Educating myself on becoming a person with a disability.
#amyloidosis
#disability
#identity
#inclusion
#invisibility
open.substack.com/pub/recently...
Educating myself on becoming a...
Bluesky SocialBluesky
Recent searches
Search options
#amyloidosis
0 posts0 participants0 posts today
Continued thread
started a #wikipedia article on biochemist Lawreen Connors (1954-2024), director of the Amyloidosis Center at Boston University: https://en.wikipedia.org/wiki/Lawreen_Connors @wikiwomeninred #WomeninSTEM #BostonUniversity @bostoncollege @tuftsuniversity #WoburnMA #OgdensburgNY #amyloid #amyloidosis #Diedin2024
research article from 2011:
Loss of functional albumin triggers acceleration of transthyretin amyloid fibril formation in familial amyloidotic polyneuropathy
https://www.nature.com/articles/labinvest201171
"Human serum albumin, the most abundant protein in plasma, serves as a transporter of various ligands and an antioxidant in blood circulation. Human serum albumin is a mixture of a reduced form (human mercaptalbumin: HMA) and an oxidized form (human nonmercaptalbumin: HNA). Albumin is the major antioxidant in plasma, and a large proportion of all the serum antioxidant properties can be attributed to albumin. Previous work has shown the total reactive antioxidant potential in plasma, considered as an index of the level of antioxidants, decreased in patients with FAP. In addition, more recent work demonstrated that albumin suppressed amyloid formation of amyloid-β(Aβ), a component of amyloid fibrils in Alzheimer's disease, by reducing oxidative stress. These data suggest that albumin functing as an antioxidant may perform a crucial role in amyloid formation in FAP."
NatureLoss of functional albumin triggers acceleration of transthyretin amyloid fibril formation in familial amyloidotic polyneuropathy - Laboratory InvestigationTransthyretin (TTR)-related familial amyloidotic polyneuropathy (FAP) is characterized by systemic accumulation of amyloid fibrils caused by a point mutation in the TTR gene. Despite the urgent need for alternative therapeutic strategies, the pathogenesis of FAP still remains elusive. In our study reported here, we focused on albumin, the most abundant protein in plasma, and described the role of albumin in the TTR amyloid-formation process. Patients with FAP evidenced significantly decreased serum albumin levels as the disease progressed. Biacore analysis showed that albumin had a binding affinity for TTR and exhibited higher affinity for TTR amyloid than native TTR. Albumin functioning as an antioxidant effectively suppressed TTR amyloid formation. In patients with FAP, albumin was significantly oxidized as the disease progressed. Moreover, loss of functional albumin accelerated TTR deposition in analbuminemic rats possessing a human variant TTR gene. Taken together, these results indicate that albumin may have an inhibitory role in the TTR amyloid-formation process.