Front Matter

(Rick Simeone) #1

238 Maternal Antibodies to Fetal Brain Neurons and Autism


these killed neurons. These antigens could enter the maternal immune system
and the adaptive immune system of the mother could form antibodies to these
antigens that enter the fetus’s brain and further damage the fetal brain develop­
ment. Here, we hypothesize that the five criteria must be met and kept in mind:
1) Only selective types of progenitor neurons are destroyed initially due to
synthetic chemicals.
2) The mothers only produce antibodies to specific neuronal antigens [i.e.,
lactose dehydrogenase (LDH) A, LDH B, STIP1, CRMP1, or perhaps against
oxytocin and AVP receptors; see below].
3) The release of neuroantigens may be more relevant during the early stages
of fetal brain development (i.e., weeks 4–8 of gestation) with regards to
development of autism and other neurodevelopmental disorders. The
rationale for this theory is that in the early stages, any elimination of brain
progenitor cells would have a much broader impact on the overall brain
construction and neural damage, as compared with later exposure, since at
later stages the blood–brain barrier (BBB) and a much thicker placental/
amniotic barrier may filter out many of the neurotoxic chemicals compared
with earlier stages of pregnancy.
4) After exposure to a neuroantigens(s) in the maternal circulation, it would take
several weeks to form antibodies to those early expressed neuroantigens.
5) The anti‐neuronal antibodies formed during the first trimester may not
always be harmful to the fetal brain during the later stages of brain develop­
ment (second and third trimester fetal brain) due to development of the
BBB and/or due to lack of expressions of the particular neuroantigens (due
to enormous and rapid brain differentiation).

Why are Fetal Neuroantigens Immunogenic


to the Maternal Immune System?


In an earlier paragraph we used the term “unique antigens,” which warrants
scientific clarification. In immunological terms, the human body does not
form antibodies to its own antigens. This is due to self‐tolerance of antigens.
However, there are few sites in human organs where this “self‐tolerance” does
not apply. These sites are called immunologically “privileged” sites and include
the brain, the retina of the eye, and male testes.
Therefore, if any antigens leak from these sites, the body will form antibodies
to the leaked antigens. This is the primary reason why in infection by the
mumps virus of only one testis that results in leakage of testicular antigens,
the  antibodies made against the testis antigens can destroy the other testis.
This would be due to antibodies not the virus! Furthermore, sperm are also
considered a “foreign” antigen by the body and in some cases immune response
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