Alzheimer's disease: the two-hit hypothesis

被引:341
作者
Zhu, XW [1 ]
Raina, AK [1 ]
Perry, G [1 ]
Smith, MA [1 ]
机构
[1] Case Western Reserve Univ, Inst Pathol, Cleveland, OH 44106 USA
关键词
D O I
10.1016/S1474-4422(04)00707-0
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
There are many lines of evidence showing that oxidative stress and aberrant mitogenic changes have important roles in the pathogenesis of Alzheimer's disease (AD). However, although both oxidative stress and cell cycle-related abnormalities are early events, occurring before any cytopathology, the relation between these two events, and their role in pathophysiology was, until recently, unclear. However, on the basis of studies of mitogenic and oxidative stress signalling pathways in AD, we proposed a "two-hit hypothesis" which states that although either oxidative stress or abnormalities in mitotic signalling can independently serve as initiators, both processes are necessary to propagate disease pathogenesis. In this paper, we summarise evidence for oxidative stress and abnormal mitotic alterations in AD and explain the two-hit hypothesis by describing how both mechanisms are necessary and invariant features of disease.
引用
收藏
页码:219 / 226
页数:8
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共 137 条
[31]   Phosphorylated mitogen-activated protein kinase (MAPK/ERK-P), protein kinase of 38kDa (p38-P), stress-activated protein kinase (SAPK/JNK-P), and calcium/calmodulin-dependent kinase II (CaM kinase II) are differentially expressed in tau deposits in neurons and glial cells in tauopathies [J].
Ferrer, I ;
Blanco, R ;
Carmona, M ;
Puig, B .
JOURNAL OF NEURAL TRANSMISSION, 2001, 108 (12) :1397-1415
[32]   Phosphorylated c-MYC expression in Alzheimer disease, Pick's disease, progressive supranuclear palsy and corticobasal degeneration [J].
Ferrer, I ;
Blanco, R ;
Carmona, M ;
Puig, B .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2001, 27 (05) :343-351
[33]  
Ferrer I, 2001, BRAIN PATHOL, V11, P144
[34]  
GARTNER U, 1995, NEUROREPORT, V6, P1441
[35]   Elevated expression of p21ras is an early event in Alzheimer's disease and precedes neurofibrillary degeneration [J].
Gärtner, U ;
Holzer, M ;
Arendt, T .
NEUROSCIENCE, 1999, 91 (01) :1-5
[36]   Involvement of cell cycle elements, cyclin-dependent kinases, pRb, and E2F•DP, in B-amyloid-induced neuronal death [J].
Giovanni, A ;
Wirtz-Brugger, F ;
Keramaris, E ;
Slack, R ;
Park, DS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (27) :19011-19016
[37]  
Gomez-Pinilla F, 1990, Neuroreport, V1, P211
[38]  
Good PF, 1996, AM J PATHOL, V149, P21
[39]  
GRANA X, 1995, ONCOGENE, V11, P211
[40]   Presenilin-1 regulates the neuronal threshold to excitotoxicity both physiologically and pathologically [J].
Grilli, M ;
Lozza, G ;
Brusa, R ;
Casarini, M ;
Uberti, D ;
Rozmahel, R ;
Westaway, D ;
St George-Hyslop, P ;
Memo, M ;
Ongini, E .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (23) :12822-12827