Research: BDNF in MS, Science is never simple

Tongiorgi E, Sartori A, Baj G, Bratina A, Di Cola F, Zorzon M, Pizzolato G. Altered serum content of brain-derived neurotrophic factor isoforms in multiple sclerosis. J Neurol Sci. 2012 Jul 24. [Epub ahead of print]

In multiple sclerosis
(MS), brain-derived neurotrophic factor (BDNF) provides
neuroprotection, but can also promote disease through the maintenance of
autoreactive T cells. One aspect that has not been explored yet in MS
is related to the opposite functions of BDNF protein isoforms consisting
of the pro-BDNF precursor, which has pro-apoptotic effects, and two
proteolytic isoforms, the mature BDNF with pro-survival effects and
truncated BDNF, with unknown functions. Using ELISA and
semi-quantitative Western-blot we determined the relative serum levels
of BDNF isoforms in 20 relapsing-remitting MS patients without any
disease modifying therapy and 20 age and gender-matched healthy controls
and searched for clinical correlates. Total serum BDNF was lower in MS
than in HC.  Using Western-blot analysis, we show that the
percentage of serum mature BDNF and pro-BDNF with respect to total
serum BDNF was significantly decreased, while truncated BDNF was
increased. No correlation between BDNF isoform percentage and clinical
or demographic features was found. Serum Fas (sFas) was increased. These
results support and expand the current hypothesis on the role of BDNF
in multiple sclerosis,
in that low pro-BDNF and high sFas might result in a failure to limit
autoreactive T cells by apoptotic deletion and decreased mature BDNF may
not provide enough neuroprotection, while truncated BDNF percent
increase could be a compensatory mechanism. 

BDNF acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses. This can limit nerve damage in animal models of MS. These authors state that BDNF levels were lower in than in healthy controls. Others have agreed that it is lower. But others have said the opposite and others have suggested that enhanced BDNF signalling means less T cell death and less nerve death and it has been suggested that this contributes to nerve protection after alemtuzumab. As often occurs in science there is disagreement. This is common in science you look for repetition and if you are really interested you need to do it yourself so that you know the reality.

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