Microglia in the pathogenesis of autism spectrum disorders

@article{Koyama2015MicrogliaIT,
  title={Microglia in the pathogenesis of autism spectrum disorders},
  author={Ryuta Koyama and Yuji Ikegaya},
  journal={Neuroscience Research},
  year={2015},
  volume={100},
  pages={1-5}
}

Figures from this paper

Microglia as possible therapeutic targets for autism spectrum disorders.
Deficient autophagy in microglia impairs synaptic pruning and causes social behavioral defects
TLDR
It is shown that deletion of atg7 from myeloid cell-specific lysozyme M-Cre mice resulted in social behavioral defects and repetitive behaviors, characteristic features of ASDs, and the role of microglial autophagy in the regulation of the synapse and neurobehaviors is shown.
Microbiota and Microglia Interactions in ASD
TLDR
It is demonstrated how pre- and postnatal environmental stimuli can modulate microglial cell phenotype and function, underpinning the notion that reciprocal interactions between microglia and intestinal microbes could play a crucial role in ASD aetiology.
Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS.
TLDR
An overview of how the field of activity-dependent pruning research has evolved, led to exciting new questions and guided the identification of new, therapeutically relevant mechanisms that result in aberrant circuit development in neurodevelopmental disorders is given.
Involvement of Neuroinflammation during Brain Development in Social Cognitive Deficits in Autism Spectrum Disorder and Schizophrenia
  • Y. Nakagawa, K. Chiba
  • Psychology, Biology
    The Journal of Pharmacology and Experimental Therapeutics
  • 2016
TLDR
The brain aberration in ASD and schizophrenia is summarized and a possible mechanism underlying social cognitive deficits in these disorders based on their distinct ages of onset is provided.
Neuroimmune and Inflammatory Signals in Complex Disorders of the Central Nervous System
TLDR
This review discusses the ability of the early developing brain to respond to a focal lesion with a rapid compensatory plasticity of intact axons and the role of microglial activation and proinflammatory cytokines in brain repair and the involvement of neuroinflammatory conditions that alter neuroimmune interactions in four different pathologies.
Brain Fires in Autism Spectrum Disorders
TLDR
It is reported that the elevated blood levels of two inflammatory molecules, IL-6 and TNF, identify a subgroup of children with ASD, who benefit most from a promising treatment with the natural flavonoid luteolin that combats brain inflammation.
Microglia Gone Rogue: Impacts on Psychiatric Disorders across the Lifespan
TLDR
Taking into account the recent identification of microglia-specific markers, and the availability of compounds that target these cells selectively in vivo, the prospect of disease intervention via the microglial route is considered.
GABA and Glutamate Imbalance in Autism and Their Reversal as Novel Hypothesis for Effective Treatment Strategy
TLDR
It is hypothesized that an integrated treatment strategy with GABA supplements, regulation of chloride and magnesium levels, vitamin D supplements, probiotics to enhance GABAA receptor and glutamate decarboxylase (GAD) expression, and memantine to activate glutamate transporters and inhibit NMDA receptors, could collectively reduce glutamate levels, maintain functional GABA receptors and thus treat repetitive behavior, impaired social behavior, and seizure activity in individuals with autism.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 48 REFERENCES
Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior
TLDR
It is shown that deficient synaptic pruning is associated with weak synaptic transmission, decreased functional brain connectivity, deficits in social interaction and increased repetitive-behavior phenotypes that have been previously associated with autism and other neurodevelopmental and neuropsychiatric disorders.
Synaptic Pruning by Microglia Is Necessary for Normal Brain Development
TLDR
It is shown that microglia actively engulf synaptic material and play a major role in synaptic pruning during postnatal development in mice and this work suggests that deficits in microglian function may contribute to synaptic abnormalities seen in some neurodevelopmental disorders.
Genetic Controls Balancing Excitatory and Inhibitory Synaptogenesis in Neurodevelopmental Disorder Models
TLDR
The current effort is to define the cascade of events linking transcription, translation and the role of specific synaptic proteins in the maintenance of excitatory versus inhibitory synapses during neural circuit formation, including mechanisms that fine-tune excitation and inhibition during the refinement of functional synaptic circuits, and later modulate this balance throughout life.
Hyperactivity of Newborn Pten Knock-out Neurons Results from Increased Excitatory Synaptic Drive
TLDR
It was determined that increased synaptic drive was sufficient to drive hypertrophic Pten knock-out neurons beyond their altered action potential threshold, and this work contributes a developmental mechanism for the increased activity of Pten-depleted neurons.
Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits
Maternal immune activation and abnormal brain development across CNS disorders
TLDR
The emerging evidence that mIA is a shared environmental risk factor across CNS disorders that varies as a function of interactions between genetic and additional environmental factors is critically reviewed.
The Emerging Biology of Autism Spectrum Disorders
Expression patterns of the diverse genes disrupted in autism spectrum disorders in the developing brain give a fresh perspective on the underlying biology. Autism spectrum disorders (ASD) are a
Neuroglial activation and neuroinflammation in the brain of patients with autism
TLDR
It is indicated that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain.
Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression
TLDR
Treatment of IRSp53−/− mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist, normalized social interaction and suggested that deviation of NMDar function in either direction leads to social deficits and that correcting the deviation has beneficial effects.
...
1
2
3
4
5
...