Please use this identifier to cite or link to this item:
Title: Cell death targets and potential modulators in Alzheimer’s disease
Authors: Castro, Rui E.
Santos, Maria M. M.
Glória, Paulo M. C.
Ribeiro, Carlos J. A.
Ferreira, Duarte M. S.
Xavier, Joana M.
Moreira, Rui
Rodrigues, Cecília M. P.
Keywords: Alzheimer’s disease
Bcl-2 family
Death receptors
Small molecules
Issue Date: 2010
Citation: Castro, Rui E.; Santos, Maria M. M.; Glória, Paulo M. C. ; Ribeiro, Carlos J. A.; Ferreira, Duarte M. S.; Xavier, Joana M.; Moreira, Rui; Rodrigues, Cecília M. P.Cell Death Targets and Potential Modulators in Alzheimer’s Disease, Current Pharmaceutical Design , 16, 2851-2864, 2010.
Abstract: Apoptosis is now recognized as a normal feature in the development of the nervous system and may also play a role in neurodegenerative disorders, such as Alzheimer’s disease. Cell surface receptors, caspases, mitochondrial factors or p53 participate in the modulation and execution of cell death. Therefore, the ability to understand and manipulate the cell death machinery is an obvious goal of medical research. Potential therapeutic approaches to modulate disease by regulating apoptosis are being tested, and include the traditional use of small molecules to target specific players in the apoptosis cascade. As our understanding of apoptosis increases, further opportunities will arise for more specific therapies that will result in improved efficacy. This review focuses on molecular mechanisms of apoptosis in Alzheimer’s disease and highlights the potential use of small molecule modulators to treat neurodegenerative disorders.
Peer review: yes
ISSN: 1381-6128
Publisher Version:
Appears in Collections:FF-DQFT - Artigos em Revistas Internacionais

Files in This Item:
File Description SizeFormat 
CPD_2010_Cecilia.pdf404,11 kBAdobe PDFView/Open    Request a copy

FacebookTwitterDeliciousLinkedInDiggGoogle BookmarksMySpace
Formato BibTex MendeleyEndnote Degois 

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.