hachyderm.io is one of the many independent Mastodon servers you can use to participate in the fediverse.
Hachyderm is a safe space, LGBTQIA+ and BLM, primarily comprised of tech industry professionals world wide. Note that many non-user account types have restrictions - please see our About page.

Administered by:

Server stats:

9.4K
active users

#amyloidosis

1 post1 participant0 posts today

research article from 2011:

Loss of functional albumin triggers acceleration of transthyretin amyloid fibril formation in familial amyloidotic polyneuropathy
nature.com/articles/labinvest2

"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.

Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press.

But amyloid plaque can build up in body organs other than the brain, and the resulting diseases — AL amyloidosis, ATTR amyloidosis and more — cause much suffering.

Read about recent research:
👉 @KnowableMag: arevie.ws/AmyloidosisKnowable
👉 Annual Review of Biochemistry: arevie.ws/AmyloidosisReview

Amyloidosis is a rare disease when an amyloid protein builds up in organs. Amyloidosis can affect various organs and cause symptoms such as heart failure, kidney damage, nerve pain, and digestive problems. Amyloidosis is also linked to neurodegenerative diseases such as Alzheimer’s and Parkinson’s, which involve amyloid accumulation in the brain.

#amyloidosis #protein #disease

inverse.com/health/amyloidosis