Do you wonder how SSRIs really work...

[Guest guest]

If you ever wondered how SSRIs work in children with autism you will find the

following articles very interesting. I am sure you have heard that the s

Hopkins article released in 2004 was supposed to change the world for autistic

children and their families. The s Hopkins article said that the brain's

immune system is triggered in autism. When s Hopkins refer to the brain's

immune system they refer to microglia cells. Microglia are the brain's immune

cells that when activated can cause neuroinflammation which lead to many of the

symptoms autistic children have.

Now, I am sure you have heard that SSRIs/antidepressants help increase blood

flow to the brain and that it is also has neuroprotective properties. I never

understood the mechanism behind it until recently. The research articles below

explain how antidepressants inhibit microglial activation which result in

reduction of neuroinflammation. When neuroinflammation is reduced more oxygen

carrying blood can circulate the brain increasing brain function and therefore

reducing autistic symptoms in children.

This provides a simple explanation of how SSRIs work and opens the door to other

treatments that can be used to inhibit microglial activation in children with

autism.

's Story - Stop Calling It Autism!

http://www.stopcallingitautism.net

Stop Calling It Autism!

Stay tuned for the first and largest autism/immune system medical disease

registry that will be launching very soon.

http://www.stopcallingitautism.org

s Hopkins School of Medicine

http://www.neuro.jhmi.edu/neuroimmunopath/autism_faqs.htm

What type of immune reactions are present in the brain of autistic patients?

In our study, we have demonstrated a marked increase in neuroglial responses,

characterized by activation of microglia and astroglia, in the brains of

autistic patients. These increased neuroglial responses are likely part of

neuroinflammatory reactions associated with the central nervous system's (CNS)

innate immune system.

Anti-Inflammatory Effects of Antidepressants

http://www.bentham.org/cmccnsa/sample/cnsamc9-1/0003T.pdf

Inhibitory effects of SSRIs on IFN-ã induced microglial activation through the

regulation of intracellular calcium.

http://www.ncbi.nlm.nih.gov/pubmed/20654672

Microglia, which are a major glial component of the central nervous system

(CNS), have recently been suggested to mediate neuroinflammation through the

release of pro-inflammatory cytokines and nitric oxide (NO). Microglia are also

known to play a critical role as resident immunocompetent and phagocytic cells

in the CNS. Immunological dysfunction has recently been demonstrated to be

associated with the pathophysiology of depression. However, to date there have

only been a few studies on the relationship between microglia and depression. We

therefore investigated if antidepressants can inhibit microglial activation in

vitro. Our results showed that the selective serotonin reuptake inhibitors

(SSRIs) paroxetine and sertraline significantly inhibited the generation of NO

and tumor necrosis factor (TNF)-á from interferon (IFN)-ã-activated 6-3

microglia. We further investigated the intracellular signaling mechanism

underlying NO and TNF-á release from IFN-ã-activated 6-3 microglia. Our results

suggest that paroxetine and sertraline may inhibit microglial activation through

inhibition of IFN-ã-induced elevation of intracellular Ca(2+). Our results

suggest that the inhibitory effect of paroxetine and sertraline on microglial

activation may not be a prerequisite for antidepressant function, but an

additional beneficial effect.