RE: interleukin-6/

[Guest guest]

To find the answer to your question, you would visit Amy Yasko's Autism Answers

website -- she is the person who pioneered the genetic testing for kids with

autism. You can ask her personally in an on-line chat. I believe you can also

consult with her for $300. For that price, she will interpret the results of

your child's test, but you will not be her patient (2+ year wait list for that).

-

" K. Fischer " <elfischer@...> wrote:

These posts on IL-6 caught my eye, as when my son was first having

issues at 2.5 we did some extensive testing through a “DAN” doctor, but

then elected not to pursue the protocol. In any event, some of the

testing that we did was a “genetic” profile of various SNP mutations

thought to maybe affect ASD kids which included all sorts of areas, the

profile showed whether there were mutations in genes and whether my son

had a normal SNP or whether there was a mutation from one or both of his

parents. Anyway, IL-6 was listed under vascular integrity section and

my son showed a mutation from both of us. I have always wondered what

this meant. Of course, the DAN doc who ordered it couldn’t explain the

significance and I quite frankly just forgot about it. Now that I am

aware of the theory and all of the current research out there on

the immune system and inflammation, I am curious whether anyone knows

anything about possible genetic predispositions to problems with the

immune system. I am curious as to whether his particular mutation

existed prior to whatever environmental insult (virus, bacteria, etc)

affected his immune system and caused the downward spiral or whether the

insult caused the particular genetic SNP to “overexpress” (for lack of a

better word). Does this make sense? ? Does it even matter as far as

treatment goes, I presume not? Sorry for the ramble, this is just very

interesting.

Prenatal exposure to interleukin-6 results in inflammatory

neurodegeneration

m J Physiol Regul Integr Comp Physiol 290: R1345-R1356, 2006

DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Prenatal exposure to interleukin-6 results in inflammatory

neurodegeneration

in hippocampus with NMDA/GABAA dysregulation and impaired spatial

learning

Anne-Maj sson,1 Eva Jennische,2 Hans-Arne Hansson,2 and Agneta

Holmäng1

1Cardiovascular Institute and Wallenberg Laboratory and 2Institute of

Anatomy and Cell Biology, Göteborg University, Sahlgrenska Academy,

Göteborg, Sweden

During pregnancy, infection or immune responses induce cytokine release,

which might influence fetal neurodevelopment, leading to

neurodegenerative

disease in adulthood. Because the hippocampus is a key area for learning

and

memory, we evaluated 4- and 24-wk-old rats for the effects of early and

late

prenatal exposure to interleukin-6 (IL-6) on hippocampal morphology,

expression of mRNA for IL-6, the -aminobutyric acid receptor (GABAA5),

the

NR1 subunit of the N-methyl-D-aspartate receptor, and glial fibrillary

acidic protein (GFAP), caspase-3 protein and mRNA levels, and learning

abilities. Late exposure increased serum IL-6 and hippocampal expression

of

IL-6 mRNA at 4 and 24 wk. All adult rats showed neuronal loss in the

hilus

and astrogliosis; males had losses mainly in the CA2 and CA3 regions,

and

females in CA1. Expression of GABAA5, NR1, and GFAP mRNA increased in

late-exposed males and females at 4 and 24 wk. mRNA and protein levels

of

the apoptosis marker caspase-3 were increased in all late-exposed rats

except males at 4 wk. Evaluation of hippocampus-dependent working memory

in

the water maze at 20 wk of age showed increases in escape latency

and

time spent near the pool wall in all IL-6 adult rats, especially

females.

These findings suggest that fetal IL-6 exposure, especially in late

pregnancy, leads to increased IL-6 levels in the circulation and

hippocampus, abnormalities of hippocampal structural and morphology, and

decreased learning during adulthood.

intrauterine exposure; hippocampus; cytokine; spatial learning; water

maze

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