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Journal of Current Pediatric Research | Volume: 23
March 14-15, 2019 | London, UK
International Conference on
Pediatrics & Neonatal Healthcare
There is increasing evidences that favour the prenatal
beginning of schizophrenia. These evidences point toward
intra-uterine environmental factors that act specifically
during the second pregnancy trimester producing a direct
damage of the brain of the fetus. The current available
technology doesn’t allow observing what is happening at
cellular level since the human brain is not exposed to a direct
analysis in that stage of the life in subjects at high risk of
developing schizophrenia.
Methods:
In 1977 we began a direct electron microscopic
research of the brain of fetuses at high risk fromschizophrenic
mothers in order to finding differences at cellular level in
relation to controls.
Results:
In these studies, we have observed within the
nuclei of neurons the presence of complete and incomplete
viral particles that reacted in positive form with antibodies
to herpes simplex hominis type I [HSV-1] virus, and
mitochondria alterations.
Conclusion:
The importance of these findings can have
practical applications in the prevention of the illness
keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. A study of the gametes
or the amniotic fluid cells in women at risk of having a
schizophrenic offspring is considered. Of being observed
the same alterations that those observed previously in the
cells of the brain of the studied foetuses, it would intend to
these women in risk of having a schizophrenia descendant,
previous information of the results, the voluntary medical
interruption of the pregnancy or an early anti HSV-1 viral
treatment as preventive measure of the later development
of the illness.
e:
segundo@infomed.sld.cuDirect evidence of viral infection and mitochondrial alterations in the Brain of fetuses at high risk for
Schizophrenia
Segundo Mesa Castillo
Psychiatric Hospital of Havana, Cuba
Curr Pediatr Res, Volume 23
DOI: 10.4066/0971-9032-C1-012