β-Amyloid peptides and amyloid plaques in Alzheimer's disease.

Gouras GK1, Olsson TT, Hansson O. 2017-03-30
"

1Department of Experimental Medical Science, Lund University, Lund, Sweden

"

Abstract:
Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the importance of differentiating between various forms of Aβ, and suggest that a better understanding of Aβ's precise pathophysiological role in the disease is important for correctly targeting it for potential future therapy.

Creative Peptides has accumulated a huge library of peptide knowledge including frontier peptide articles, application of peptides, useful tools, and more!

 Orexin A (OXA) and orexin B (OXB) are hypothalamic neuropeptides discovered in 1998, which bind to two G-protein ...

Peptides are the ideal drug molecules because of their high affinity, high selectivity, low toxicity, and easy synthesis. Sci ...

 Myristoyl pentapeptide-8, a cosmetic peptide, is a synthetic peptide containing arginine, aspartic acid, glycine ...

 Caprooyl tetrapeptide-3, an anti-wrinkle peptide, a reaction product of caproic acid and tetrapeptide-3, compris ...

 Cetrorelix acetate (C70H92ClN17O14, referred to as cetrorelix), a synthetic decapeptide with 5 amino acids in th ...

Contact Us

USA

Address:

Tel: |

Email:

Germany

Address:

Copyright © 2024 Creative Peptides. All rights reserved.