PMID- 16787836
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20070709
LR  - 20230320
IS  - 1029-8428 (Print)
IS  - 1029-8428 (Linking)
VI  - 2
IP  - 2-3
DP  - 2000
TI  - Neurotrophic factors in neurodegenerative disorders: model of Parkinson's 
      disease.
PG  - 115-37
AB  - Neurotrophic factors are compounds that enhance neuronal survival and 
      differentiation. Most of these compounds exert their pharmacological actions on 
      selective types of neurons, and therefore, are considered promising new 
      therapeutic agents for the treatment of different neurodegenerative disorders 
      characterized by selective degeneration of certain neuronal groups. Those 
      compounds have been used in humans for several neurological disorders including 
      amyotrophic lateral sclerosis--ciliary derived neurotrophic factor (CNTF) and 
      brain derived neurotrophic factor (BDNF), Alzheimer's disease and peripheral 
      neuropathy--nerve growth factor (NGF) and Parkinson's disease (PD)--glial derived 
      neurotrophic factor (GDNF). In spite of well founded clinical experiments by 
      previous experimental work in animal models some of these trials have been 
      negative. For instance, animal models of PD have shown that several neurotrophic 
      factors, including GDNF and other compounds, reduce apoptosis and increase 
      resistance of dopamine neurons to neurotoxins in vitro. These compounds prevent 
      or recover the damage to dopamine neurons of rodents and primates produced by 
      chemical or mechanical acute lesions including 6-OH-DA, MPTP, methamphetamine and 
      axotomy. The differences between the promising results obtained in experimental 
      models and the lack of clinical results or excessive toxicity found in humans 
      could be attributed to the following reasons: (a) Lack of relevance between the 
      pathogenesis of the experimental lesion and the corresponding neurodegenerative 
      disorder. (b) Poor correlation between results obtained in acute, self-limited, 
      selective deficit produced to experimental animals and those available in more 
      complex, chronic and progressive disorders involving patients. (c) Inadequate 
      delivery of the active product to the target area in the human brain. (d) Poor 
      information from acute experiments in animals which does not predict long-term 
      effects of chronic infusion in humans. Further experimental work, therefore, is 
      needed to transfer these neurotrophic factors to the clinic.
FAU - Garcia de Yebenes, J
AU  - Garcia de Yebenes J
AD  - Servicio de Neurologia, Fundacion Jimenez Diaz, Avda de Reyes Catolicos 2, Madrid 
      28040, Spain. jgyebenes@fjd.es
FAU - Yebenes, J
AU  - Yebenes J
FAU - Mena, M A
AU  - Mena MA
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
EDAT- 2006/06/22 09:00
MHDA- 2006/06/22 09:01
CRDT- 2006/06/22 09:00
PHST- 2006/06/22 09:00 [pubmed]
PHST- 2006/06/22 09:01 [medline]
PHST- 2006/06/22 09:00 [entrez]
AID - 10.1007/BF03033789 [doi]
PST - ppublish
SO  - Neurotox Res. 2000;2(2-3):115-37. doi: 10.1007/BF03033789.