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Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. [1] It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant – alters the normal activity of the nervous system in such a ...
The magnitude of ethanol neurotoxicity in fetuses leading to fetal alcohol syndrome has been shown to be dependent on antioxidant levels in the brain such as vitamin E. [108] As the fetal brain is relatively fragile and susceptible to induced stresses, severe deleterious effects of alcohol exposure can be seen in important areas such as the ...
The effects of early-life exposures to anesthesia on the brain in humans are controversial. Evidence from nonhuman primate research suggests significant developmental neurotoxicity and long-term social impairment, with a dose–response relationship where repeated exposures cause a more severe impact than single ones.
The cerebral atrophy that alcoholics often present with is due to alcohol induced neurotoxicity. [7] [11] Evidence of neurodegeneration can be supported by an increased microglia density and expression of proinflammatory cytokines in the brain. Animal studies find that heavy and regular binge drinking causes neurodegeneration in corticolimbic ...
[3] [4] Some research suggests that serotonergic neurotoxicity might represent neuroadaptive mechanisms rather than neuronal damage per se. [5] [6] Dopaminergic neurotoxins can induce a Parkinson's disease-like condition in animals and humans. [1] [7] Serotonergic neurotoxins have been associated with cognitive and memory deficits and ...
Olney's lesions, also known as NMDA receptor antagonist neurotoxicity (NAT), is a form of brain damage consisting of selective death of neurons but not glia, observed in restricted brain regions of rats and certain other animal models exposed to large quantities of psychoactive drugs that inhibit the normal operation of the neuronal NMDA receptor.
The presence of neurofibrillary tangles in the brain is one of the key hallmarks of Alzheimer’s disease. These irregular clumps of protein are closely associated with disease progression.
[18] [37] It has been shown, in vivo, that supplementing with pyridoxal or pyridoxal phosphate increases pyridoxine concentrations in humans, meaning there are metabolic pathways from each vitamer of B 6 to the all other forms. [38] [39] Consuming high amounts of vitamin B 6 from food has not been reported to cause adverse effects. [24] [30] [40]