PMID- 24074845
OWN - NLM
STAT- MEDLINE
DCOM- 20150220
LR  - 20140701
IS  - 1476-8305 (Electronic)
IS  - 1028-415X (Linking)
VI  - 17
IP  - 5
DP  - 2014 Sep
TI  - Molecular mechanisms of cognitive impairment in iron deficiency: alterations in 
      brain-derived neurotrophic factor and insulin-like growth factor expression and 
      function in the central nervous system.
PG  - 193-206
LID - 10.1179/1476830513Y.0000000084 [doi]
AB  - OBJECTIVE: The present review examines the relationship between iron deficiency 
      and central nervous system (CNS) development and cognitive impairment, focusing 
      on the cellular and molecular mechanisms related to the expression and function 
      of growth factors, particularly the insulin-like growth factors I and II 
      (IGF-I/II) and brain-derived neurotrophic factor (BDNF), in the CNS. METHODS: 
      Nutritional deficiencies are important determinants in human cognitive 
      impairment. Among these, iron deficiency has the highest prevalence worldwide. 
      Although this ailment is known to induce psychomotor deficits during development, 
      the precise molecular and cellular mechanisms underlying these alterations have 
      not been properly elucidated. This review summarizes the available information on 
      the effect of iron deficiency on the expression and function of growth factors in 
      the CNS, with an emphasis on IGF-I/II and BDNF. RESULTS AND DISCUSSION: Recent 
      studies have shown that specific growth factors, such as IGF-I/II and BDNF, have 
      an essential role in cognition, particularly in processes involving learning and 
      memory, by the activation of intracellular-signaling pathways involved in cell 
      proliferation, differentiation, and survival. It is known that nutritional 
      deficiencies promote reductions in systemic and CNS concentrations of growth 
      factors, and that altered expression of these molecules and their receptors in 
      the CNS leads to psychomotor and developmental deficits. Iron deficiency may 
      induce these deficits by decreasing the expression and function of IGF-I/II and 
      BDNF in specific areas of the brain.
FAU - Estrada, Jose A
AU  - Estrada JA
FAU - Contreras, Irazu
AU  - Contreras I
FAU - Pliego-Rivero, F Bernardo
AU  - Pliego-Rivero FB
FAU - Otero, Gloria A
AU  - Otero GA
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20131126
PL  - England
TA  - Nutr Neurosci
JT  - Nutritional neuroscience
JID - 100892202
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Somatomedins)
SB  - IM
MH  - Anemia, Iron-Deficiency/complications/*pathology
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Cell Differentiation
MH  - Cell Proliferation
MH  - Central Nervous System/metabolism/physiopathology
MH  - *Cognition
MH  - Cognition Disorders/complications/*pathology
MH  - Disease Models, Animal
MH  - Humans
MH  - Learning
MH  - Memory
MH  - Signal Transduction
MH  - Somatomedins/genetics/*metabolism
OTO - NOTNLM
OT  - Central nervous system
OT  - Growth factors
OT  - Iron deficiency
EDAT- 2013/10/01 06:00
MHDA- 2015/02/24 06:00
CRDT- 2013/10/01 06:00
PHST- 2013/10/01 06:00 [entrez]
PHST- 2013/10/01 06:00 [pubmed]
PHST- 2015/02/24 06:00 [medline]
AID - nns199_1378529235863 [pii]
AID - 10.1179/1476830513Y.0000000084 [doi]
PST - ppublish
SO  - Nutr Neurosci. 2014 Sep;17(5):193-206. doi: 10.1179/1476830513Y.0000000084. Epub 
      2013 Nov 26.