The neurodevelopmental theory in the aetiology of schizophrenia is
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
The
neurodevelopmental theory in the aetiology of schizophrenia is
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
neurodevelopmental theory in the aetiology of schizophrenia is
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
The
neurodevelopmental theory in the aetiology of schizophrenia is
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
neurodevelopmental theory in the aetiology of schizophrenia is
considered one of the most consistent at present. Evidence from
epidemiological and neuropathological studies indicates that the
pathogenic process that culminate in the development of schizophrenia
are initiated early in life and has been associated with a variety of
prenatal environmental insults to the developing brain, including
infection. Although the infectious agents have been proposed as one of
the risk factors for schizophrenia the data on the association of a
specific infectious agent with prenatal brain evidence is absent.
Understanding of the structural abnormalities would allow a better
identification of neurodevelopmental processes that contribute to risk
for schizophrenia. We have hypothesized that at ultra high-risk fetuses
would have alterations at cellular level that would let us differentiate
them to the comparison subjects. A reappraisal of our ultrastructural
studies carried out in samples of the left temporal lobe of foetuses at
ultra high risk of developing schizophrenia is presented. The findings
obtained are compatible with an active infection of the central nervous
system by herpes simplex hominis type I [HSV1] virus. The present
results are the first direct evidence that demonstrate the presence of
this virus in the central nervous system of foetuses from schizophrenic
mothers in the critical period of foetal development. The importance of
this finding can have practical applications in the prevention of the
illness keeping in mind its direct relation to the aetiology and
physiopathology of schizophrenia. - See more at:
http://infection.omicsgroup.com/abstract/2015/direct-evidence-of-viral-infection-and-mitochondrial-alterations-in-the-brain-of-fetuses-at-high-risk-for-schizophrenia#sthash.E7Wj586W.dpuf
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