Abstract:
:Parkinson's disease (PD) is caused by the degeneration of dopaminergic neurons of substantia nigra projecting to striatum. The cause of idiopathic PD is obscure, and most cases are sporadic. It is widely accepted that there is a genetic component of the disease, and the earlier the age of onset, the greater the likelihood that genetic factors play a dominant role. Oxidative stress of the substantia nigra seems to contain the driving force for neurodegeneration, leading to a destructive "toxic cycle." The most prevalent therapy is levodopa administration, but it is not efficacious after several years of treatment. Several alternative therapies are currently being explored, such as neuroprotective approaches. Compounds with potentially neuroprotective efficacy such as selegiline, dopamine agonists, riluzole, creatine, and coenzyme Q10 are currently being tested. Trophic factors represent another class of neuroprotective compounds, but their intracerebral administration is difficult to achieve. In this respect, a potentially useful therapeutic approach is grafting cell vectors that release trophic molecules that stimulate regeneration in the damaged nigrostriatal system. Promising results have been obtained with fibroblasts engineered to secrete glial cell line-derived neurotrophic factor (GDNF) or brain-derived neurotrophic factor (BDNF) or viral vectors expressing GDNF. We have tested the suitability of intrastriatal grafts of chromaffin cells obtained from the Zuckerkandl's organ, which exert beneficial effects in parkinsonian rats, and release trophic factors such as GDNF and transforming growth factor-beta1 (TGF-beta1).
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Fernandez-Espejo Edoi
10.1385/MN:29:1:15subject
Has Abstractpub_date
2004-02-01 00:00:00pages
15-30issue
1eissn
0893-7648issn
1559-1182pii
MN:29:1:15journal_volume
29pub_type
杂志文章,评审abstract::(-)-Epigallocatechin-3‑gallate (EGCG), the predominant constituent of green tea, has been demonstrated to be neuroprotective against acute ischemic stroke. However, the long-term actions of EGCG on neurogenesis and functional recovery after ischemic stroke have not been identified. In this study, C57BL/6 mice underwen...
journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-9924-0
更新日期:2017-07-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-018-0978-z
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-012-8383-5
更新日期:2013-06-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-9711-y
更新日期:2017-03-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 已发布勘误
doi:10.1007/s12035-018-1095-8
更新日期:2018-10-01 00:00:00
abstract::The development of in vitro amplification systems allows detecting femtomolar amounts of prion protein scrapie (PrP(Sc)) in human cerebrospinal fluid (CSF). We performed a CSF study to determine the effects of prion disease type, codon 129 genotype, PrP(Sc) type, and other disease-related factors on the real-time quak...
journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-014-8709-6
更新日期:2015-02-01 00:00:00
abstract::Early-onset familial Alzheimer's disease (AD) is most commonly associated with the mutations in presenilin-1 (PS1). PS1 is the catalytic component of the γ-secretase complex, which cleaves amyloid precursor protein to produce amyloid-β (Aβ), the major cause of AD. Presenilin enhancer 2 (Pen2) is critical for activatin...
journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-014-8969-1
更新日期:2015-12-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-017-0795-9
更新日期:2018-07-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-014-9076-z
更新日期:2016-03-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-0048-3
更新日期:2017-09-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-015-9638-8
更新日期:2017-01-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-013-8620-6
更新日期:2014-06-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-019-01687-6
更新日期:2019-12-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-015-9620-5
更新日期:2016-12-01 00:00:00
abstract::Inhalational general anesthetics, such as sevoflurane and isoflurane, modulate a subset of brain Kv1 potassium channels. However, the Kv1.2 channel is resistant to propofol, a commonly used intravenous alkylphenol anesthetic. We hypothesize that propofol binds to a presumed pocket involving the channel's S4-S5 linker,...
journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-017-0437-2
更新日期:2018-02-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-014-8667-z
更新日期:2014-12-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,meta分析,评审
doi:10.1007/s12035-015-9271-6
更新日期:2016-05-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-018-1263-x
更新日期:2019-04-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-012-8241-5
更新日期:2012-04-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/BF02816114
更新日期:1994-08-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-015-9236-9
更新日期:2015-10-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-012-8275-8
更新日期:2012-06-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1385/MN:26:1:109
更新日期:2002-08-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-0047-4
更新日期:2017-09-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1385/MN:32:2:157
更新日期:2005-10-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-0171-1
更新日期:2017-10-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-018-1211-9
更新日期:2019-04-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-015-9518-2
更新日期:2016-11-01 00:00:00
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journal_title:Molecular neurobiology
pub_type: 杂志文章,评审
doi:10.1007/s12035-015-9641-0
更新日期:2017-01-01 00:00:00
abstract::The aim of this study was to examine if nicotine was able to improve cognition deficits in a mouse model of chronic mild stress. Twenty-four male C57BL/6 mice were divided into three groups: control, stress, and stress with nicotine treatment. The animal model was established by combining chronic unpredictable mild st...
journal_title:Molecular neurobiology
pub_type: 杂志文章
doi:10.1007/s12035-016-0012-2
更新日期:2017-08-01 00:00:00