Neuroprotective strategies for basal ganglia degeneration: Parkinson's and Huntington's diseases

被引:225
作者
Alexi, T [1 ]
Borlongan, CV
Faull, RLM
Williams, CE
Clark, RG
Gluckman, PD
Hughes, PE
机构
[1] Univ Auckland, Sch Med, Res Ctr Dev Med & Biol, Auckland, New Zealand
[2] Univ Auckland, Sch Med, Dept Anat & Radiol, Auckland, New Zealand
[3] Univ Auckland, Sch Med, Dept Pharmacol & Clin Pharmacol, Auckland, New Zealand
[4] NIDA, Intramural Res Program, NIH, Baltimore, MD USA
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
neurotrophic factors; excitotoxicity; metabolic compromise; oxidative stress; energy supplements; antioxidants; cell transplantation; immunosuppressants; immunophilins; apoptosis; striatum; substantia nigra; caudate-putamen;
D O I
10.1016/S0301-0082(99)00032-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
There are three main mechanisms of neuronal cell death which may act separately or cooperatively to cause neurodegeneration. This lethal triplet of metabolic compromise, excitotoxicity, and oxidative stress causes neuronal cell death that is both necrotic and apoptotic in nature. Aspects of each of these three mechanisms are believed to play a role in the neurodegeneration that occurs in both Parkinsons and Huntington's diseases. Strategies to rescue or protect injured neurons usually involve promoting neuronal growth and function or interfering with neurotoxic processes. Considerable research has been done on testing a large array of neuroprotective agents using animal models which mimic these disorders. Some of these approaches have progressed to the clinical arena. Here, we review neuroprotective strategies which have been found to successfully ameliorate the neurodegeneration associated with Parkinson's and Huntington's diseases. First, we will give an overview of the mechanisms of cell death and the background of Parkinson's and Huntington's diseases. Then we will elaborate on a range of neuroprotective strategies, including neurotrophic factors, anti-excitotoxins, antioxidants, bioenergetic supplements, anti-apoptotics, immunosuppressants, and cell transplantation techniques. Most of these approaches hold promise as potential therapies in the treatment of these disorders. (C) 2000 Elsevier Science Ltd. All lights reserved.
引用
收藏
页码:409 / 470
页数:62
相关论文
共 738 条
[1]   A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe [J].
Abbas, N ;
Lücking, CB ;
Ricard, S ;
Dürr, A ;
Bonifati, V ;
De Michele, G ;
Bouley, S ;
Vaughan, JR ;
Gasser, T ;
Marconi, R ;
Broussolle, E ;
Brefel-Courbon, C ;
Harhangi, BS ;
Oostra, AB ;
Fabrizio, E ;
Böhme, GA ;
Pradier, L ;
Wood, NW ;
Filla, A ;
Meco, G ;
Denefle, P ;
Agid, Y ;
Brice, A .
HUMAN MOLECULAR GENETICS, 1999, 8 (04) :567-574
[2]   A COMPARISON OF NEUROTROPHIC EFFECTS OF EPIDERMAL GROWTH-FACTOR AND BASIC FIBROBLAST GROWTH-FACTOR IN PRIMARY CULTURED NEURONS FROM VARIOUS REGIONS OF FETAL-RAT BRAIN [J].
ABE, K ;
TAKAYANAGI, M ;
SAITO, H .
JAPANESE JOURNAL OF PHARMACOLOGY, 1990, 54 (01) :45-51
[3]   Methamphetamine causes lipid peroxidation and an increase in superoxide dismutase activity in the rat striatum [J].
Açikgöz, O ;
Gönenç, S ;
Kayatekin, BM ;
Uysal, N ;
Pekçetin, Ç ;
Semin, I ;
Güre, A .
BRAIN RESEARCH, 1998, 813 (01) :200-202
[4]   Oxidative DNA damage in the parkinsonian brain: An apparent selective increase in 8-hydroxyguanine levels in substantia nigra [J].
Alam, ZI ;
Jenner, A ;
Daniel, SE ;
Lees, AJ ;
Cairns, N ;
Marsden, CD ;
Jenner, P ;
Halliwell, B .
JOURNAL OF NEUROCHEMISTRY, 1997, 69 (03) :1196-1203
[5]   A non-invasive transport system for GDNF across the blood-brain barrier [J].
Albeck, DS ;
Hoffer, BJ ;
Quissell, D ;
Sanders, LS ;
Zerbe, G ;
Granholm, ACE .
NEUROREPORT, 1997, 8 (9-10) :2293-2298
[6]   TROPHIC ACTIONS OF TRANSFORMING GROWTH-FACTOR-ALPHA ON MESENCEPHALIC DOPAMINERGIC-NEURONS DEVELOPING IN CULTURE [J].
ALEXI, T ;
HEFTI, F .
NEUROSCIENCE, 1993, 55 (04) :903-918
[7]   Neurotrophin-4/5 selectively protects nigral calbindin-containing neurons in rats with medial forebrain bundle transections [J].
Alexi, T ;
Hefti, F .
NEUROSCIENCE, 1996, 72 (04) :911-921
[8]   Metabolic compromise with systemic 3-nitropropionic acid produces striatal apoptosis in Sprague-Dawley rats but not in BALB/c ByJ mice [J].
Alexi, T ;
Hughes, PE ;
Knüsel, B ;
Tobin, AJ .
EXPERIMENTAL NEUROLOGY, 1998, 153 (01) :74-93
[9]   Protective effects of neurotrophin-4/5 and transforming growth factor-alpha. On striatal neuronal phenotypic degeneration after excitotoxic lesioning with quinolinic acid [J].
Alexi, T ;
Venero, JL ;
Hefti, F .
NEUROSCIENCE, 1997, 78 (01) :73-86
[10]   3-nitropropionic acid's lethal triplet: cooperative pathways of neurodegeneration [J].
Alexi, T ;
Hughes, PE ;
Faull, RLM ;
Williams, CE .
NEUROREPORT, 1998, 9 (11) :R57-R64