Apoptosis

A form of programmed cell death that begins when a cell receives internal or external signals, then proceeds through a series of characteristic stages typically including rounding-up of the cell, retraction of pseudopods, reduction of cellular volume (pyknosis), chromatin condensation, nuclear fragmentation (karyorrhexis), and plasma membrane blebbing, and ends with the death of the cell. – NCI Thesaurus, U.S. National Cancer Institute

Antioxidant / Apoptosis / GI / Mercury / Neuroinflammation / Neurons / Vagus Nerve

Methylmercury Interactions With Gut Microbiota and Potential Modulation of Neurogenic Niches in the Brain

Excerpt:
“Accumulating evidence implies the gut-brain axis as a pathway for MeHg harmful neurotoxic effects and a potential factor for later neurodegenerative disorders. The MeHg may induce a hormesis-related neuronal toxicity. Hormesis is an important redox dependent aging-associated neurodegenerative/ neuroprotective issue (Calabrese et al., 2010). The use of antioxidants, such as plant polyphenols (Calabrese et al., 2010; Leri et al., 2020) and protective nutrients (Oria et al., 2020) may be beneficial in reducing the MeHg-driven neuroinflammatory state and associated cell death with the interplay of the intestinal microbiota.”

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  • November 3, 2020
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
Apoptosis / Thimerosal

Effect of Thimerosal on the Neurodevelopment of Premature Rats.

CONCLUSIONS:
The negative adverse consequences on neurodevelopment observed in the present study are consistent with previous studies; this study raised serious concerns about adverse neurodevelopmental disorder such as autism in humans following the ongoing worldwide routine administration of thimerosal containing vaccines to infants.

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  • November 15, 2013
Adjuvant / Aluminum / Apoptosis / Hepatitis B Vaccine / Mitochondria / Toxicants / Vaccine adverse events

Hepatitis B vaccine induces apoptotic death in Hepa1-6 cells

Excerpt:
‘We conclude that exposure of Hepa1-6 cells to a low dose of adjuvanted hepatitis B vaccine leads to loss of mitochondrial integrity, apoptosis induction, and cell death, apoptosis effect was observed also in C2C12 mouse myoblast cell line after treated with low dose of vaccine (0.3, 0.1, 0.05 μg/ml).”

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  • January 17, 2012
Adjuvant / Aluminum / Apoptosis / Astrocytes / Inflammation / Neurons / Toxicants

Aluminum adjuvant linked to Gulf War illness induces motor neuron death in mice

Excerpt:
“Significant cognitive deficits in water-maze learning were observed in the combined aluminum and squalene group (4.3 errors per trial) compared with the controls (0.2 errors per trial) after 20 wk. Apoptotic neurons were identified in aluminum-injected animals that showed significantly increased activated caspase-3 labeling in lumbar spinal cord (255%) and primary motor cortex (192%) compared with the controls. Aluminum-treated groups also showed significant motor neuron loss (35%) and increased numbers of astrocytes (350%) in the lumbar spinal cord. The findings suggest a possible role for the aluminum adjuvant in some neurological features associated with GWI and possibly an additional role for the combination of adjuvants.”

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  • February 20, 2007
Aluminum / Apoptosis / Genes / Inflammation / Neuroinflammation / NF-KappaB / Toxicants

Nanomolar aluminum induces pro-inflammatory and pro-apoptotic gene expression in human brain cells in primary culture

Excerpt:
“The promoters of genes up-regulated by aluminum are enriched in binding sites for the stress-inducible transcription factors HIF-1 and NF-kappaB, suggesting a role for aluminum, HIF-1 and NF-kappaB in driving atypical, pro-inflammatory and pro-apoptotic gene expression. The effect of aluminum on specific stress-related gene expression patterns in human brain cells clearly warrant further investigation.”

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  • September 20, 2005

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