20 Papers

20 Papers / ASD Subtypes / Autism Biomarkers / Autoimmunity / Genes / GI / Glial Cells / Immune / Neuroinflammation / Post-mortem / Review

Neuroinflammation and autism: toward mechanisms and treatments

Excerpts:

“In our clinical work and review of the literature, we have been impressed by the possible role of autoimmune disorders as influencing the pathophysiology of a distinct, objectively defined etiologic subtype of ASDs.”

“The notion that environmental factors contribute to ASD prevalence continues to evolve. Once-influential theories suggesting links among exposure to vaccines containing attenuated virus or toxins, conditions such as inflammatory bowel disease, and ASDs have fallen from favor since the retraction of a key study (Wakefield et al, 1998). It is important to emphasize, however, that the major reason for retraction was poor scientific method rather than theoretical flaws. Although ASDs are currently within the realm of psychiatrists and neurologists, it is becoming clear that at least some subtypes represent whole-body disorders, offering exciting new possibilities for therapy.”

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  • November 13, 2012
20 Papers / Acetaminophen / Adjuvant / Aluminum / CDC / Fever / Glutathione / Immune / Measles / Mercury / MMR / Review / Toxicants / Vaccine adverse events

Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure

Excerpt:
“We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever.”

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  • November 7, 2012
20 Papers / Cytokines / Genes / IL-1β / IL-4 / IL-6 / Immune / Review / Toxicants

Cytokine dysregulation in autism spectrum disorders (ASD): Possible role of the environment

Abstract

Autism spectrum disorders (ASD) are neurodevelopmental diseases that affect an alarming number of individuals. The etiological basis of ASD is unclear, and evidence suggests it involves both genetic and environmental factors. There are many reports of cytokine imbalances in ASD. These imbalances could have a pathogenic role, or they may be markers of underlying genetic and environmental influences. Cytokines act primarily as mediators of immunological activity, but they also have significant interactions with the nervous system. They participate in normal neural development and function, and inappropriate activity can have a variety of neurological implications. It is therefore possible that cytokine dysregulation contributes directly to neural dysfunction in ASD. Further, cytokine profiles change dramatically in the face of infection, disease, and toxic exposures. Therefore, imbalances may represent an immune response to environmental contributors to ASD. The following review is presented in two main parts. First, we discuss select cytokines implicated in ASD, including IL-1Β, IL-6, IL-4, IFN-γ, and TGF-Β, and focus on their role in the nervous system. Second, we explore several neurotoxic environmental factors that may be involved in the disorders, and focus on their immunological impacts. This review represents an emerging model that recognizes the importance of both genetic and environmental factors in ASD etiology. We propose that the immune system provides critical clues regarding the nature of the gene by environment interactions that underlie ASD pathophysiology.

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  • August 17, 2012
20 Papers / 3 Studies / Adjuvant / Aluminum / Autoimmunity / Immune / Toxicants / Vaccine Schedule

Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?

Excerpt:
“Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r=0.92, p<0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3-4months of age (Pearson r=0.89-0.94, p=0.0018-0.0248). The application of the Hill's criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal."

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  • August 23, 2011
20 Papers / Encephalopathy / Parental reports / Review / VICP

Unanswered Questions: A Review of Compensated Cases of Vaccine-Induced Brain Injury

Excerpts:
“This empirical investigation, published in a peer-reviewed law journal, examines claims that the VICP compensated for vaccine-induced encephalopathy and seizure disorder. The VICP has compensated approximately 2,500 claims of vaccine injury since the inception of the program. This study found 83 cases of acknowledged vaccine-induced brain damage that include autism, a disorder that affects speech, social communication and behavior.”

“This finding of autism in compensated cases of vaccine injury is significant. U.S. government spokespeople have been asserting no vaccine-autism link for more than a decade. This finding calls into question the decisions of the Court of Federal Claims in the Omnibus Autism Proceeding in 2009 and 2010 and the statement of Health and Human Services on its website that “HHS has never concluded in any case that autism was caused by vaccination.”

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  • January 23, 2011
20 Papers / Antioxidant / Dendritic cells / Glial Cells / Glutamate / Lipids / Oxidative Stress / Purkinje cells / Regression / Review / ROS

The Neurobiology of Autism

Exceprts:
We also discuss evidence implicating oxidative stress, neuroglial activation and neuroimmunity in autism.

“Oxidative stress is another possible cause of Purkinje cell loss and other neuroanatomical changes described in autistic brains (reviewed in (37, 113)). Oxidative stress occurs when the levels of reactive oxygen species exceed the antioxidant capacities of a cell, often leading to cell death. Because of its very high oxygen demands and limited anti-oxidant capacity, the brain is thought to be relatively vulnerable to oxidative stress (111). Several studies have shown decreased levels of antioxidants such as superoxide dismutase, transferrin and ceruloplasmin in the blood or serum of patients with ASD (38, 108, 222). Significant elevations in biomarker profiles indicating increased oxidative stress, such as increased lipid peroxidation, have also been documented in autism (38, 107, 229).Interestingly, in one report the alterations in antioxidant proteins were linked specifically to regressive autism, suggesting a postnatal environmental effect (38). Polymorphisms in metabolic pathway genes may contribute to the increased oxidative stress in autism (108). Advanced glycationend products have also been reported to be elevated in both the brain tissue and serum of autistic patients, a change which can also lead to increased oxidative damage (23,110).”

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  • October 17, 2007
20 Papers / Genes / GI / Immune / Inflammation / Neuroinflammation / Review

Autism: A brain disorder or a disorder that affects the brain?

Abstract

Autism is defined behaviorally, as a syndrome of abnormalities involving language, social reciprocity and hyperfocus or reduced behavioral flexibility. It is clearly heterogeneous, and it can be accompanied by unusual talents as well as by impairments, but its underlying biological and genetic basis in unknown. Autism has been modeled as a brain-based, strongly genetic disorder, but emerging findings and hypotheses support a broader model of the condition as a genetically influenced and systemic. These include imaging, neuropathology and psychological evidence of pervasive (and not just specific) brain and phenotypic features; postnatal evolution and chronic persistence of brain, behavior and tissue changes (e.g. inflammation) and physical illness symptomatology (e.g. gastrointestinal, immune, recurrent infection); overlap with other disorders; and reports of rate increases and improvement or recovery that support a role for modulation of the condition by environmental factors (e.g. exacerbation or triggering by toxins, infectious agents, or others stressors, or improvement by treatment). Modeling autism more broadly encompasses previous work, but also encourages the expansion of research and treatment to include intermediary domains of molecular and cellular mechanisms, as well as chronic tissue, metabolic and somatic changes previously addressed only to a limited degree. The heterogeneous biologies underlying autism may conceivably converge onto the autism profile via multiple mechanisms on the one hand and processing and connectivity abnormalities on the other may illuminate relevant final common pathways and contribute to focusing on the search for treatment targets in this biologically and etiologically heterogeneous behavioral syndrome.

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  • December 1, 2006
20 Papers / Encephalopathy / Immune / Mercury / Review / Thimerosal / Toxicants / Vaccine adverse events / Vaccine Schedule

Neurological adverse events associated with vaccination

Excerpt:
“Among the “major” neurological complications, usually manifesting more than 48 hours after vaccination and which might be the cause of permanent damage to the central nervous system (CNS), the following are listed: seizures – especially if there is no increase in body temperature, hypotonic-hyporesponsive episodes, postvaccinal encephalitis, postvaccinal encephalopathy [6, 8-11] and autism [10, 12-14].”

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  • June 24, 2002

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