Amyloid pathology and protein kinase C (PKQ): Possible therapeutics effects of PKC activators

被引:18
作者
Olariu, A [1 ]
Yamada, K
Nabeshima, T
机构
[1] NIMH, Unit Neuroplastic, NIH, Bethesda, MD 20892 USA
[2] Kanazawa Univ, Grad Sch Nat Sci & Technol, Div Life Sci, Neuropharmacol Lab, Kanazawa, Ishikawa 9201192, Japan
[3] Nagoya Univ, Grad Sch Med, Dept Neuropsychopharmacol & Hosp Pharm, Nagoya, Aichi 4668560, Japan
关键词
amyloid protein; Alzheimer's disease; signal transduction; protein kinase C; cell death;
D O I
10.1254/jphs.CPJ04004X
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Amyloid beta-protein (Abeta) is one of the most studied peptides in human neurodegenerative disorders. Although much has been learned about the biochemistry of this peptide, fundamental questions such as when and how the Abeta becomes pathologic remain unanswered. In this article we review the recent findings on the biology and pathology of Abeta and the role protein kinase C (PKC) plays in these processes. The potential neuroprotective role of PKC and the possible therapeutic effects of PKC activators in Alzheimer's disease (AD) will be discussed. Briefly, comments will be also addressed on the role of PKC in cell death and neurogenesis in AD.
引用
收藏
页码:1 / 5
页数:5
相关论文
共 31 条
  • [1] Protein kinase C anchoring deficit in postmortem brains of Alzheimer's disease patients
    Battaini, F
    Pascale, A
    Lucchi, L
    Pasinetti, GM
    Govoni, S
    [J]. EXPERIMENTAL NEUROLOGY, 1999, 159 (02) : 559 - 564
  • [2] Restoring production of hippocampal neurons in old age
    Cameron, HA
    McKay, RDG
    [J]. NATURE NEUROSCIENCE, 1999, 2 (10) : 894 - 897
  • [3] Aβ, aging, and Alzheimer's disease:: A tale, models, and hypotheses
    Chaney, MO
    Baudry, J
    Esh, C
    Childress, J
    Luehrs, DC
    Kokjohn, TA
    Roher, AE
    [J]. NEUROLOGICAL RESEARCH, 2003, 25 (06) : 581 - 589
  • [4] DECREASED LEVELS OF PROTEIN KINASE-C IN ALZHEIMER BRAIN
    COLE, G
    DOBKINS, KR
    HANSEN, LA
    TERRY, RD
    SAITOH, T
    [J]. BRAIN RESEARCH, 1988, 452 (1-2) : 165 - 174
  • [5] Mitotic signaling by β-amyloid causes neuronal death
    Copani, A
    Condorelli, F
    Caruso, A
    Vancheri, C
    Sala, A
    Stella, AMG
    Canonico, PL
    Nicoletti, F
    Sortino, MA
    [J]. FASEB JOURNAL, 1999, 13 (15) : 2225 - 2234
  • [6] GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES
    CORDER, EH
    SAUNDERS, AM
    STRITTMATTER, WJ
    SCHMECHEL, DE
    GASKELL, PC
    SMALL, GW
    ROSES, AD
    HAINES, JL
    PERICAKVANCE, MA
    [J]. SCIENCE, 1993, 261 (5123) : 921 - 923
  • [7] The use of formic acid to embellish amyloid plaque detection in Alzheimer's disease tissues misguides key observations
    D'Andrea, MR
    Reiser, PA
    Polkovitch, DA
    Gumula, NA
    Branchide, B
    Hertzog, BM
    Schmidheiser, D
    Belkowski, S
    Gastard, MC
    Andrade-Gordon, P
    [J]. NEUROSCIENCE LETTERS, 2003, 342 (1-2) : 114 - 118
  • [8] β-amyloid activates the mitogen-activated protein kinase cascade via hippocampal α7 nicotinic acetylcholine receptors:: In vitro and in vivo mechanisms related to Alzheimer's disease
    Dineley, KT
    Westerman, M
    Bui, D
    Bell, K
    Ashe, KH
    Sweatt, JD
    [J]. JOURNAL OF NEUROSCIENCE, 2001, 21 (12) : 4125 - 4133
  • [9] Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice
    Etcheberrigaray, R
    Tan, M
    Dewachter, I
    Kuipéri, C
    Van der Auwera, I
    Wera, S
    Qiao, LX
    Bank, B
    Nelson, TJ
    Kozikowski, AP
    Van Leuven, F
    Alkon, DL
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (30) : 11141 - 11146
  • [10] Phosphorylation of presenilin 1 at the caspase recognition site regulates its proteolytic processing and the progression of apoptosis
    Fluhrer, R
    Friedlein, A
    Haass, C
    Walter, J
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (03) : 1585 - 1593