Mitochondria
Mitochondria
And
Neurological Disorders
And
The Human Mitochondrial Neurotoxin, Hexachlorophene
The purpose of this paper is to raise some questions. They are based on a review of the biomedical research on mitochondria, neurological disorders, and the human neurotoxin, hexachlorophene. The questions, based upon the review, are raised in the hope that those with more specific expertise will see the value of exploring the quite real possibility that brain imaging of those who were exposed to hexachlorophene may show a specific pattern of neurological abnormalities. Will these brain imaging results of adults who were exposed to hexachlorophene as babies correlate with the specific pattern of neurological abnormalities shown in autopsies of the babies who died after being exposed to hexachlorophene?
Some questions raised are these: Today, who has those hexachlorophene-related mitochondrial abnormalities? We know babies and children are more vulnerable because the skin is more permeable, but what are the other exposure vulnerabilities. Are they, for some, also caused by an interaction with their specific genetics? Could brain imaging show abnormalities in the myelin of the cerebellum and other areas of the brain that are characteristic of this particular mitochondrial neurotoxin? Is there sufficient evidence to go ahead and assess a possible causal relationship between specific behavioral symptoms related to structural and functional brain abnormalities? Could brain imaging show a relationship between therapeutic variables, behavioral symptoms, and changes in structural and functional brain abnormalities?
Other mitochondrial neurotoxins (for example, triethyltins, cuprizone, MPTP,3-NP) have been used as causal variables in model neurological disorders (for example, Huntington's, ALS, Parkinson's, etc.). Each of these neurotoxins have different neurological effects. For example, a recent study(Klivenyi,P 2005) contrasted the effects of the toxin model for Parkinson's(MPTP) and the toxin model for Huntington's(3-NP). Both mitochondrial neurotoxins caused changes in amino acids. But they caused two different amino acid neurotransmitter effects. It would seem quite reasonable that a similar research approach would show that hexachlorophene would result in a third specific amino acid neurotransmitter effect. We know it has its own neurological disorder pattern.
From the past epidemiological study of the autopsies of the babies, we already know that it is a specific human mitochondrial neurotoxin. Hexachlorophene's effects, now, can be studied in adults by means of brain imaging. It's an opportunity that wasn't there before; it's an opportunity we should take advantage of now.
And
Neurological Disorders
And
The Human Mitochondrial Neurotoxin, Hexachlorophene
The purpose of this paper is to raise some questions. They are based on a review of the biomedical research on mitochondria, neurological disorders, and the human neurotoxin, hexachlorophene. The questions, based upon the review, are raised in the hope that those with more specific expertise will see the value of exploring the quite real possibility that brain imaging of those who were exposed to hexachlorophene may show a specific pattern of neurological abnormalities. Will these brain imaging results of adults who were exposed to hexachlorophene as babies correlate with the specific pattern of neurological abnormalities shown in autopsies of the babies who died after being exposed to hexachlorophene?
Some questions raised are these: Today, who has those hexachlorophene-related mitochondrial abnormalities? We know babies and children are more vulnerable because the skin is more permeable, but what are the other exposure vulnerabilities. Are they, for some, also caused by an interaction with their specific genetics? Could brain imaging show abnormalities in the myelin of the cerebellum and other areas of the brain that are characteristic of this particular mitochondrial neurotoxin? Is there sufficient evidence to go ahead and assess a possible causal relationship between specific behavioral symptoms related to structural and functional brain abnormalities? Could brain imaging show a relationship between therapeutic variables, behavioral symptoms, and changes in structural and functional brain abnormalities?
Other mitochondrial neurotoxins (for example, triethyltins, cuprizone, MPTP,3-NP) have been used as causal variables in model neurological disorders (for example, Huntington's, ALS, Parkinson's, etc.). Each of these neurotoxins have different neurological effects. For example, a recent study(Klivenyi,P 2005) contrasted the effects of the toxin model for Parkinson's(MPTP) and the toxin model for Huntington's(3-NP). Both mitochondrial neurotoxins caused changes in amino acids. But they caused two different amino acid neurotransmitter effects. It would seem quite reasonable that a similar research approach would show that hexachlorophene would result in a third specific amino acid neurotransmitter effect. We know it has its own neurological disorder pattern.
From the past epidemiological study of the autopsies of the babies, we already know that it is a specific human mitochondrial neurotoxin. Hexachlorophene's effects, now, can be studied in adults by means of brain imaging. It's an opportunity that wasn't there before; it's an opportunity we should take advantage of now.
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1 Comments:
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