Journal
NEUROLOGIA
Volume 33, Issue 1, Pages 47-58Publisher
ELSEVIER ESPANA SLU
DOI: 10.1016/j.nrl.2015.03.012
Keywords
Atzheinier disease; Beta-amytaid; Beta-secretase; Gamma-secretase; Amyteid hypothese
Categories
Ask authors/readers for more resources
Introduction: Alzheimer disease (AD) is a major neurodegenerative disorder which eventually results in total intellectual disability. The high global prevalence and the socioeconomic burden associated with the disease pose major challenges for public health in the 21st century. In this review we focus on both existing treatments and the therapies being developed, which principally target the beta-amytoid protein. Discussion: The amyloidogenic hypothesis proposes that beta-amyloid plays a key role in AD. Several pharmacological approaches aim to reduce the formation of p-amyloid peptides by inhibiting the beta-secretase and gamma-secretase enzymes. In addition, both passive and active immunotherapies have been developed for the purpose of inhibiting beta-amyloid peptide aggregation. Conclusions: Progress in identifying the molecular basis of AD may provide better models for understanding the causes of this neurodegenerative disease. The lack of efficacy of solane-zumab (a humanised monoclonal antibody that promotes beta-amyloid clearance in the brain), demonstrated by 2 recent Phase in clinical trials in patients with mild AD, suggests that the amyloidogenic hypothesis needs to be revised. 2015 Sociedad Espanola de Neurologia. Published by Elsevier Espana, S.L.U.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available