Organophosphate-induced brain damage: Mechanisms, neuropsychiatric and neurological consequences, and potential therapeutic strategies

Organophosphate (OP)-induced brain damage is defined as progressive damage to the brain, resulting from the cholinergic neuronal excitotoxicity and dysfunction induced by OP-induced irreversible AChE inhibition. This delayed secondary neuronal damage that occurs mainly in the cholinergic regions of...

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Bibliographic Details
Published in:Neurotoxicology (Park Forest South) Vol. 33; no. 3; pp. 391 - 400
Main Author: Chen, Yun
Format: Journal Article
Language:English
Published: Amsterdam Elsevier B.V 01.06.2012
Elsevier
Subjects:
Acetylcholinesterase
Acetylcholinesterase - metabolism
Animals
Antidotes - therapeutic use
Biological and medical sciences
Brain - drug effects
Brain - enzymology
Brain - pathology
Brain - physiopathology
Cholinergic neuronal excitotoxicity
Cholinesterase Inhibitors - poisoning
Excitatory Amino Acid Antagonists - therapeutic use
Humans
Medical sciences
Nerve agents
Neurological impairments
Neuroprotective Agents - therapeutic use
Neuroprotective strategies
Neuropsychiatric disorders
Neurotoxicity Syndromes - diagnosis
Neurotoxicity Syndromes - enzymology
Neurotoxicity Syndromes - etiology
Neurotoxicity Syndromes - physiopathology
Neurotoxicity Syndromes - psychology
Neurotoxicity Syndromes - therapy
Organophosphate Poisoning
Organophosphates
Secondary neuronal damage
Toxicology
Treatment Outcome
Neuroprotective strategies
Neuropsychiatric disorders
Secondary neuronal damage
Acetylcholinesterase
Nerve agents
Cholinergic neuronal excitotoxicity
Neurological impairments
Organophosphates
Neuroprotection
Toxicity
Nervous system
Esterases
Mechanism of action
Nervous system diseases
Secondary
Enzyme
Neuroprotective agent
Carboxylic ester hydrolases
Cerebral disorder
Toxin
Neuron
Treatment
Central nervous system disease
Neurotoxin
Mental disorder
Hydrolases
Organophosphorus compounds
Lesion
ISSN:0161-813X, 1872-9711, 1872-9711
Online Access:Get full text
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Summary:Organophosphate (OP)-induced brain damage is defined as progressive damage to the brain, resulting from the cholinergic neuronal excitotoxicity and dysfunction induced by OP-induced irreversible AChE inhibition. This delayed secondary neuronal damage that occurs mainly in the cholinergic regions of the brain that contain dense accumulations of cholinergic neurons and the majority of cholinergic projection, might be largely responsible for persistent profound neuropsychiatric and neurological impairments (memory, cognitive, mental, emotional, motor and sensory deficits) in the victims of OP poisoning. Neuroprotective strategies for attenuating OP-induced brain damage should target different development stages of OP-induced brain damage, and may include but not limited to: (1) Antidote therapies with atropine and related efficient anticholinergic drugs; (2) Anti-excitotoxic therapies targeting attenuation of cerebral edema and inflammatory reaction, blockage of calcium influx, inhibition of apoptosis program, and the control of seizures; (3) Neuroprotective strategies using cytokines, antioxidants and NMDAR antagonists (a single drug or a combination of drugs) to slow down the process of secondary neuronal damage; and (4) Therapies targeting individual symptoms or clusters of chronic neuropsychiatric and neurological symptoms. These neuroprotective strategies may help limit or prevent secondary neuronal damage at the early stage of OP poisoning and attenuate the subsequent neuropsychiatric and neurological impairments, thus reducing the long-term disability caused by exposure to OPs.
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ISSN:0161-813X
1872-9711
1872-9711
DOI:10.1016/j.neuro.2012.03.011