A Fibril Structure of Amyloid β-Protein Proves Promising

Alzheimer’s is currently an irreversible brain disorder that affects memory, cognitive skills and eventually the ability to carry out even simple tasks. The cause of Alzheimer’s disease, which is the most common form of dementia, is not yet fully understood. It is likely a combination of age-related changes in the brain, genetic differences, environmental factors and differences in lifestyle. ¹ Although there are no cures for Alzheimer’s or any form of Dementia, the World Health Organization stated that people can reduce the risk of dementia by getting regular exercise, not smoking, avoiding harmful use of alcohol, controlling their weight, eating a healthy diet, and maintaining healthy blood pressure, cholesterol and blood sugar levels.²

 Alzheimers is thought to be caused by a build-up of amyloid plaques in and around brain cells.   These plaques are formed primarily by fragments 1-40 and 1-42 of Amyloid β-Protein.  However, the truncated version, 11-40, is also found in abundance in cerebrospinal fluid.³ Both truncated forms, Amyloid β-Protein (11-40) and [Pyr11]-Amyloid β-Protein (11-40), are found in Alzheimer’s Disease and Down’s Syndrome brains.⁴   Working with Amyloid β-Protein and be a challenge due to its high rate of aggregation.  This can be minimized by the use of 26-O-acyl isoAβ 1-42, a water-soluble isopeptide that can be used to prepare Amyloid β-Protein (1-42) through a pH-induced acyl shift. The inclusion of the isopeptide bond disrupts aggregation, alleviating the common difficulty when working with Amyloid β-Protein (1-42).⁵

The FDA has granted accelerated approval for Alzheimer’s drug Aduhelm. Aduhelm represents a first-of-its-kind treatment for Alzheimer’s disease. It is the first new treatment approved for Alzheimer’s since 2003 and is the first therapy that targets the fundamental pathophysiology of the disease.⁶ Researchers evaluated Aduhelm in three separate studies representing a total of 3,482 patients. Patients receiving the treatment had significant dose-and time-dependent reduction of amyloid beta plaque, while patients in the control arm of the studies had no reduction of amyloid beta plaque.⁶ This is very promising news in the fight against Alzheimer’s.

Amyloid β-Protein (11-40) (Human)
PAB-4492-v

[Pyr11]-Amyloid β-Protein (11-40) (Human)
PAB-4493-v

Amyloid beta (1-42)
AA-1

Our complete Amyloid β-Protein product line can be found here.  We can also prepare custom Amyloid β-Protein fragments.  Contact one of our peptide specialists today for a quotation.

References:

1. National Institute on Aging Dec, 24^th, 2019 What Causes Alzheimers Disease
2. World Health Organization. Sept 21^st, 2020. Dementia
3. D. Barritt & J.H. Viles, J. Biol. Chem., 290, 27791 (2015). (Pharmacol.)
4. Liu, et al., Acta Neuropathol., 112, 163 (2006). (Pharmacol.)
5. Yoshiya, et al., Bioorg. Med. Chem. Lett., 24, 3861 (2014).
6. Food Drug Administration, Accelerated Approval for Alzheimer’s Drug, June 7^th