http://www.pnas.org/content/110/23/9523.abstract
Abstract
Is it possible to prevent atrophy
of key brain regions related to cognitive decline and Alzheimer’s
disease (AD)? One approach
is to modify nongenetic risk factors, for
instance by lowering elevated plasma homocysteine using B vitamins. In
an initial,
randomized controlled study on elderly
subjects with increased dementia risk (mild cognitive impairment
according to 2004
Petersen criteria), we showed that
high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg,
vitamin B12 0.5 mg)
slowed shrinkage of the whole brain volume
over 2 y. Here, we go further by demonstrating that B-vitamin treatment
reduces,
by as much as seven fold, the cerebral
atrophy in those gray matter (GM) regions specifically vulnerable to the
AD process,
including the medial temporal lobe. In the
placebo group, higher homocysteine levels at baseline are associated
with faster
GM atrophy, but this deleterious effect is
largely prevented by B-vitamin treatment. We additionally show that the
beneficial
effect of B vitamins is confined to
participants with high homocysteine (above the median, 11 µmol/L) and
that, in these participants,
a causal Bayesian network analysis
indicates the following chain of events: B vitamins lower homocysteine,
which directly
leads to a decrease in GM atrophy, thereby
slowing cognitive decline. Our results show that B-vitamin
supplementation can
slow the atrophy of specific brain regions
that are a key component of the AD process and that are associated with
cognitive
decline. Further B-vitamin supplementation
trials focusing on elderly subjets with high homocysteine levels are
warranted
to see if progression to dementia can be
prevented.
Do not self-prescribe. I told this to a nurse, she said overdosing on B vitamins is not good.
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