Neuroglial activation and neuroinflammation in the brain of patients with autism

By D. Vargas, C. Nascimbene, C. Krishnan, A. Zimmerman, C. Pardo. Annals of Neurology, 2005

2,160 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Genetics, Neurology

View Paper: https://www.semanticscholar.org/paper/9ef2056c187cc47843d8493c7c391e6d34ec140b

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Citations in the corpus

Mapping early brain development in autism. (2007, neutral): “Vargas et al. (2005) reported glial activation and pro-and anti-inﬂammatory molecules in frontal cortex.”
Elevated Immune Response in the Brain of Autistic Patients (2009, background): “However, there is only one study that has been conducted to investigate the inflammatory cytokine profile in the brain of autistic patients using protein arrays (Vargas et al, 2005).”
Microglial activation and increased microglial density observed in the dorsolateral prefrontal cortex in autism. (2010, background): “Recently, a single study has qualitatively reorted microglial and astroglial activation in the cerebellum and nterior cingulate and middle frontal gyri (7).”
Autism risk factors: genes, environment, and gene-environment interactions (2012, background): “Another study consistently reported microglial activation in the dorsolateral prefrontal cortex in brains of patients with ASD.68 This neuroglial response may result from either a primary disturbance of neuroglial function or unknown factors that disturb prenatal or postnatal CNS development.”
Consensus Paper: Pathological Role of the Cerebellum in Autism (2012, background): “One striking feature is the presence of ongoing neuroinflammation in postmortem brain tissue from individuals with AD, a finding that is consistent over a broad age range (5–44 years of age) [73].”
The role of immune dysfunction in the pathophysiology of autism (2011, positive): “These findings include prominent microglia activation and, increased inflammatory cytokine and chemokine production, including interferon (IFN)-c, IL-1b, IL-6, IL-12p40, tumor necrosis factor (TNF)-a and chemokine C–C motif ligand (CCL)-2 in the brain tissue and cerebral spinal fluid (Li et al., 200”
Elevated plasma cytokines in autism spectrum disorders provide evidence of immune dysfunction and are associated with impaired behavioral outcome (2010, background): “creased IL-8 levels, a chemoattractant cytokine important in inflammatory process, a finding that corresponds to similar increases of IL-8 seen in the brain and CSF of individuals with ASD (Vargas et al., 2005; Li et al., 2009).”
Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012, neutral): “Taken together, thesedatademonstrate that phagocytic signaling through CR3 and its ligand C3 is one molecular mechanism by which microglia engulf RGC inputs.”
The complement system: an unexpected role in synaptic pruning during development and disease. (2012, background): “…tissue have suggested that abnormal microglial function and/or complement cascade activation may play a role in autism and psychiatric disorders such as schizophrenia (Pardo et al. 2005, Vargas et al. 2005, Hashimoto 2008, Monji et al. 2009, Chen et al. 2010, Morgan et al. 2010, Havik et al. 2011).”
Early behavioral intervention, brain plasticity, and the prevention of autism spectrum disorder (2008, background): “…affecting gray matter at an early age, that may reflect reduced synapse density perhaps secondary to migratory/apoptotic abnormalities (Fatemi & Halt, 2001), column density/packing abnormalities (Casanova, 2004) and/or active processes such as reactive gliosis and edema (Vargas et al., 2005).”
High intelligence: A risk factor for psychological and physiological overexcitabilities (2018, background): “Vargas et al. (2005) investigated the presence of immune activation in postmortem brain specimens and CSF from subjects with autism.”
Advancing the understanding of autism disease mechanisms through genetics (2016, neutral): “Neuropathological and positron emission tomography (PET) imaging studies have identified microglial infiltration and activation in the frontal, prefrontal, cingulate, frontoinsular and visual cortices and in the cerebellum 217–220 .”
The epidemiology of autism spectrum disorders. (2007, positive): “Postmortem central nervous sytstem tissue from individuals with autism shows evidence of innate immune system abnormalities, particularly in the cerebellum, which are thought to represent a chronic inflammatory process (171).”