Signature tau neuropathology in CBD

[Swarfmaker]

I have found reports about 4 substances that may be able to prevent
tau protein corruption, and disaggregate aggregations already formed:
Methylene blue, cinnamon proantocyanidins (related to tannins), grape
seed extract polyphenols, and niacinamide (a form of B3). If tau
protein corruption is a key step in the process of the disease, then
using a "tau buster" should help. However, I think that there are
other steps that would have to addressed too. Of course the big
question is, what causes the problem in the first place, the "root
cause"? Could it be the result of a chemical produced by the body in
trying to fight an infections, such as the tumor necrosis factor alpha
(TNF-alpha) the body produces when fighting off helicobacter pylori in
the stomach? It could be genetic.

In any case, things like cinnamon, niacinamide, and grape seed extract
would be simple, relatively inexpensive, and probably safe to
experiment with. Do your homework, ask questions, make up your own
minds. After someone has tried these things for a case of CBD, then we
can start talking about their effectiveness. Right now, they are just
four question marks.

2002: Forman Mark S; Zhukareva Victoria; Bergeron Catherine; Chin
Steven S-M;
Grossman Murray; Clark Chris; Lee Virginia M-Y; Trojanowski John Q

Signature tau neuropathology in gray and white matter of corticobasal
degeneration.
The American journal of pathology 2002;160(6):2045-53.

Corticobasal degeneration (CBD) is an adult-onset progressive
neurodegenerative disorder characterized by L-dopa-resistant rigidity,
focal cortical deficits, and variable dementia. The neuropathological
hallmark of CBD is the deposition of filamentous inclusions in neurons
and glia composed of hyperphosphorylated tau with only four
microtubule-binding repeats (4R-tau). To characterize the regional
burden of tau pathology in CBD, we studied 12 brains with the
neuropathological diagnosis of CBD using biochemical and histochemical
techniques. Eleven brain regions were evaluated including gray and
white matter from frontal, parietal, temporal, and occipital lobes and
cerebellum as well as basal ganglia. Although the distribution of tau
pathology was variable, neuropathological and biochemical data showed
a similar burden of tau abnormalities in frontal, temporal, and
parietal lobes and basal ganglia of both hemispheres. This included
abundant, sarkosyl-insoluble 4R-tau in both gray and white matter of
two or more of these cortical regions and basal ganglia, and to a
lesser extent, cerebellar white matter. The insoluble tau pathology in
gray and white matter showed overlapping but distinct phosphorylated
epitopes suggesting cell-type and subcellular localization (ie, cell
bodies versus cell processes)-specific differences in tau
phosphorylation. In contrast, soluble tau was composed of normal 4R/3R-
tau ratios indicating no gross abnormality in tau splicing. Thus,
although clinically heterogeneous, CBD is a distinct lobar and basal
ganglionic tauopathy with selective aggregation of 4R-tau.

http://www.biomedexperts.com/Abstract.bme/12057909/Signature_tau_neuropathology_in_gray_and_white_matter_of_corticobasal_degeneration