Cdk5 is a key factor in tau aggregation and tangle formation in vivo

被引:421
作者
Noble, W
Olm, V
Takata, K
Casey, E
O, M
Meyerson, J
Gaynor, K
LaFrancois, J
Wang, LL
Kondo, T
Davies, P
Burns, M
Veeranna
Nixon, R
Dickson, D
Matsuoka, Y
Ahlijanian, M
Lau, LF
Duff, K [1 ]
机构
[1] NYU, Nathan S Kline Inst Psychiat Res, Ctr Dementia Res, 140 Old Orangeburg Rd, Orangeburg, NY 10962 USA
[2] Yeshiva Univ Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10461 USA
[3] Mayo Clin, Jacksonville, FL 32224 USA
[4] Pfizer Inc, Global Res & Dev, CNS Discovery, Groton, CT 06340 USA
关键词
D O I
10.1016/S0896-6273(03)00259-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Tau aggregation is a common feature of neurodegenerative diseases such as Alzheimer's disease, and hyperphosphorylation of tau has been implicated as a fundamental pathogenic mechanism in this process. To examine the impact of cdk5 in tau aggregation and tangle formation, we crossed transgenic mice overexpressing the cdk5 activator p25, with transgenic mice overexpressing mutant (P301L) human tau. Tau was hyperphosphorylated at several sites in the double transgenics, and there was a highly significant accumulation of aggregated tau in brainstem and cortex. This was accompanied by increased numbers of silver-stained neurofibrillary tangles (NFTs). Insoluble tau was also associated with active GSK. Thus, cdk5 can initiate a major impact on tau pathology progression that probably involves several kinases. Kinase inhibitors may thus be beneficial therapeutically.
引用
收藏
页码:555 / 565
页数:11
相关论文
共 50 条
[41]   Glycogen synthase kinase-3β phosphorylates protein tau and rescues the axonopathy in the central nervous system of human four-repeat tau transgenic mice [J].
Spittaels, K ;
Van den Haute, C ;
Van Dorpe, J ;
Geerts, H ;
Mercken, M ;
Bruynseels, K ;
Lasrado, R ;
Vandezande, K ;
Laenen, I ;
Boon, T ;
Van Lint, J ;
Vandenheede, J ;
Moechars, D ;
Loos, R ;
Van Leuven, F .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (52) :41340-41349
[42]   TAU-PROTEIN KINASE-I IS ESSENTIAL FOR AMYLOID BETA-PROTEIN-INDUCED NEUROTOXICITY [J].
TAKASHIMA, A ;
NOGUCHI, K ;
SATO, K ;
HOSHINO, T ;
IMAHORI, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (16) :7789-7793
[43]   Aβ amyloidosis induces the initial stage of tau accumulation in APPSw mice [J].
Tomidokoro, Y ;
Ishiguro, K ;
Harigaya, Y ;
Matsubara, E ;
Ikeda, M ;
Park, JM ;
Yasutake, K ;
Kawarabayashi, T ;
Okamoto, K ;
Shoji, M .
NEUROSCIENCE LETTERS, 2001, 299 (03) :169-172
[44]   p35/Cdk5 pathway mediates soluble amyloid-β peptide-induced tau phosphorylation in vitro [J].
Town, T ;
Zolton, J ;
Shaffner, R ;
Schnell, B ;
Crescentini, R ;
Wu, YJ ;
Zeng, J ;
DelleDonne, A ;
Obregon, D ;
Tan, J ;
Mullan, M .
JOURNAL OF NEUROSCIENCE RESEARCH, 2002, 69 (03) :362-372
[45]   A survey of Cdk5 activator p35 and p25 levels in Alzheimer's disease brains [J].
Tseng, HC ;
Zhou, Y ;
Shen, Y ;
Tsai, LH .
FEBS LETTERS, 2002, 523 (1-3) :58-62
[46]   M-Calpain (calcium-activated neutral proteinase) in Alzheimer's disease brains [J].
Tsuji, T ;
Shimohama, S ;
Kimura, J ;
Shimizu, K .
NEUROSCIENCE LETTERS, 1998, 248 (02) :109-112
[47]  
Veeranna, 1998, J NEUROSCI, V18, P4008
[48]   Inhibition of neuronal cyclin-dependent kinase-5 by staurosporine and purine analogs is independent of activation by munc-18 [J].
Veeranna ;
Shetty, KT ;
Amin, N ;
Grant, P ;
Albers, RW ;
Pant, HC .
NEUROCHEMICAL RESEARCH, 1996, 21 (05) :629-636
[49]   Rapid tyrosine phosphorylation of neuronal proteins including tau and focal adhesion kinase in response to amyloid-β peptide exposure:: Involvement of src family protein kinases [J].
Williamson, R ;
Scales, T ;
Clark, BR ;
Gibb, G ;
Reynolds, CH ;
Kellie, S ;
Bird, IN ;
Varndell, IM ;
Sheppard, PW ;
Everall, I ;
Anderton, BH .
JOURNAL OF NEUROSCIENCE, 2002, 22 (01) :10-20
[50]   Preferential labeling of Alzheimer neurofibrillary tangles with antisera for tau protein kinase (TPK)I glycogen synthase kinase-3 beta and cyclin-dependent kinase 5, a component of TPK II [J].
Yamaguchi, H ;
Ishiguro, K ;
Uchida, T ;
Takashima, A ;
Lemere, CA ;
Imahori, K .
ACTA NEUROPATHOLOGICA, 1996, 92 (03) :232-241