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2020 ; 173
(ä): 1-34
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The putative etiology and prevention of autism
#MMPMID32711807
Steinman G
Prog Mol Biol Transl Sci
2020[]; 173
(ä): 1-34
PMID32711807
show ga
Since the initial psychological report by Leo Kanner in 1943, relatively little
formal biochemical/neurological research on the cause of autism, other than
peripheral searches for genomic mutations, had been carried until the end of the
20th century. As a result of studies on twin sets and the conclusion that autism
was largely a hereditary defect, numerous investigations have sought various
genetic faults in particular. However, such studies were able to reveal a
plausible etiology for this malady in only a small percentage of instances. Key
bio-molecular characteristics of this syndrome have been uncovered when the
potential roles of the glia were studied in depth. Findings related to
biochemical deficiencies appearing early in the newborn, such as depressed IGF-1
(insulin-like growth factor #1) in neurogenesis/myelination, are becoming
emphasized in many laboratories. Progress leading to timely diagnoses and
subsequent prevention of central nervous system dysconnectivity now seems
plausible. The tendency for an infant to develop autism may currently be
determinable and preventable before irreversible psychosocial disturbances become
established. These discussions about glial function will be inter-spersed with
comments about their apparent relevance to autism. The concluding portion of this
presentation will be a detailed review and summation of this diagnosis and
prevention proposition.
|Animals
[MESH]
|Autistic Disorder/blood/*etiology/genetics/*prevention & control
[MESH]
free
free
free
