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[reason]

Like all tissues, those of the blood-brain barrier in blood vessel walls deteriorate due to the cellular and molecular damage of aging. Researchers here correlate that deterioration with progressive cognitive impairment, further reinforcing existing data on the contribution of blood vessel functional decline to age-related damage in the brain:

The blood-brain barrier (BBB) limits entry of blood-derived products, pathogens, and cells into the brain that is essential for normal neuronal functioning and information processing. Post-mortem tissue analysis indicates BBB damage in Alzheimer's disease (AD). The timing of BBB breakdown remains, however, elusive. Using an advanced dynamic contrast-enhanced MRI protocol with high spatial and temporal resolutions to quantify regional BBB permeability in the living human brain, we show an age-dependent BBB breakdown in the hippocampus, a region critical for learning and memory that is affected early in AD.

The BBB breakdown in the hippocampus and its CA1 and dentate gyrus subdivisions worsened with mild cognitive impairment that correlated with injury to BBB-associated pericytes, as shown by the cerebrospinal fluid analysis. Our data suggest that BBB breakdown is an early event in the aging human brain that begins in the hippocampus and may contribute to cognitive impairment.

Link: http://dx.doi.org/10...ron.2014.12.032

View the full article at FightAging

[resveratrol_guy]

...yet another reason to use bone marrow therapy of some sort to address early (i.e. predominantly vascular) Alzheimer's disease before it creates widespread tauopathy. It's my somewhat controversial opinion that the vast majority of Alzheimer's begins with exactly the sort of damage that you've mentioned here.

[resveratrol_guy]

Needs references? Sure. There's a lot on Google (alzheimers pericyte neovascularization cd34 bone marrow, etc.) basically linking perictye (not to be confused with parasite) dysfunction and excessive but incompetent cerebral neovascularization to Alzheimer's disease, and plenty also linking bone marrow or CD34+ therapy to vascular repair, especially in rodents. The bottom line seems to be: pericyte damage -> incompetent BBB function -> incompetent neovascularization due to failed repair -> more neuronal damage. With each iteration of the process, more and more vascular surface area is created, but it leaks, so the rate of neuronal poisoning increases with time. In principle, intervening rapidly in the initial BBB pathology might stave off Alzheimer's indefinitely. My friend and I both underwent variations of this procedure; in her case, it was clearly early dementia of some form.