One of the hallmarks of AD (Alzheimer's disease) is the formation of senile plaques in the brain, which contain fibrils composed of Aβ (amyloid β-peptide). According to the ‘amyloid cascade’ hypothesis, the aggregation of Aβ initiates a sequence of events leading to the formation of neurofibrillary tangles, neurodegeneration, and on to the main symptom of dementia. However, emphasis has now shifted away from fibrillar forms of Aβ and towards smaller and more soluble ‘oligomers’ as the main culprit in AD. The present chapter commences with a brief introduction to the disease and its current treatment, and then focuses on the formation of Aβ from the APP (amyloid precursor protein), the genetics of early-onset AD, which has provided strong support for the amyloid cascade hypothesis, and then on the development of new drugs aimed at reducing the load of cerebral Aβ, which is still the main hope for providing a more effective treatment for AD in the future.
Skip Nav Destination
Review Article| August 18 2014
Amyloid β-peptide and Alzheimer's disease
David Allsop ;
Essays Biochem (2014) 56: 99–110.
- Views Icon Views
- Share Icon Share
Sarah Perrett, David Allsop, Jennifer Mayes; Amyloid β-peptide and Alzheimer's disease. Essays Biochem 18 August 2014; 56 99–110. doi: https://doi.org/10.1042/bse0560099
Download citation file:
Don't already have an account? Register
Get Access To This Article
Buy This Article