PMID- 22836016
OWN - NLM
STAT- MEDLINE
DCOM- 20130114
LR  - 20171116
IS  - 1878-5883 (Electronic)
IS  - 0022-510X (Linking)
VI  - 320
IP  - 1-2
DP  - 2012 Sep 15
TI  - Altered serum content of brain-derived neurotrophic factor isoforms in multiple 
      sclerosis.
PG  - 161-5
LID - 10.1016/j.jns.2012.07.016 [doi]
AB  - 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. We demonstrate 
      that the capture and detection antibodies of the ELISA kit from Promega are able 
      to recognize all three isoforms but with different efficiency. 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. Hence, future studies on MS should take into account BDNF 
      proteolytic processing.
CI  - Copyright (c) 2012 Elsevier B.V. All rights reserved.
FAU - Tongiorgi, Enrico
AU  - Tongiorgi E
AD  - Department of Life Sciences, BRAIN Center for Neuroscience, University of 
      Trieste, Trieste, Italy. tongi@units.itn
FAU - Sartori, Arianna
AU  - Sartori A
FAU - Baj, Gabriele
AU  - Baj G
FAU - Bratina, Alessio
AU  - Bratina A
FAU - Di Cola, Francesco
AU  - Di Cola F
FAU - Zorzon, Marino
AU  - Zorzon M
FAU - Pizzolato, Gilberto
AU  - Pizzolato G
LA  - eng
PT  - Journal Article
DEP - 20120724
PL  - Netherlands
TA  - J Neurol Sci
JT  - Journal of the neurological sciences
JID - 0375403
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (FAS protein, human)
RN  - 0 (Protein Isoforms)
RN  - 0 (Protein Precursors)
RN  - 0 (brain-derived neurotrophic factor precursor)
RN  - 0 (fas Receptor)
SB  - IM
MH  - Adult
MH  - Brain-Derived Neurotrophic Factor/blood/*metabolism
MH  - Case-Control Studies
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Multiple Sclerosis/blood/*metabolism
MH  - Multiple Sclerosis, Relapsing-Remitting/blood/*metabolism
MH  - Protein Isoforms/blood/*metabolism
MH  - Protein Precursors/blood/metabolism
MH  - fas Receptor/blood/*metabolism
EDAT- 2012/07/28 06:00
MHDA- 2013/01/15 06:00
CRDT- 2012/07/28 06:00
PHST- 2011/11/08 00:00 [received]
PHST- 2012/06/23 00:00 [revised]
PHST- 2012/07/06 00:00 [accepted]
PHST- 2012/07/28 06:00 [entrez]
PHST- 2012/07/28 06:00 [pubmed]
PHST- 2013/01/15 06:00 [medline]
AID - S0022-510X(12)00350-4 [pii]
AID - 10.1016/j.jns.2012.07.016 [doi]
PST - ppublish
SO  - J Neurol Sci. 2012 Sep 15;320(1-2):161-5. doi: 10.1016/j.jns.2012.07.016. Epub 
      2012 Jul 24.