Aβ was found manipulating the level of nicotine in the brain along with the MAP kinase, another signaling receptor, to cause cell death. An example is through the nicotinic acetylcholine receptor (nAchRs), which is a receptor commonly found along the surfaces of the cells that respond to nicotine stimulation, turning them on or off. Aβ uses several routes in the central nervous system to cause cell death. Thus they are left in the brain until they are broken down, but if enough accumulate, they form plaques which are toxic to neurons. Aβ results from a mutation that occurs when protein chains are cut at the wrong locations, resulting in chains of different lengths that are unusable. Neurotoxic agents Amyloid beta Īmyloid beta (Aβ) was found to cause neurotoxicity and cell death in the brain when present in high concentrations. Additionally, neurotoxicity has been found to be a major cause of neurodegenerative diseases such as Alzheimer's disease (AD). Some of the symptoms that result from cell death include loss of motor control, cognitive deterioration and autonomic nervous system dysfunction. When present in high concentrations, they can lead to neurotoxicity and death ( apoptosis). Some of the most common naturally occurring brain toxins that lead to neurotoxicity as a result of long term drug use are amyloid beta (Aβ), glutamate, dopamine, and oxygen radicals. In some cases the level or exposure-time may be critical, with some substances only becoming neurotoxic in certain doses or time periods. This may be due to the direct action of the substance, with the impairment and neurocognitive deficits being temporary, and resolving when the substance is eliminated from the body. The presence of neurocognitive deficits alone is not usually considered sufficient evidence of neurotoxicity, as many substances may impair neurocognitive performance without resulting in the death of neurons.
The term neurotoxicity implies the involvement of a neurotoxin however, the term neurotoxic may be used more loosely to describe states that are known to cause physical brain damage, but where no specific neurotoxin has been identified. All symptoms listed above are consistent with mold mycotoxin accumulation. Chronic mold exposure in homes can lead to neurotoxicity which may not appear for months to years of exposure. They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Symptoms may appear immediately after exposure or be delayed. Neurotoxicity can result from organ transplants, radiation treatment, certain drug therapies, recreational drug use, and exposure to heavy metals, bites from certain species of venomous snakes, pesticides, certain industrial cleaning solvents, fuels and certain naturally occurring substances. This can eventually disrupt or even kill neurons, which are cells that transmit and process signals in the brain and other parts of the nervous system. It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant– alters the normal activity of the nervous system in such a way as to cause permanent or reversible damage to nervous tissue. 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. ( August 2014) ( Learn how and when to remove this template message) Please help to improve this article by introducing more precise citations. This article includes a list of general references, but it lacks sufficient corresponding inline citations.
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