Myelination is an essential part of human brain development. Nerves can only conduct pulses of energy efficiently if covered by myelin. Like insulation on an electric wire, the fatty coating of myelin keeps the pulses confined and maintains the integrity of the electrical signal so that it has a high signal-to-noise ratio. When the insulation on a wire is damaged or destroyed, the flow of electrical current may be interrupted and a short-circuit occurs.
Oligodendrocyte cells give white matter its color by manufacturing myelin. If myelin falls into disrepair, nerve axons cease to function, even though they themselves aren't damaged. Protecting oligodendrocytes after brain or spinal cord injury might keep nerve cells intact.
At birth, relatively few pathways have myelin insulation. Myelination in the human brain continues from before birth until at least 20 years of age. Up until the age of 10 or so, vast areas of the cortex are not yet myelinated. Up to the age of 20, large areas of the frontal lobes are not yet myelinated.1
Myelination begins in the developmentally oldest parts of the brain, like the brain stem, moving to the areas of the nervous system that have developed more recently, like the prefrontal lobe and cortex. Myelin spreads throughout the nervous system in stages, which vary slightly in each individual. Impairment of myelination can alter neural communication without necessarily causing severe CNS (central nervous system) damage.
The prefrontal portions of the cerebrum have a profound influence on human behavior.2 If an individual is injected with vaccines,most of which have adjuvants like mercury and aluminum compounds, as well as foreign proteins (some from other species in which the vaccines were grown) and biological organisms, unprotected nerves may be impacted. The argument for a role
of vaccines in the development of autistic disorders hinges on these biological effects upon nerves, damaging them in a way that influences behavior and learning patterns.
The argument for adjuvants evoking an auto-immune response does not hinge on any inherent neuro-toxicity of these compounds, but on the initiation of an allergic response.
The model by which adjuvants initiate an immune response is that of Experimental Allergic Encephalomyelitis (EAE). To date, EAE is recognized as the best available animal model of several degenerative human diseases, like multiple sclerosis and post-vaccinal encephalopathies. EAE3 is generally thought to be an autoimmune response to myelin basic protein (MBP). Oddly, MBP can also suppress EAE, and many observations suggest that an independent immune response to so-called "adjuvant" material is also necessary to EAE induction. Of course, this is why adjuvants are used in vaccines, to dramatically increase the likelihood of an
immune response to the administered biological material.
Thus, EAE may be a result of a pair of interactive immune responses, one against MBP, and one against the adjuvant. If so, the adjuvant should, like MBP, suppress EAE. Root-Bernstein, et al. (1986) presented data from experiments on strain 13 guinea pigs demonstrating EAE suppression by muramyl dipeptide, an active component of complete Freund's adjuvant. In the past, adjuvants have only been classified as immunopotentiators, not immunosuppressants. Apparently, adjuvants are both. This study strengthens the argument that adjuvants may be
crucial to initiating an auto-immune response leading to post-vaccine neurological symptoms.
