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Post mortem findings of link between vascular instability and Autism

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
Not a lot of detail in this story (or in the linked abstract) but interesting nonetheless :

Evidence of autism shows up in the brain's blood vessels, study finds

"In a typical brain, blood vessels are stable, thereby ensuring a stable distribution of blood," she adds. "Whereas in the autism brain, the cellular structure of blood vessels continually fluctuates, which results in circulation that is fluctuating and, ultimately, neurologically limiting."

http://www.sciencealert.com/evidence-of-autism-can-be-found-in-the-brain-s-blood-vessels-study-finds

Persistent Angiogenesis in the Autism Brain: An Immunocytochemical Study of Postmortem Cortex, Brainstem and Cerebellum

We found significant increases in both nestin and CD34, which are markers of angiogenesis localized to pericyte cells and endothelial cells, respectively.

http://link.springer.com/article/10.1007/s10803-015-2672-6
 

Thomas

Senior Member
Messages
325
Location
Canada
yes I saw that. Sounds like the old school ME hypothesis of the disease being based on an injury to the vascular system of the brain. I guess all those abnormal SPECT scans of ME patients actually do mean something and aren't just "academic".
 

anciendaze

Senior Member
Messages
1,841
Exactly how the vascular system is damaged, and why this usually doesn't get noticed, remain open questions. I am reminded of the broad medical significance of this for the brain due to recently discussing problems in an elderly relative who has had trouble with syncope and falls, also polyuria and orthostatic intolerance. I've had to repeatedly tell those involved that brains do not work very well if they aren't getting sufficient oxygenated blood, in which case psychological speculation is harmful.

In another case we noticed that syncope consistently took place about two hours after the patient was given medication for blood pressure. Reducing the dosage and increasing frequency helped.

As I've said before, syncope is not a trivial problem for public health. About 1/3 of all emergency cases are caused by syncope, and this doesn't include things like traffic accidents where subsequent trauma may hide the original cause. I could also point to common medical recognition that repeated syncope is a reasonable prognostic indicator for mental decline, and we don't even know the incidence of less dramatic vascular problems. This means vascular instability could be a major cause of patients becoming unable to care for themselves -- at any age.

Many current publications on repeated syncope are concerned with cardiac issues. Some are tied to psychiatric problems. There is a literature on transient ischemic attacks, but we don't really seem to be doing much to prevent them, and probably fall far short of diagnosing most. We are still far from understanding vascular changes outside the heart which stop short of producing syncope.

The type of linkage highest on my list at present is a runaway process of endothelial invasion by T-cells due to missing peptide signals from B-cells, though I still don't know what triggers the failure. If this is concentrated in highly vascularized tissues in the brain, or in the pituitary, it would be very hard to detect in living patients. A flow of fluid resulting from endothelial damage by invading cells might produce cerebral edema, if there were no compensation. A reduction in vasopressin/ADH secreted by the pituitary would then appear to be a compensating mechanism to avoid the immediate danger to life from cerebral edema. This is one way in which ME/CFS patients can experience episodic hypovolemia without losing blood. I'm sure other mechanisms for vascular instability due to immune activity can be postulated.

This is not a problem restricted to a tiny minority of children. It can produce mental decline at any age.

Added: a different failure mode stemming from the same cause could produce hydrocephalus, which is also often recognized in children of roughly the same age at which autism becomes apparent. Despite the apparently simple nature of this problem we still have useful explanations for only a minority of cases. Surprisingly, this also shows up in age-related mental decline normally considered quite different in nature.
 
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wastwater

Senior Member
Messages
1,271
Location
uk
The gene FOXC1 among others may lead to poorly formed brain blood vessels
I was looking at notch signalling and CADASIL
 
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natasa778

Senior Member
Messages
1,774
... The type of linkage highest on my list at present is a runaway process of endothelial invasion by T-cells due to missing peptide signals from B-cells, though I still don't know what triggers the failure. If this is concentrated in highly vascularized tissues in the brain, or in the pituitary, it would be very hard to detect in living patients. A flow of fluid resulting from endothelial damage by invading cells might produce cerebral edema, if there were no compensation. A reduction in vasopressin/ADH secreted by the pituitary would then appear to be a compensating mechanism to avoid the immediate danger to life from cerebral edema. This is one way in which ME/CFS patients can experience episodic hypovolemia without losing blood. I'm sure other mechanisms for vascular instability due to immune activity can be postulated.

This is not a problem restricted to a tiny minority of children. It can produce mental decline at any age.

Added: a different failure mode stemming from the same cause could produce hydrocephalus, which is also often recognized in children of roughly the same age at which autism becomes apparent. Despite the apparently simple nature of this problem we still have useful explanations for only a minority of cases. Surprisingly, this also shows up in age-related mental decline normally considered quite different in nature.

I have posted on GABA thread about (low dose) diuretic bumetanide being reported as having good effects in a number of children with autism, especially as bringing great cognitive/academic gains. The rationale for use is addressing GABAeric dysfunction, but of course other, more direct effects linked to what you describe above are also possible...

I'll try search this forum and wider for any reports of bumetanide (or micro dose AEDs) in ME.