A look again at the full text of the benfotiamine abstract
as given earlier by Sillewater.
" The drastic disturbance of glucose metabolism in the
brain is one of the striking features of Alzheimer’s
disease. A significant reduction in cerebral glucose
consumption can precede overt clinical symptoms or
brain atrophy, even for decades. "
" Thus, Alzheimer’s disease has been considered to be
an ‘insulin-resistant brain state’ or even a type 3 diabetes
mellitus (Steen et al., 2005). These previous studies,
therefore, indicate that a disturbance of glucose
metabolism in the brain is associated with the
pathogenesis of Alzheimer’s disease. "
" We found that chronic treatment of benfotiamine significantly
reduced the number of amyloid plaques. By contrast,
fursultiamine had no effect on the number of amyloid plaques
Furthermore, we examined the phosphorylation of tau, and
also found that only chronic treatment of benfotiamine but not
fursultiamine significantly reduced the number of the
phosphorylated tau-positive cells. Taken together, these
results indicate that benfotiamine, but not fursultiamine, exerts
robust neuroprotection against cognitive impairment and
pathological alterations in the Alzheimer’s disease mouse model. "
" ..... benfotiamine most likely exerts its beneficial effects
through thiamine-independent pathways. "
" Recently, GSK-3 has been considered to be a new mechanism
in the pathogenesis of Alzheimer’s disease. In particular,
inhibition of GSK-3 activity blocked the production of β-amyloid
peptides by interfering with APP cleavage ...... chronic
benfotiamine treatment affects the phosphorylation of both
GSK-3α and GSK-3β, and reduces their enzymatic activities. "
" ..... benfotiamine has been shown to block three major
pathways of hyperglycaemic damage (the hexosamine
pathway, the advanced glycation end product formation
pathway and the diacylglycerol-protein kinase C pathway),
as well as hyperglycaemia-associated nuclear factor-κB
activation, by activating transketolase, thus preventing the
development and progression of diabetic nerve complications. "
" Benfotiamine is a special S-acyl thiamine derivative, while
most other thiamine derivatives including fursultiamine are
disulphide derivatives. This special modification may endow
benfotiamine with unique pharmacological effects. "
" .... benfotiamine may also regulate GSK-3 activities.
GSK-3 was first identified as a kinase involved in controlling
glycogen metabolism. Now, it has been demonstrated as a
ubiquitous serine/threonine protein kinase that participates
in multiple physiological and pathological processes.
Specifically, GSK-3 is involved in insulin signalling cascade
and molecular pathogenesis of diabetes. Interestingly, recent
evidence shows that GSK-3 also contributes to the
pathogenesis of Alzheimer’s disease (Takashima, 2006).
Inhibiting GSK-3 activity has been demonstrated to reduce \
the production and accumulation of β-amyloid in APP
(amyloid precursor protein) overexpressing mice. "
" ..... benfotiamine significantly enhanced the phosphorylation
levels and reduced enzymatic activities of both GSK-3α and
-3β in the APP/PS1 mice, suggesting that a GSK-3-dependent
pathway may be involved in the beneficial effects of benfotiamine. "
The current study has a major clinical implication in preventing
and treating Alzheimer’s disease because benfotiamine has
been utilized and shown to be without any serious side-effect
as a food supplement or a drug for therapies of peripheral
nervous disorders in some countries. "
" Also, benfotiamine differs from other water-soluble and
lipophilic thiamine derivatives both in its physicochemical
properties and its structure, especially in the open thiazole
ring and S-acyl. These properties endow benfotiamine with
complicated pharmacokinetics. "
http://brain.oxfordj...133/5/1342.long
" Benfotiamine Fights Cognitive Impairment in Alzheimer's. "
http://www.naturalpr...alzheimers.aspx
LongeCity
