's Recommended Blogs
[x]
hasn't added any blog recommendations yet.
1
Blogs Instructions
's Recommended Books
[x]
hasn't added any book recommendations yet.
1 Books Instructions
's Affiliates and Organizations
[x]
hasn't added any organizations or groups yet.
1 Badges Instructions
Search This Blog
About Sachin
I am a Visiting Assistant Professor in Cellular & Biomolecular Laboratory at Michigan State University, East Lansing, MI, USA. My passion is...
View Sachin's Profile
As explained in the previous post, Aβ catabolic pathway may offer an effective way to prevent as well as treat Alzheimer's disease (AD). The enzymes involved in Aβ degradation and clearance are- Neprilysin (NEP), Insulin Degrading Enzyme (IDE), various matrix metalloproteinases (MMPs) that degrade Aβ and low-density lipoprotein receptor-related protein 1 (LRP-1) located on Blood-Brain Barrier (BBB), which causes efflux of Aβ from brain to blood.
The extracellular deposits of of the amyloid beta (Aβ) protein are the hallmarks of Alzheimer's disease(AD) brain. These Aβ deposits are result of-
1) increased production of Aβ (anabolism)- High activity and levels of β-secretase (BACE1) and γ-secretase
(presenilins) increase the amyloidogenic processing of Amyloid Precursor Protein (APP), leading to the increased production of Aβ AND/OR
1) increased production of Aβ (anabolism)- High activity and levels of β-secretase (BACE1) and γ-secretase
(presenilins) increase the amyloidogenic processing of Amyloid Precursor Protein (APP), leading to the increased production of Aβ AND/OR
