250 Maternal Antibodies to Fetal Brain Neurons and Autism
A Chicken and Egg Conundrum
Several investigators have been looking at the possibility that some mothers
with autoimmune disorders may possess antibodies to fetal brain antigens.
Therefore, with regard to antibodies to different neuroantigens that we
described in the preceding section, there is evidence that there may be maternal
antibodies that target different fetal brain antigens than LDH, YBX1, cypin,
STIP1, CRMP1, and CRMP2 that are in the 39‐ and 73‐kDa molecular weight
bands. An association between the presence of neuroantibodies and the inci
dence of numerous behavioral disorders has been described [27–29]. Antibodies
reactive to neuronal tissues have been identified in schizophrenia [27–30].Tourette Syndrome [30–32] and Obsessive Compulsive Disorder [33]
Unlike the neuroantibodies identified and well‐characterized in mothers of ASD
children, the neuroantibodies observed in children, and in other neurologic disor
ders, bind to adult, rather than fetal, brain tissue, suggesting that they are targeting
adult or older children rather than the fetal brain. In neurologic illnesses that arise
later in life, such as schizophrenia, these different kinds of neuroantibodies may be
crossing the BBB after the child is born, when the BBB is sealed! It is hypothesized
that there must be another event that increases barrier permeability, allowing anti
bodies to traverse the BBB and alter neuronal processes that cause episodic schizo
phrenia, Tourette syndrome, obsessivecompulsive disorder, and many similar
psychiatric disorders. We have been working on the potential role of synthetic
chemicals that activate Interleukin‐6 (IL‐6; [34]). IL‐6 has been shown to make the
BBB transiently leaky (see Chapter 9). The question is, if maternal neuroantibodies
are playing a role in many neurodevelopmental disorders, then how are the key
neuroantigens entering the maternal blood circulation? We hypothesize that the
leakage of brain antigens is the result of synthetic chemicals that reach the adult
brains as much as they are reaching the fetal brains. Environmental factors and tim
ing of exposure during different stages of fetal development and after birth are the
major contributors to the differing symptoms and manifestations of ASD as well as
numerous neuropsychiatric disorders, which are all rising at an alarming rate. We
believe that the real culprits are the synthetic chemicals that first damage certain
fetal brain neurons, release the neuroantigens, and enter the maternal circulation,
and the neuroantibodies produced by the mothers, cause the damage [34].Other Contributing Factors in Neuropsychiatric Disorders
Infectious Flu Virus
Influenza Vaccine and Narcolepsy
In recent years there has been a special interest in vaccination with Pandemrix–a
pandemic influenza A vaccine – and the development of narcolepsy. The