Minocycline as a potential therapeutic agent in neurodegenerative disorders characterised by protein misfolding

被引:55
作者
Noble, Wendy [1 ]
Garwood, Claire J. [1 ]
Hanger, Diane P. [1 ]
机构
[1] Kings Coll London, Inst Psychiat, Dept Neurosci, MRC Ctr Neurodegenerat Res, London SE5 8AF, England
关键词
minocycline; protein aggregation; neuroinflammation; neurodegeneration; protein misfolding; AMYOTROPHIC-LATERAL-SCLEROSIS; SLOWS DISEASE PROGRESSION; MOUSE MODEL; MICROGLIAL ACTIVATION; PRION PROTEIN; CELL-DEATH; A-BETA; ALZHEIMERS; TAU; TETRACYCLINES;
D O I
10.4161/pri.3.2.8820
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Many neurodegenerative disorders share common features including the accumulation of aggregated misfolded proteins, neuroinflammation and the induction of apoptosis. While the contributions of each of these individual elements to neuronal death remain unclear, a commonly used antibiotic, minocycline, has been shown to reduce the progression and severity of disease in several models of neurodegeneration by variously downregulating these molecular pathways. Here we discuss the evidence for the potential of minocycline as a broad-specificity therapeutic agent for those neurodegenerative diseases that are characterized by the presence of misfolded proteins.
引用
收藏
页码:78 / 83
页数:6
相关论文
共 71 条
[1]
Minocycline inhibits poly(ADP-ribose) polymerase-1 at nanomolar concentrations [J].
Alano, Conrad C. ;
Kauppinen, Tiina M. ;
Valls, Andreu Viader ;
Swanson, Raymond A. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2006, 103 (25) :9685-9690
[2]
A novel mechanism of action of tetracyclines: Effects on nitric oxide synthases [J].
Amin, AR ;
Attur, MG ;
Thakker, GD ;
Patel, PD ;
Vyas, PR ;
Patel, RN ;
Patel, IR ;
Abramson, SB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (24) :14014-14019
[3]
Blockade of PKCδ proteolytic activation by loss of function mutants rescues mesencephalic dopaminergic neurons from methylcyclopentadienyl manganese tricarbonyl (MMT)-induced apoptotic cell death [J].
Anantharam, V ;
Kitazawa, M ;
Latchoumycandane, C ;
Kanthasamy, A ;
Kanthasamy, AG .
PROTECTIVE STRATEGIES FOR NEURODEGENERATIVE DISEASES, 2004, 1035 :271-289
[4]
Phosphorylation of Ser-129 is the dominant pathological modification of α-synuclein in familial and sporadic Lewy body disease [J].
Anderson, John P. ;
Walker, Donald E. ;
Goldstein, Jason M. ;
de laat, Rian ;
Banducci, Kelly ;
Caccavello, Russell J. ;
Barbour, Robin ;
Huang, Jiping ;
Kling, Kristin ;
Lee, Michael ;
Diep, Linnea ;
Keim, Pamela S. ;
Shen, Xiaofeng ;
Chataway, Tim ;
Schlossmacher, Michael G. ;
Seubert, Peter ;
Schenk, Dale ;
Sinha, Sukanto ;
Gai, Wei Ping ;
Chilcote, Tamie J. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (40) :29739-29752
[5]
Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms [J].
Andorfer, C ;
Kress, Y ;
Espinoza, M ;
de Silva, R ;
Tucker, KL ;
Barde, YA ;
Duff, K ;
Davies, P .
JOURNAL OF NEUROCHEMISTRY, 2003, 86 (03) :582-590
[6]
Tau, tangles, and Alzheimer's disease [J].
Binder, LI ;
Guillozet-Bongaarts, AL ;
Garcia-Sierra, F ;
Berry, RW .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2005, 1739 (2-3) :216-223
[7]
Clinical potential of minocycline for neurodegenerative disorders [J].
Blum, D ;
Chtarto, A ;
Tenenbaum, L ;
Brotchi, J ;
Levivier, M .
NEUROBIOLOGY OF DISEASE, 2004, 17 (03) :359-366
[8]
Reduced retina microglial activation and improved optic nerve integrity with minocycline treatment in the DBA/2J mouse model of glaucoma [J].
Bosco, Alejandra ;
Inman, Denise M. ;
Steele, Michael R. ;
Wu, Guangming ;
Soto, Ileana ;
Marsh-Armstrong, Nicholas ;
Hubbard, Walter C. ;
Calkins, David J. ;
Horner, Philip J. ;
Vetter, Monica L. .
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2008, 49 (04) :1437-1446
[9]
Programmed cell death mechanisms in neurological disease [J].
Bredesen, Dale E. .
CURRENT MOLECULAR MEDICINE, 2008, 8 (03) :173-186
[10]
Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1 [J].
Bruijn, LI ;
Houseweart, MK ;
Kato, S ;
Anderson, KL ;
Anderson, SD ;
Ohama, E ;
Reaume, AG ;
Scott, RW ;
Cleveland, DW .
SCIENCE, 1998, 281 (5384) :1851-1854