New insights into brain BDNF function in normal aging and Alzheimer disease

被引:485
作者
Tapia-Arancibia, Lucia [1 ,2 ]
Aliaga, Esteban [3 ]
Silhol, Michelle [1 ,2 ]
Arancibia, Sandor [1 ,2 ]
机构
[1] Univ Montpellier 2, INSERM, U710, F-34095 Montpellier, France
[2] EPHE, F-75007 Paris, France
[3] Univ Valparaiso, Fac Ciencias, Dept Fisiol, Ctr Neurobiol & Plasticidad Desarrollo, Valparaiso, Chile
关键词
Aging; BDNF; ProBDNF; TrkB receptor; beta-amyloid peptide; Alzheimer disease;
D O I
10.1016/j.brainresrev.2008.07.007
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The decline observed during aging involves multiple factors that influence several systems. it is the case for learning and memory processes which are severely reduced with aging. it is admitted that these cognitive effects result from impaired neuronal plasticity, which is altered in normal aging but mainly in Alzheimer disease. Neurotrophins and their receptors, notably BDNF, are expressed in brain areas exhibiting a high degree of plasticity (i.e. the hippocampus, cerebral cortex) and are considered as genuine molecular mediators of functional and morphological synaptic plasticity. Modification of BDNF and/or the expression of its receptors (TrkB.FL, TrkB.T1 and TrkB.T2) have been described during normal aging and Alzheimer disease. Interestingly, recent findings show that some physiologic or pathologic age-associated changes in the central nervous system could be offset by administration of exogenous BDNF and/or by stimulating its receptor expression. These molecules may thus represent a physiological reserve which could determine physiological or pathological aging. These data suggest that boosting the Expression or activity of these endogenous protective systems may be a promising therapeutic alternative to enhance healthy aging. (C) 2008 Elsevier B.V. All rights reserved
引用
收藏
页码:201 / 220
页数:20
相关论文
共 317 条
[21]   The p75 neurotrophin receptor and neuronal apoptosis [J].
Barrett, GL .
PROGRESS IN NEUROBIOLOGY, 2000, 61 (02) :205-229
[22]  
Baxter GT, 1997, J NEUROSCI, V17, P2683
[23]   Elevation of cytoskeletal protein breakdown in aged Wistar rat brain [J].
Bernath, E ;
Kupina, N ;
Liu, MC ;
Hayes, RL ;
Meegan, C ;
Wang, KKW .
NEUROBIOLOGY OF AGING, 2006, 27 (04) :624-632
[24]   Fast actions of neurotrophic factors [J].
Berninger, B ;
Poo, MM .
CURRENT OPINION IN NEUROBIOLOGY, 1996, 6 (03) :324-330
[25]   Biochemical and functional interactions between the neurotrophin receptors trk and p75NTR [J].
Bibel, M ;
Hoppe, E ;
Barde, YA .
EMBO JOURNAL, 1999, 18 (03) :616-622
[26]   ALTERNATE 5' EXONS IN THE RAT BRAIN-DERIVED NEUROTROPHIC FACTOR GENE - DIFFERENTIAL PATTERNS OF EXPRESSION ACROSS BRAIN-REGIONS [J].
BISHOP, JF ;
MUELLER, GP ;
MOURADIAN, MM .
MOLECULAR BRAIN RESEARCH, 1994, 26 (1-2) :225-232
[27]   Delineating Somatostatin's Neuronal Actions [J].
Blake, A. D. ;
Badway, A. C. ;
Strowski, M. Z. .
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS, 2004, 3 (02) :153-160
[28]   LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN DENTATE AREA OF ANESTHETIZED RABBIT FOLLOWING STIMULATION OF PERFORANT PATH [J].
BLISS, TVP ;
LOMO, T .
JOURNAL OF PHYSIOLOGY-LONDON, 1973, 232 (02) :331-356
[29]   Neurotrophin-evoked depolarization requires the sodium channel NaV1.9 [J].
Blum, R ;
Kafitz, KW ;
Konnerth, A .
NATURE, 2002, 419 (6908) :687-693
[30]  
BOTHWELL M, 1995, ANNU REV NEUROSCI, V18, P223, DOI 10.1146/annurev.ne.18.030195.001255