PMID- 23870838
OWN - NLM
STAT- MEDLINE
DCOM- 20140402
LR  - 20130920
IS  - 1558-1497 (Electronic)
IS  - 0197-4580 (Linking)
VI  - 34
IP  - 12
DP  - 2013 Dec
TI  - Reduced neuroplasticity in aged rats: a role for the neurotrophin brain-derived 
      neurotrophic factor.
PG  - 2768-76
LID - S0197-4580(13)00269-8 [pii]
LID - 10.1016/j.neurobiolaging.2013.06.014 [doi]
AB  - Aging is a physiological process characterized by a significant reduction of 
      neuronal plasticity that might contribute to the functional defects observed in 
      old subjects. Even if the neurobiological mechanisms that contribute to such 
      impairment remain largely unknown, a role for neurotrophic molecules, such as the 
      neurotrophin brain-derived neurotrophic factor (BDNF), has been postulated. On 
      this basis, the purpose of this study was to provide a detailed investigation of 
      the BDNF system, at transcriptional and translational levels, in the ventral and 
      dorsal hippocampus and in the prefrontal cortex of middle-aged and old rats, 
      compared with in adult animals. The expression of major players in BDNF 
      regulation and response, including the transcription factors, calcium-responsive 
      transcription factor, cyclic adenosine monophosphate (cAMP) responsive 
      element-binding protein (CREB), and neuronal Per Arnt Sim (PAS) domain protein 4, 
      and the high-affinity receptor tropomyosin receptor kinase B (TrkB), was also 
      analyzed. Our results demonstrate that the BDNF system is affected at different 
      levels in aged rats with global impairment including reduced transcription, 
      impaired protein synthesis and processing, and decreased activation of the TrkB 
      receptors. These modifications might contribute to the cognitive deficits 
      associated with aging and suggest that pharmacological strategies aimed at 
      restoring reduced neurotrophism might be useful to counteract age-related 
      cognitive decline.
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Calabrese, Francesca
AU  - Calabrese F
AD  - Department of Pharmacological and Biomolecular Sciences, Universita' degli Studi 
      di Milano, Milan, Italy.
FAU - Guidotti, Gianluigi
AU  - Guidotti G
FAU - Racagni, Giorgio
AU  - Racagni G
FAU - Riva, Marco A
AU  - Riva MA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130717
PL  - United States
TA  - Neurobiol Aging
JT  - Neurobiology of aging
JID - 8100437
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Transcription Factors)
RN  - 0 (calcium response transcription factor 1, rat)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Aging/*genetics/*physiology
MH  - Animals
MH  - Brain/metabolism
MH  - Brain-Derived Neurotrophic Factor/metabolism/*physiology
MH  - Cognition Disorders/drug therapy/etiology
MH  - Cyclic AMP Response Element-Binding Protein/physiology
MH  - Male
MH  - Molecular Targeted Therapy
MH  - Neuronal Plasticity/*physiology
MH  - Protein Biosynthesis/genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, trkB/physiology
MH  - Transcription Factors/physiology
MH  - Transcription, Genetic/genetics
OTO - NOTNLM
OT  - Aging
OT  - BDNF
OT  - Carf
OT  - Cognition
OT  - Creb
OT  - Npas4
OT  - Transcription factors
OT  - TrkB
EDAT- 2013/07/23 06:00
MHDA- 2014/04/03 06:00
CRDT- 2013/07/23 06:00
PHST- 2013/02/05 00:00 [received]
PHST- 2013/06/01 00:00 [revised]
PHST- 2013/06/18 00:00 [accepted]
PHST- 2013/07/23 06:00 [entrez]
PHST- 2013/07/23 06:00 [pubmed]
PHST- 2014/04/03 06:00 [medline]
AID - S0197-4580(13)00269-8 [pii]
AID - 10.1016/j.neurobiolaging.2013.06.014 [doi]
PST - ppublish
SO  - Neurobiol Aging. 2013 Dec;34(12):2768-76. doi: 
      10.1016/j.neurobiolaging.2013.06.014. Epub 2013 Jul 17.