Brain Advance Access originally published online on October 3, 2006
Brain 2006 129(11):2840-2855; doi:10.1093/brain/awl280
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Review Articles |
Therapeutic approaches to Alzheimer's disease
1 Department of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg Erlangen, Germany 2 Novartis Institutes for Biomedical Research, Basel Switzerland
*Correspondence to: Jens Wiltfang, Department of Psychiatry, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany E-mail: jens.wiltfang{at}psych.imed.uni-erlangen.de
Alzheimer's disease is an age-related progressive neurodegenerative disorder with an enormous unmet medical need. It is the most common form of dementia affecting 
5% of adults over 65 years. In view of our ageing society the number of patients, as well as the economical and social impact, is expected to grow dramatically in the future. Currently available medications appear to be able to produce moderate symptomatic benefits but not to stop disease progression. The search for novel therapeutic approaches targeting the presumed underlying pathogenic mechanisms has been a major focus of research and it is expected that novel medications with disease-modifying properties will emerge from these efforts in the future. In this review, currently available drugs as well as novel therapeutic strategies, in particular those targeting amyloid and tau pathologies, are discussed.
Key Words: amyloid plaques; neurofibrillary tangles; tau pathology; therapeutic strategies
Abbreviations: Aß, amyloid-ß peptide; AchE, acetylcholinesterase; APP, amyloid precursor protein; NFTs, neurofibrillary tangles; NMDA, N-methyl-D-aspartate; PHFs, paired helical filaments; PS1 and PS2, presenilin-1 and -2
Received July 4, 2006. Revised August 25, 2006. Accepted August 31, 2006.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  K. E. Paleologou, A. W. Schmid, C. C. Rospigliosi, H.-Y. Kim, G. R. Lamberto, R. A. Fredenburg, P. T. Lansbury Jr., C. O. Fernandez, D. Eliezer, M. Zweckstetter, et al. Phosphorylation at Ser-129 but Not the Phosphomimics S129E/D Inhibits the Fibrillation of {alpha}-Synuclein J. Biol. Chem., June 13, 2008; 283(24): 16895 - 16905. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. J. Wruck, M. E. Gotz, T. Herdegen, D. Varoga, L.-O. Brandenburg, and T. Pufe Kavalactones Protect Neural Cells against Amyloid {beta} Peptide-Induced Neurotoxicity via Extracellular Signal-Regulated Kinase 1/2-Dependent Nuclear Factor Erythroid 2-Related Factor 2 Activation Mol. Pharmacol., June 1, 2008; 73(6): 1785 - 1795. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Nelissen, M. Vandenbulcke, K. Fannes, A. Verbruggen, R. Peeters, P. Dupont, K. Van Laere, G. Bormans, and R. Vandenberghe A{beta} amyloid deposition in the language system and how the brain responds Brain, August 1, 2007; 130(8): 2055 - 2069. [Abstract] [Full Text] [PDF]
|
|