PMID- 25623403
OWN - NLM
STAT- MEDLINE
DCOM- 20160519
LR  - 20150127
IS  - 1530-0277 (Electronic)
IS  - 0145-6008 (Linking)
VI  - 39
IP  - 1
DP  - 2015 Jan
TI  - Increased serum neurotrophin levels related to alcohol use disorder in a young 
      population sample.
PG  - 30-3
LID - 10.1111/acer.12592 [doi]
AB  - BACKGROUND: The diagnosis of alcohol use disorder is based on clinical signs and 
      on the measurement of biological markers. However, these markers are neither 
      sufficiently sensitive, nor specific enough, for determining the effects of 
      alcohol abuse on the central nervous system. Serum neurotrophins are important 
      regulators of neural survival, development, function, and plasticity and have 
      been found to be reduced in alcohol use disorder. The aim of this study was to 
      investigate the alterations in serum neurotrophin levels (brain-derived 
      neurotrophic factor [BDNF], glial-derived neurotrophic factor [GDNF], and nerve 
      growth factor [NGF]) in alcohol use disorder in a young population, and thus 
      possibly representing the early stages of the illness. METHODS: This is a 
      cross-sectional study, nested in a population-based study of people aged 18 to 
      35, involving 795 participants. The participants responded to the CAGE 
      questionnaire, and a CAGE score of >/=2 was considered to be a positive screen for 
      the abuse/dependence or moderate to severe alcohol use disorder. Serum BDNF, 
      GDNF, and NGF levels were measured by ELISA. RESULTS: In the CAGE >/= 2 group, GDNF 
      (p </= 0.001) and NGF (p </= 0.001) serum levels were significantly increased, and 
      the BDNF elevation was near a statistical significance (p = 0.068) when compared 
      to the CAGE < 2 group. A significantly positive correlation was observed only in 
      the CAGE >/= 2 group for BDNF/GDNF (r = 0.37, p < 0.001) and GDNF/NGF (r = 0.84, 
      p < 0.001) levels. The correlation between the NGF and BDNF levels was 
      significantly positive in both groups (r = 0.28, p < 0.001 for the CAGE < 2 
      group, and r = 0.30, p = 0.008 for the CAGE >/= 2 group). CONCLUSIONS: These 
      results suggest that elevated neurotrophins are candidate markers for the early 
      stages of alcohol misuse.
CI  - Copyright (c) 2015 by the Research Society on Alcoholism.
FAU - Lhullier, Alfredo C
AU  - Lhullier AC
AD  - Escola de Psicologia, Centro de Ciencias da Vida e da Saude, Universidade 
      Catolica de Pelotas, Pelotas, Brazil.
FAU - Moreira, Fernanda P
AU  - Moreira FP
FAU - da Silva, Ricardo A
AU  - da Silva RA
FAU - Marques, Melina B
AU  - Marques MB
FAU - Bittencourt, Guilherme
AU  - Bittencourt G
FAU - Pinheiro, Ricardo T
AU  - Pinheiro RT
FAU - Souza, Luciano D M
AU  - Souza LD
FAU - Portela, Luis Valmor
AU  - Portela LV
FAU - Lara, Diogo R
AU  - Lara DR
FAU - Jansen, Karen
AU  - Jansen K
FAU - Wiener, Carolina D
AU  - Wiener CD
FAU - Oses, Jean Pierre
AU  - Oses JP
LA  - eng
PT  - Journal Article
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Biomarkers)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Alcoholism/*blood
MH  - Biomarkers/blood
MH  - Brain-Derived Neurotrophic Factor/*blood
MH  - Cross-Sectional Studies
MH  - Female
MH  - Glial Cell Line-Derived Neurotrophic Factor/*blood
MH  - Humans
MH  - Male
MH  - Nerve Growth Factor/*blood
MH  - Young Adult
OTO - NOTNLM
OT  - Alcohol Abuse and Dependence
OT  - Alcohol Epidemiology
OT  - Brain-Derived Neurotrophic Factor
OT  - Glial-Derived Neurotrophic Factor
OT  - Nerve Growth Factor
EDAT- 2015/01/28 06:00
MHDA- 2016/05/20 06:00
CRDT- 2015/01/28 06:00
PHST- 2014/04/10 00:00 [received]
PHST- 2014/10/01 00:00 [accepted]
PHST- 2015/01/28 06:00 [entrez]
PHST- 2015/01/28 06:00 [pubmed]
PHST- 2016/05/20 06:00 [medline]
AID - 10.1111/acer.12592 [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 2015 Jan;39(1):30-3. doi: 10.1111/acer.12592.