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http://www.medpagetoday.com/MeetingCove ... id=5517461

Evidence of microbleeds was detected in 28 of the patients. These patients had significantly more white matter hyperintensities in the MRI scans (mean score 10.5 versus 7 among those with no microbleeds, P=0.001), and there were trends in the microbleed patients toward more large-vessel and lacunar infarcts.

Why would patients with microbleeds have more white matter hyperintensities? This is in patients with Alzheimer's disease. In CCSVI there is suspected to be diapedesis or leakage of red blood cells into the brain. Is this similar to a microbleed? If microbleeds contribute to the formation of a white matter hyperintensity in Alzheimer's disease, it would lend support to the idea that diapedesis in CCSVI contributes to the formation of our white matter lesions.

http://www.medpagetoday.com/Neurology/A ... id=5517461

Genetic Risk for Alzheimer's Manifests Early

In a family of SPEN1 E280A mutation carriers, those ages 18 to 26 had elevated levels of beta amyloid in both cerebrospinal fluid (CSF) and blood (P=0.008 and P=0.01, respectively), reported Eric Reiman, MD, of Banner Alzheimer's Institute in Phoenix, and colleagues online in The Lancet Neurology.

In a second study in the same population, fibrillar amyloid beta began to accumulate at around age 28 and plateaued around age 37, long before the expected onset of symptomatic disease, the researchers said.

In Alzheimer's, they've been able to identify people with a mutation that leads to Alzheimer's, and so they've been able to see that even though these people look healthy in their 20s and 30s, there are elevated levels of amyloid beta in the blood and CSF. The levels of amyloid beta are presumably a marker for elevated levels within the brain itself as well.

How would the outflow obstructions of CCSVI affect this situation? If someone were unfortunate enough to have both the Alzheimer's gene and jugular or azygous outflow obstructions, would the impaired drainage promote greater accumulation of beta amyloid?

I thought the amyloid beta accumulates in the CSF, cleared, if it is working correctly by the glymphatic drainage...

Microbleeds sounds a lot like the blood-borne leakage apparent when gadolinium is injected into the bloodstream and leaks around perivascular new lesion sites...

Wow, CCSVI Alliance has just released a summary of research links on blood flow issues with Alzheimer's, Parkinson's, and OND's.


http://www.ccsvi.org/index.php/the-basi ... l-diseases

Haven't gotten all of the Haacke work with Parkinson's (71% have some sort of CCSVI, but a different sort?) to link yet but it looks like Alzheimer's is atherosclerosis of the Circle of Willis at least (Alex E Roher and others at The Longtine Center for Neurodegenerative Biochemistry, Banner Sun Health Research Institute, Sun City and other institutes in AZ)

The autopsy research is very obvious to me.

Amazing stuff.