Literature DB >> 12540055

p38 mitogen activated protein kinase as a therapeutic target for Alzheimer's disease.

Stacie A Dalrymple1.   

Abstract

The characteristic pathological hallmarks of Alzheimer's disease (AD) include neuritic plaques, neurofibrillary tangles, and inflammatory changes. Current therapies, such as molecules that target enhancing cholinergic activity, can improve cognitive function in the short term but, unfortunately, have no impact on progression of the disease. Although many molecular targets have been suggested to play a causative role in AD progression, clinical data demonstrating a link between the blockade of such targets and amelioration or halting of disease progression are lacking. Even so, there are many interesting candidate targets, and current research efforts in these areas promises to deliver a wealth of new possibilities for treating AD in the future. This brief review will focus on p38 mitogen-activated protein kinase as a possible target for therapeutic intervention in AD.

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Year:  2002        PMID: 12540055     DOI: 10.1385/JMN:19:3:295

Source DB:  PubMed          Journal:  J Mol Neurosci        ISSN: 0895-8696            Impact factor:   3.444


  36 in total

1.  Early-onset Alzheimer's disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene.

Authors:  M C Chartier-Harlin; F Crawford; H Houlden; A Warren; D Hughes; L Fidani; A Goate; M Rossor; P Roques; J Hardy
Journal:  Nature       Date:  1991-10-31       Impact factor: 49.962

2.  p38 kinase is activated in the Alzheimer's disease brain.

Authors:  K Hensley; R A Floyd; N Y Zheng; R Nael; K A Robinson; X Nguyen; Q N Pye; C A Stewart; J Geddes; W R Markesbery; E Patel; G V Johnson; G Bing
Journal:  J Neurochem       Date:  1999-05       Impact factor: 5.372

3.  Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP.

Authors:  J Lewis; D W Dickson; W L Lin; L Chisholm; A Corral; G Jones; S H Yen; N Sahara; L Skipper; D Yager; C Eckman; J Hardy; M Hutton; E McGowan
Journal:  Science       Date:  2001-08-24       Impact factor: 47.728

4.  Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer's disease: potential significance for tau protein phosphorylation.

Authors:  J G Sheng; R A Jones; X Q Zhou; J M McGinness; L J Van Eldik; R E Mrak; W S Griffin
Journal:  Neurochem Int       Date:  2001 Nov-Dec       Impact factor: 3.921

5.  Phosphorylated mitogen-activated protein kinase (MAPK/ERK-P), protein kinase of 38 kDa (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.

Authors:  I Ferrer; R Blanco; M Carmona; B Puig
Journal:  J Neural Transm (Vienna)       Date:  2001       Impact factor: 3.575

6.  Activation of p38 kinase links tau phosphorylation, oxidative stress, and cell cycle-related events in Alzheimer disease.

Authors:  X Zhu; C A Rottkamp; H Boux; A Takeda; G Perry; M A Smith
Journal:  J Neuropathol Exp Neurol       Date:  2000-10       Impact factor: 3.685

Review 7.  Polymorphisms in inflammatory genes and the risk of Alzheimer disease.

Authors:  P L McGeer; E G McGeer
Journal:  Arch Neurol       Date:  2001-11

8.  Activation of the JNK/p38 pathway occurs in diseases characterized by tau protein pathology and is related to tau phosphorylation but not to apoptosis.

Authors:  C Atzori; B Ghetti; R Piva; A N Srinivasan; P Zolo; M B Delisle; S S Mirra; A Migheli
Journal:  J Neuropathol Exp Neurol       Date:  2001-12       Impact factor: 3.685

9.  Anti-inflammatory effects of a p38 mitogen-activated protein kinase inhibitor during human endotoxemia.

Authors:  Judith Branger; Bernt van den Blink; Sebastiaan Weijer; Jeffrey Madwed; Carina L Bos; Abhya Gupta; Chan-Loi Yong; Stephen H Polmar; Dariusz P Olszyna; C Erik Hack; Sander J H van Deventer; Maikel P Peppelenbosch; Tom van der Poll
Journal:  J Immunol       Date:  2002-04-15       Impact factor: 5.422

10.  Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease.

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Journal:  Nature       Date:  1995-06-29       Impact factor: 49.962

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  6 in total

1.  The p38 MAP Kinase Family as Regulators of Proinflammatory Cytokine Production in Degenerative Diseases of the CNS.

Authors:  Adam D Bachstetter; Linda J Van Eldik
Journal:  Aging Dis       Date:  2010-09-24       Impact factor: 6.745

2.  Chronic nicotine administration exacerbates tau pathology in a transgenic model of Alzheimer's disease.

Authors:  Salvatore Oddo; Antonella Caccamo; Kim N Green; Kevin Liang; Levina Tran; Yiling Chen; Frances M Leslie; Frank M LaFerla
Journal:  Proc Natl Acad Sci U S A       Date:  2005-02-10       Impact factor: 11.205

3.  Signal transduction in Alzheimer disease: p21-activated kinase signaling requires C-terminal cleavage of APP at Asp664.

Authors:  Thuy-Vi V Nguyen; Veronica Galvan; Wei Huang; Surita Banwait; Huidong Tang; Junli Zhang; Dale E Bredesen
Journal:  J Neurochem       Date:  2007-11-06       Impact factor: 5.372

4.  A novel p38 alpha MAPK inhibitor suppresses brain proinflammatory cytokine up-regulation and attenuates synaptic dysfunction and behavioral deficits in an Alzheimer's disease mouse model.

Authors:  Lenka Munoz; Hantamalala Ralay Ranaivo; Saktimayee M Roy; Wenhui Hu; Jeffrey M Craft; Laurie K McNamara; Laura Wing Chico; Linda J Van Eldik; D Martin Watterson
Journal:  J Neuroinflammation       Date:  2007-09-04       Impact factor: 8.322

5.  Insight into the Structural Determinants of Imidazole Scaffold-Based Derivatives as TNF-α Release Inhibitors by in Silico Explorations.

Authors:  Yuan Wang; Mingwei Wu; Chunzhi Ai; Yonghua Wang
Journal:  Int J Mol Sci       Date:  2015-08-25       Impact factor: 5.923

6.  p38 MAPK Inhibition Improves Synaptic Plasticity and Memory in Angiotensin II-dependent Hypertensive Mice.

Authors:  Hai-Long Dai; Wei-Yuan Hu; Li-Hong Jiang; Le Li; Xue-Feng Gaung; Zhi-Cheng Xiao
Journal:  Sci Rep       Date:  2016-06-10       Impact factor: 4.379

  6 in total

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