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Alzheimer’s, Parkinson’s, Multiple Sclerosis, Depression & Bipolar Disorder All Linked to Metal Toxicants
By Dr. Marianna Pochelli ND
Guest Writer for Wake Up World
Metal toxicants entering the part of the brain that deals with stress and panic have been linked to disorders dealing with the central nervous system. Increasing evidence indicates that damage to the locus ceruleus (LC), is present in a wide range of neurodegenerative diseases including demyelinating and psychiatric disorders.
There are a growing number of Clinicians and Scientists who are convinced that excitotoxins and heavy metals play a critical role in the development of several neurological disorders, including migraines, seizures, infections, abnormal neural development, certain endocrine disorders, specific types of obesity, and especially the neurodegenerative diseases; a group of diseases which includes ALS, Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and olivopontocerebellar degeneration.
The locus ceruleus (LC) is a nucleus in the pons (part of the brainstem) involved with physiological responses to stress and panic. It is the principal site for brain synthesis of the hormone and neurotransmitter norepinephrine (noradrenaline). It has been known for many years that toxicants (ie., poisons that are put into the environment or human body by human activity) that block the uptake of noradrenaline can damage the LC of experimental animals. The recent finding that a metal toxicant, inorganic mercury, selectively enters the cytoplasm of human LC neuron has prompted researchers to investigate how these toxicants cause many of these CNS disorders.
The Locus Ceruleus is Upregulated by Stress
An increased output of noradrenaline from the LC can be elicited by a wide range of acute and chronic stressors, in particular those that are physical (e.g., pain), psychological (e.g., anxiety), or social (e.g., isolation). Chronic stressors can keep noradrenergic neurons in a highly active state permanently. Stressors can increase the uptake of circulating toxicants that use neurotransmitter transporters to enter LC neurons.
Stress has been implicated in the onset or relapse of a number of neurodegenerative, demyelinating and psychiatric conditions. The increased activity of the LC during stress, with a concomitant increase in neurotransmitter release and re-uptake, encourage circulating toxicants to enter the terminal axons of LC neurons.
Studies indicating which elements of the LC-Toxicant hypothesis relate to particular CNS disorders.
| Locus ceruleus
involved |
Metal toxicant
associated |
Stress before
onset/relapse |
Blood-brain
barrier dysfunction |
Inflammation
implicated |
|
| Alzheimer’s disease | Yes | Yes | Yes | Yes | Yes |
| Parkinson’s disease | Yes | Yes | Yes | Yes | Yes |
| Amyotrophic lateral sclerosis | Yes | Yes | Yes | Yes | Yes |
| Multiple sclerosis | Yes | Yes | Yes | Yes | Yes |
| Major depression | Yes | Yes | Yes | Yes | Yes |
| Bipolar disorder | Yes | Yes | Yes | Yes | Yes |
CNS Regions are Innervated by the Locus Ceruleus
About 70% of all CNS noradrenaline comes from the LC innervate in particular CNS regions that are involved in Alzheimer’s disease (hippocampus, neocortex, basal forebrain), amyotrophic lateral sclerosis (brain stem and spinal motor neurons), and mood disorders (amygdala). The substantia nigra, which is damaged in Parkinson’s disease, also receives innervation from the LC.
The normal human brain contains about 32,000 LC neurons and is estimated to contain capillaries with a total length of 640 kilometres. This means that, on average, each LC neuron is responsible for innervating 20 meters of capillaries. No other neuronal system has such widespread contact with circulating blood.
Noradrenaline plays an important part in maintaining the integrity of the blood-brain barrier and in responding to stressors by increasing cerebral blood flow. With their large exposure to the blood circulation, LC neurons could take up toxicants even if they were at low levels in the blood.Noradrenaline also suppresses inflammation, mostly because of its affects on microglia, which have a high expression of adrenoreceptors. Inflammation would be further increased if a permeable blood-brain barrier, caused by noradrenaline depletion, allowed inflammatory cells to enter the CNS.
