Glial Cells

(neuroglia) Any of the cells that hold nerve cells in place and help them work the way they should. The types of neuroglia include oligodendrocytes, astrocytes, microglia, and ependymal cells. – U.S. National Cancer Institute

20 Papers / 3 Studies / Adjuvant / Aluminum / Autophagy / Blood brain barrier / Cytokines / Dendritic cells / Genes / Glial Cells / IL-6 / Immune / Inflammation / Neuroinflammation / Oxidative Stress / Review / Toxicants

Inflammation and Autophagy: A Convergent Point between Autism Spectrum Disorder (ASD)-Related Genetic and Environmental Factors: Focus on Aluminum Adjuvants

Excerpts:
“As a result of these pieces of evidence (epidemiological, clinical and preclinical data) pointing to a potential causal association between early ABA (aluminum-based adjuvants) exposure and increased ASD risk, new hypotheses regarding neurological and immunological consequences of ABA-containing vaccines and novel clinical strategies (i.e., postponing of ABA-containing vaccines and replacement of ABAs with calcium phosphate are now being considered.“

“Our review presents the lack of fundamental scientific data demonstrating that Al adjuvants are safe and do not induce any long-term side effects. It also supports further investigation related to the effects of early Al adjuvant exposures occurring in combination with genetic susceptibility factors, including autophagy, immune and inflammation process genes. As accumulating evidence shows that modulating the levels of autophagy may increase the risk of NDDs, such studies will elucidate a new etiology for these complex disorders and contribute to develop potential new diagnostic and therapeutic tools.”

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  • August 31, 2022
Glial Cells / Immune / Males / Mitochondria / TSPO

[11C]PBR28 MR–PET imaging reveals lower regional brain expression of translocator protein (TSPO) in young adult males with autism spectrum disorder

Press Release from Harvard Magazine:

“Inflammation link for autism
A neuroimaging study has shown that the brains of young men with autism spectrum disorder have low levels of translocator protein, a substance that appears to play a role in inflammation and metabolism.

This discovery by a team of HMS researchers at Massachusetts General Hospital provides an important insight into the possible origins of autism spectrum disorder.

This developmental disorder, which affects one in fifty-nine children in the United States, emerges in early childhood and is characterized by difficulty communicating and interacting with others. Although the cause is unknown, growing evidence has linked it to neuroinflammation.

One sign of neuroinflammation is elevated levels of translocator protein, which can be measured in the brain using positron-emission tomography and anatomic magnetic resonance imaging.

The research team used these imaging tools to scan the brains of fifteen young adult males with the disorder. The group included both high- and low-functioning participants with varying degrees of intellectual ability. As a control, the team scanned the brains of eighteen non-autistic young men of similar age.

The scans showed that the brains of the young men with the disorder had lower levels of the protein, compared with the brains of non-autistic participants. In fact, those participants with the most severe symptoms of the disorder tended to have the lowest expression of the protein.

The brain regions found to have low expression of the protein have previously been linked to autism spectrum disorder and are thought to govern social and cognitive capacities such as processing emotions, interpreting facial expressions, and empathy.

The researchers point out that the translocator protein has multiple complex roles, some of which promote brain health. Adequate levels of the protein are, for example, necessary for normal functioning of mitochondria. Earlier research has linked malfunctioning mitochondria in brain cells to autism spectrum disorder.

Zürcher NR et al., Molecular Psychiatry, February 2020

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  • February 19, 2020
Aluminum / Astrocytes / Glial Cells / Inflammation / Lymphocytes / Neuroinflammation

Intracellular Aluminium in Inflammatory and Glial Cells in Cerebral Amyloid Angiopathy: A Case Report

Discussion: The observation of predominantly intracellular aluminium in these tissues was novel and something similar has only previously been observed in cases of autism. The results suggest a strong inflammatory component in this case and support a role for aluminium in this rare and unusual case of CAA.

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  • April 24, 2019
20 Papers / Aluminum / CRPS / Cytokines / Fever / Glial Cells / HPV vaccine / IL-1β / IL-6 / Immune / Inflammation / Mercury / Neuroinflammation / Review / ROS / TNF-α / Vaccine adverse events

Post-vaccination inflammatory syndrome: a new syndrome

Except:
“There is a growing body of work to support the role of inflammatory cytokines in ASD. An emerging focus of research into the etiology of ASD has suggested neuroinflammation as one of the major candidates underlying the biologica model [5]. Plasma levels of IL-1β, IL-6 and IL-8 were increased in children with ASD and correlated with regressive autism, as well as impaired communication and aberrant behavior [6-8]. Vargas [9] showed an active neuroinflammatory process in the cerebral cortex, white matter, and in the cerebellum of autistic patients. Immunocytochemichal studies showed marked activation of microglia [5].”

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  • January 1, 2019
Aluminum / Genes / Glial Cells / Inflammation

Aluminium in brain tissue in autism

Abstract
Autism spectrum disorder is a neurodevelopmental disorder of unknown aetiology. It is suggested to involve both genetic susceptibility and environmental factors including in the latter environmental toxins. Human exposure to the environmental toxin aluminium has been linked, if tentatively, to autism spectrum disorder. Herein we have used transversely heated graphite furnace atomic absorption spectrometry to measure, for the first time, the aluminium content of brain tissue from donors with a diagnosis of autism. We have also used an aluminium-selective fluor to identify aluminium in brain tissue using fluorescence microscopy. The aluminium content of brain tissue in autism was consistently high. The mean (standard deviation) aluminium content across all 5 individuals for each lobe were 3.82(5.42), 2.30(2.00), 2.79(4.05) and 3.82(5.17) μg/g dry wt. for the occipital, frontal, temporal and parietal lobes respectively. These are some of the highest values for aluminium in human brain tissue yet recorded and one has to question why, for example, the aluminium content of the occipital lobe of a 15 year old boy would be 8.74 (11.59) μg/g dry wt.? Aluminium-selective fluorescence microscopy was used to identify aluminium in brain tissue in 10 donors. While aluminium was imaged associated with neurones it appeared to be present intracellularly in microglia-like cells and other inflammatory non-neuronal cells in the meninges, vasculature, grey and white matter. The pre-eminence of intracellular aluminium associated with non-neuronal cells was a standout observation in autism brain tissue and may offer clues as to both the origin of the brain aluminium as well as a putative role in autism spectrum disorder.

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  • March 18, 2018
20 Papers / Adjuvant / Aluminum / Apoptosis / COMT / Cytokines / Dendritic cells / Detoxification / Genes / GI / Glial Cells / Glutathione / Immune / Inflammation / Mercury / Methionine / Methylation / Mitochondria / MTHFR / Neuroinflammation / Neurons / Oxidative Stress / Pregnancy / Review / Seizure / Thimerosal / Toxicants / Transsulfuration

Autism is an Acquired Cellular Detoxification Deficiency Syndrome with Heterogeneous Genetic Predisposition

Excerpt:
“The literature strongly supports that autism is most accurately seen as an acquired cellular detoxification deficiency syndrome with heterogeneous genetic predisposition that manifests pathophysiologic consequences of accumulated, run-away cellular toxicity. At a more general level, it is a form of a toxicant-induced loss of tolerance of toxins, and of chronic and sustained ER overload (“ER hyperstress”), contributing to neuronal and glial apoptosis via the unfolded protein response (UPR). Inherited risk of impaired cellular detoxification and circulating metal re-toxification in neurons and glial cells accompanied by chronic UPR is key.”

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  • March 16, 2018
Adjuvant / Aluminum / Cytokines / Genes / Glial Cells / Glutathione / Inflammation / Mitochondria / Oxidative Stress

The putative role of environmental aluminium in the development of chronic neuropathology in adults and children. How strong is the evidence and what could be the mechanisms involved?

Abstract
The conceptualisation of autistic spectrum disorder and Alzheimer’s disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant. Such administration has the potential to induce pathology via several routes such as provoking dysfunction and/or activation of glial cells which play an indispensable role in the regulation of central nervous system homeostasis and neurodevelopment. Other routes include the generation of oxidative stress, depletion of reduced glutathione, direct and indirect reductions in mitochondrial performance and integrity, and increasing the production of proinflammatory cytokines in both the brain and peripherally. The mechanisms whereby environmental aluminium could contribute to the development of the highly specific pattern of neuropathology seen in Alzheimer’s disease are described. Also detailed are several mechanisms whereby significant quantities of aluminium introduced via immunisation could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminium salts in immunisations should be discontinued and that adults should take steps to minimise their exposure to environmental aluminium.

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  • July 27, 2017
20 Papers / 3 Studies / Adjuvant / ASD Subtypes / Astrocytes / Cytokines / Detoxification / Endothelial Cells / Genes / Glial Cells / Glutathione / HLA / Immune / Inflammation / Males / Mercury / Mitochondria / Oxidative Stress / Sulfhydryl Groups / Thimerosal / Toxicants

The Putative Role of Environmental Mercury in the Pathogenesis and Pathophysiology of Autism Spectrum Disorders and Subtypes

Excerpt:
“Environmental mercury is neurotoxic at doses well below the current reference levels considered to be safe, with evidence of neurotoxicity in children exposed to environmental sources including fish consumption and ethylmercury-containing vaccines. Possible neurotoxic mechanisms of mercury include direct effects on sulfhydryl groups, pericytes and cerebral endothelial cells, accumulation within astrocytes, microglial activation, induction of chronic oxidative stress, activation of immune-inflammatory pathways and impairment of mitochondrial functioning. (Epi-)genetic factors which may increase susceptibility to the toxic effects of mercury in ASD include the following: a greater propensity of males to the long-term neurotoxic effects of postnatal exposure and genetic polymorphisms in glutathione transferases and other glutathione-related genes and in selenoproteins. Furthermore, immune and inflammatory responses to immunisations with mercury-containing adjuvants are strongly influenced by polymorphisms in the human leukocyte antigen (HLA) region and by genes encoding effector proteins such as cytokines and pattern recognition receptors. Some epidemiological studies investigating a possible relationship between high environmental exposure to methylmercury and impaired neurodevelopment have reported a positive dose-dependent effect.”

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  • July 22, 2017
Glial Cells / Males / Neurons / Toxicants

Gestational Exposure to Air Pollution Alters Cortical Volume, Microglial Morphology, and Microglia-Neuron Interactions in a Sex-Specific Manner

Excerpts:

“…several large scale epidemiological studies have recently linked prenatal air pollution exposure with an increased risk of neurodevelopmental disorders such as autism spectrum disorder (ASD).”

“We have demonstrated that prenatal exposure to DEP in mice, i.e., to the pregnant dams throughout gestation, results in a persistent vulnerability to behavioral deficits in adult offspring, especially in males, which is intriguing given the greater incidence of ASD in males to females (∼4:1).”

“DEP exposure increased inflammatory cytokine protein and altered the morphology of microglia, consistent with activation or a delay in maturation, only within the embryonic brains of male mice…”

“Consistent with this hypothesis, we found increased microglial-neuronal interactions in male offspring that received DEP compared to all other groups. Taken together, these data suggest a mechanism by which prenatal exposure to environmental toxins may affect microglial development and long-term function, and thereby contribute to the risk of neurodevelopmental disorders.”

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  • May 31, 2017

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