I am editing a new autism manuscript (not by me) and need some additional
readers, so I will first summarize the context and synaptobrevin-related
rationale:
The etiology of autism is not well understood; a variety of causes are
suspected, and certain syndromes (eg, fragile X) are known as
capable of inducing autistic-like traits. Currently, the NIH is funding
research into genetic indicators associated with autism, even as a goodly
number of parents and private physicians and others are developing data
suggesting that additional factors need be considered.
I have been reading and editing a document that I believe to be a highly
significant contribution to understanding the etiology of autism, in at
least a subset of autistics and quite possibly a large subset. The author
(Ellen R Bolte) and I are now ready to seek some additional readers to
peruse the manuscript -- which is the reason for this posting.
Ellen has recently submitted a near-final draft of the paper to an
established journal and has several weeks to collect some poignant
criticisms and modify the manuscript accordingly.
The title of the manuscript is:
Autism and Clostridium tetani: an hypothesis
Ellen R Bolte
*****
The basic rationale of Ellen's paper includes but is not limited to the
following points:
Synaptobrevins are gene-encoded molecules that span the membranes of
synaptic vesicles and participate in neuronal signaling. Toxins from
Clostridium tetani are known to incapacitate synaptobrevin function on
synaptic vesicles. Although generally we think of tetanus as a severe
illness resulting from C. tetani infections, medical literature indicates
that subacute infections can occur, even in persons who have been
immunized against tetanus. Furthermore, already in the literature are
studies documenting retrograde axonal, transsynaptic transport of C.
tetani toxin from peripheral sources, via the spinal cord and sympathetic
nervous system, to various brain regions known to be affected in autism.
Ellen's basic hypothesis is that subacute Clostridium tetani infections,
localized in the intestine or elsewere, would generate sufficient toxin so
as to induce autism and autistic-like traits in persons so infected. The
well-documented facts that subacute C. tetani infections occur and that
C. tetani toxin trans-axonally migrates toward various parts of the
brain and then deleteriously affects synaptobrevin function suggests
that Ellen's hypothesis may well be valid.
*****
The above statements are just part of the rationale and are here presented
to convey a sense of the content and argument so that listees can decide
whether or not they would like to peruse such a challenging but very well
documented manuscript.
Consider Ellen's hypothesis at a most basic level: if a person's synaptic
vesicles have loss of function due to toxin-destroyed synaptobrevins, then
many aspects of perception and of responses to perception would be
disabled, thereby inducing autistic-like traits or even autism.
*****
If you are interested in reading her manuscript during the next several
weeks and would communicate to us your critique and/or suggestions, please
contact me directly by e-mail (ie, not via post to newsgroup) and I will
e-mail a copy to you.
Teresa
Teresa.Binstock at uchsc.edu
Teresa C. Binstock, Researcher
Developmental & Behavioral Neuroanatomy
B140 The Children's Hospital
1056 E. 19th Avenue
Denver CO USA
80218
Autism and Clostridium tetani: an hypothesis.
Ellen R Bolte
copyright 1996
manuscript submitted
Because this posting describes and summarizes a
manuscript that has been recently submitted, this e-
mail's contents are copyrighted by:
Teresa C. Binstock
and
Ellen R Bolte
eof
