c57bl-6-mouse-offspring
#5
Ruthy Glass, Sara Norton, Nicholas Fox, Alexander W Kusnecov
Stimulation of the immune system during pregnancy, known as maternal immune activation (MIA), can cause long-lasting neurobiological and behavioral changes in the offspring. This phenomenon has been implicated in the etiology of developmental psychiatric disorders, such as autism and schizophrenia. Much of this evidence is predicated on animal models using bacterial agents such as LPS and/or viral mimics such as Poly I:C, both of which act through toll-like receptors. However, fewer studies have examined the role of direct activation of maternal T-cells during pregnancy using microbial agents...
May 14, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29771335/loss-of-fragile-x-protein-fmrp-impairs-homeostatic-synaptic-downscaling-through-tumor-suppressor-p53-and-ubiquitin-e3-ligase-nedd4-2
#6
Kwan Young Lee, Kathryn A Jewett, Hee Jung Chung, Nien-Pei Tsai
Synaptic scaling allows neurons to homeostatically readjust synaptic strength upon chronic neural activity perturbations. Although altered synaptic scaling has been implicated to underlie imbalanced brain excitability in neurological disorders such as autism spectrum disorders and epilepsy, the molecular dysregulation and restoration of synaptic scaling in those diseases have not been demonstrated. Here, we showed that the homeostatic synaptic downscaling is absent in the hippocampal neurons of Fmr1 KO mice, the mouse model of the most common inherited autism, Fragile X Syndrome (FXS)...
May 16, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29771287/term-or-preterm-cesarean-section-delivery-does-not-lead-to-long-term-detrimental-consequences-in-mice
#7
Morgane Chiesa, Damien Guimond, Roman Tyzio, Alexandre Pons-Bennaceur, Natalia Lozovaya, Nail Burnashev, Diana C Ferrari, Yehezkel Ben-Ari
Epidemiological studies have provided contradictory data on the deleterious sequels of cesarean section (C-section) delivery and their links with developmental brain disorders such as Autism Spectrum Disorders. To gain better insight on these issues, we have now compared physiological, morphological, and behavioral parameters in vaginal, term, and preterm C-section delivered mice. We report that C-section delivery does not lead to long-term behavioral alterations though preterm C-section delivery modifies communicative behaviors in pups...
May 16, 2018: Cerebral Cortex
https://www.readbyqxmd.com/read/29768199/the-autism-related-protein-chd8-cooperates-with-c-ebp%C3%AE-to-regulate-adipogenesis
#8
Yasuyuki Kita, Yuta Katayama, Taichi Shiraishi, Takeru Oka, Tetsuya Sato, Mikita Suyama, Yasuyuki Ohkawa, Keishi Miyata, Yuichi Oike, Michiko Shirane, Masaaki Nishiyama, Keiichi I Nakayama
The gene encoding the chromatin remodeler CHD8 is the most frequently mutated gene in individuals with autism spectrum disorder (ASD). Heterozygous mutations in CHD8 give rise to ASD that is often accompanied by macrocephaly, gastrointestinal complaints, and slender habitus. Whereas most phenotypes of CHD8 haploinsufficiency likely result from delayed neurodevelopment, the mechanism underlying slender habitus has remained unknown. Here, we show that CHD8 interacts with CCAAT/enhancer-binding protein β (C/EBPβ) and promotes its transactivation activity during adipocyte differentiation...
May 15, 2018: Cell Reports
https://www.readbyqxmd.com/read/29762671/motor-impairments-correlate-with-social-deficits-and-restricted-neuronal-loss-in-an-environmental-model-of-autism
#9
Tareq Al Sagheer, Obelia Haida, Anais Balbous, Maureen Francheteau, Emmanuel Matas, Pierre-Olivier Fernagut, Mohamed Jaber
Background: Motor impairments are amongst the earliest and most consistent signs of autism spectrum disorders (ASD) but are not used as diagnostic criteria. In addition, the relationship between motor and cognitive impairments and their respective neural substrates remain unknown. Methods: Here, we aimed at determining whether a well-acknowledged animal model of ASD, the valproic acid (VPA) model, displays motor impairments and whether they may correlate with social deficits and neuronal loss within motor brain areas...
May 12, 2018: International Journal of Neuropsychopharmacology
https://www.readbyqxmd.com/read/29760409/histone-deacetylase-inhibitor-ms-275-restores-social-and-synaptic-function-in-a-shank3-deficient-mouse-model-of-autism
#10
Kaijie Ma, Luye Qin, Emmanuel Matas, Lara J Duffney, Aiyi Liu, Zhen Yan
Autism is a neurodevelopmental disorder characterized by social deficits and repetitive behaviors. Genetic screening has identified synaptic, transcriptional, and chromatin genes disrupted in autistic patients. Haploinsufficiency of Shank3, which encodes a scaffold protein at glutamatergic synapses, is causally linked to autism. Using a Shank3-deficient mouse model that exhibits prominent autism-like phenotypes, we have found that histone acetylation in the prefrontal cortex (PFC) is abnormally low, which can be reversed by MS-275 (also known as Entinostat, SNDX-275), a class I histone deacetylase (HDAC) inhibitor that is selectively potent in PFC...
April 19, 2018: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/29752066/the-microglial-innate-immune-receptor-trem2-is-required-for-synapse-elimination-and-normal-brain-connectivity
#11
Fabia Filipello, Raffaella Morini, Irene Corradini, Valerio Zerbi, Alice Canzi, Bernadeta Michalski, Marco Erreni, Marija Markicevic, Chiara Starvaggi-Cucuzza, Karel Otero, Laura Piccio, Francesca Cignarella, Fabio Perrucci, Matteo Tamborini, Marco Genua, Lawrence Rajendran, Elisabetta Menna, Stefania Vetrano, Margaret Fahnestock, Rosa Chiara Paolicelli, Michela Matteoli
The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. Microglial defects in phagocytosis of toxic aggregates or apoptotic membranes were proposed to be at the origin of the pathological processes in the presence of Trem2 inactivating mutations. Here, we show that TREM2 is essential for microglia-mediated synaptic refinement during the early stages of brain development...
May 3, 2018: Immunity
https://www.readbyqxmd.com/read/29748850/from-aggression-to-autism-new-perspectives-on-the-behavioral-sequelae-of-monoamine-oxidase-deficiency
#12
REVIEW
Marco Bortolato, Gabriele Floris, Jean C Shih
The two monoamine oxidase (MAO) enzymes, A and B, catalyze the metabolism of monoamine neurotransmitters, such as serotonin, norepinephrine, and dopamine. The phenotypic outcomes of MAO congenital deficiency have been studied in humans and animal models, to explore the role of these enzymes in behavioral regulation. The clinical condition caused by MAOA deficiency, Brunner syndrome, was first described as a disorder characterized by overt antisocial and aggressive conduct. Building on this discovery, subsequent studies were focused on the characterization of the role of MAOA in the neurobiology of antisocial conduct...
May 10, 2018: Journal of Neural Transmission
https://www.readbyqxmd.com/read/29724786/autism-associated-neuroligin-4-mutation-selectively-impairs-glycinergic-synaptic-transmission-in-mouse-brainstem-synapses
#13
Bo Zhang, Ozgun Gokce, W Dylan Hale, Nils Brose, Thomas C Südhof
In human patients, loss-of-function mutations of the postsynaptic cell-adhesion molecule neuroligin-4 were repeatedly identified as monogenetic causes of autism. In mice, neuroligin-4 deletions caused autism-related behavioral impairments and subtle changes in synaptic transmission, and neuroligin-4 was found, at least in part, at glycinergic synapses. However, low expression levels precluded a comprehensive analysis of neuroligin-4 localization, and overexpression of neuroligin-4 puzzlingly impaired excitatory but not inhibitory synaptic function...
May 3, 2018: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/29720545/multifocal-demyelinating-motor-neuropathy-and-hamartoma-syndrome-associated-with-a-de-novo-pten-mutation
#14
Boglarka Bansagi, Vietxuan Phan, Mark R Baker, Julia O'Sullivan, Matthew J Jennings, Roger G Whittaker, Juliane S Müller, Jennifer Duff, Helen Griffin, James A L Miller, Grainne S Gorman, Hanns Lochmüller, Patrick F Chinnery, Andreas Roos, Laura E Swan, Rita Horvath
OBJECTIVE: To describe a patient with a multifocal demyelinating motor neuropathy with onset in childhood and a mutation in phosphatase and tensin homolog ( PTEN ), a tumor suppressor gene associated with inherited tumor susceptibility conditions, macrocephaly, autism, ataxia, tremor, and epilepsy. Functional implications of this protein have been investigated in Parkinson and Alzheimer diseases. METHODS: We performed whole-exome sequencing in the patient's genomic DNA validated by Sanger sequencing...
May 2, 2018: Neurology
https://www.readbyqxmd.com/read/29700290/brain-region-specific-disruption-of-shank3-in-mice-reveals-a-dissociation-for-cortical-and-striatal-circuits-in-autism-related-behaviors
#15
Alexandra L Bey, Xiaoming Wang, Haidun Yan, Namsoo Kim, Rebecca L Passman, Yilin Yang, Xinyu Cao, Aaron J Towers, Samuel W Hulbert, Lara J Duffney, Erin Gaidis, Ramona M Rodriguiz, William C Wetsel, Henry H Yin, Yong-Hui Jiang
We previously reported a new line of Shank3 mutant mice which led to a complete loss of Shank3 by deleting exons 4-22 (Δe4-22) globally. Δe4-22 mice display robust ASD-like behaviors including impaired social interaction and communication, increased stereotypical behavior and excessive grooming, and a profound deficit in instrumental learning. However, the anatomical and neural circuitry underlying these behaviors are unknown. We generated mice with Shank3 selectively deleted in forebrain, striatum, and striatal D1 and D2 cells...
April 27, 2018: Translational Psychiatry
https://www.readbyqxmd.com/read/29698767/regulation-of-neural-differentiation-synaptic-scaling-and-animal-behavior-by-mecp2-phophorylation
#16
Xiaofen Zhong, Hongda Li, Jason Kim, Qiang Chang
Highly expressed in the mammalian brain and widely distributed across the genome, MeCP2 is a key player in recognizing modified DNA and interpreting the epigenetic information encoded in different DNA methylation/hydroxymethylation patterns. Alterations in sequence or copy number of the X-linked human MECP2 gene cause either Rett syndrome (RTT) or MECP2 duplication syndrome. Alterations in MECP2 levels have also been identified in patients with autism. To fully understand the significant role of MECP2 in regulating the development and function of the nervous system, it is important to study all aspects of MeCP2 function...
April 23, 2018: Neurobiology of Learning and Memory
https://www.readbyqxmd.com/read/29696935/impaired-hippocampal-synaptic-plasticity-and-enhanced-excitatory-transmission-in-a-novel-animal-model-of-autism-spectrum-disorders-with-telomerase-reverse-transcriptase-overexpression
#17
Jeehae Rhee, Kwanghoon Park, Ki Chan Kim, Chan Young Shin, ChiHye Chung
Recently, we have reported that animals with telomerase reverse transcriptase (TERT) overexpression exhibit reduced social interaction, decreased preference for novel social interaction and poor nest-building behaviors-symptoms that mirror those observed in human autism spectrum disorders (ASD). Overexpression of TERT also alters the excitatory/inhibitory (E/I) ratio in the medial prefrontal cortex. However, the effects of TERT overexpression on hippocampal-dependent learning and synaptic efficacy have not been investigated...
April 26, 2018: Molecules and Cells
https://www.readbyqxmd.com/read/29685134/oral-sensitization-to-whey-proteins-induces-age-and-sex-dependent-behavioral-abnormality-and-neuroinflammatory-responses-in-a-mouse-model-of-food-allergy-a-potential-role-of-mast-cells
#18
Danielle L Germundson, Nicholas A Smith, Lane P Vendsel, Andrea V Kelsch, Colin K Combs, Kumi Nagamoto-Combs
BACKGROUND: Growing evidence has strengthened the association of food allergy with neuropsychiatric symptoms such as depression, anxiety, and autism. However, underlying mechanisms by which peripheral allergic responses lead to behavioral dysfunction are yet to be determined. Allergen-activated mast cells may serve as mediators by releasing histamine and other inflammatory factors that could adversely affect brain function. We hypothesized that eliciting food allergy in experimental animals would result in behavioral changes accompanied by mast cell accumulation in the brain...
April 23, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29678176/prenatal-and-early-life-diesel-exhaust-exposure-causes-autism-like-behavioral-changes-in-mice
#19
Yu-Chi Chang, Toby B Cole, Lucio G Costa
BACKGROUND: Escalating prevalence of autism spectrum disorders (ASD) in recent decades has triggered increasing efforts in understanding roles played by environmental risk factors as a way to address this widespread public health concern. Several epidemiological studies show associations between developmental exposure to traffic-related air pollution and increased ASD risk. In rodent models, a limited number of studies have shown that developmental exposure to ambient ultrafine particulates or diesel exhaust (DE) can result in behavioral phenotypes consistent with mild ASD...
April 20, 2018: Particle and Fibre Toxicology
https://www.readbyqxmd.com/read/29668850/altered-neocortical-gene-expression-brain-overgrowth-and-functional-over-connectivity-in-chd8-haploinsufficient-mice
#20
Philipp Suetterlin, Shaun Hurley, Conor Mohan, Kimberley L H Riegman, Marco Pagani, Angela Caruso, Jacob Ellegood, Alberto Galbusera, Ivan Crespo-Enriquez, Caterina Michetti, Yohan Yee, Robert Ellingford, Olivier Brock, Alessio Delogu, Philippa Francis-West, Jason P Lerch, Maria Luisa Scattoni, Alessandro Gozzi, Cathy Fernandes, M Albert Basson
Truncating CHD8 mutations are amongst the highest confidence risk factors for autism spectrum disorder (ASD) identified to date. Here, we report that Chd8 heterozygous mice display increased brain size, motor delay, hypertelorism, pronounced hypoactivity, and anomalous responses to social stimuli. Whereas gene expression in the neocortex is only mildly affected at midgestation, over 600 genes are differentially expressed in the early postnatal neocortex. Genes involved in cell adhesion and axon guidance are particularly prominent amongst the downregulated transcripts...
April 13, 2018: Cerebral Cortex
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