amyloid polyneuropathy

Article: Familial amyloid polyneuropathy.

Amyloid polyneuropathy (Portuguese)

Thus, Senile systemic amyloidosis and familial amyloid polyneuropathy are often treatable diseases that are misdiagnosed.

Currently, the main target diseases being studied are familial amyloid polyneuropathy (FAP) and Alzheimer's disease.

Susceptibility and modifier genes in Portuguese transthyretin V30M amyloid polyneuropathy: complexity in a single-gene disease.

Myenteric plexuses often participate in familial amyloid polyneuropathy and in a few cases with AL and AA.

Vyndaqel or Tafamidis was approved for the treatment of Familial amyloid Polyneuropathy by the European Medicines Agency in late 2011.

Vyndaqel or Tafamidis is a European Medicines Agency approved drug for the treatment of familial amyloid polyneuropathy caused by transthyretin amyloisis.

Cachexia is seen in patients with cancer, AIDS, chronic obstructive lung disease, multiple sclerosis, congestive heart failure, tuberculosis, familial amyloid polyneuropathy, mercury poisoning (acrodynia) and hormonal deficiency.

Familial amyloid polyneuropathy (FAP), also called transthyretin-related hereditary amyloidosis, transthyretin amyloidosis or Corino de Andrade's disease, is an autosomal dominant neurodegenerative disease.

Tafamidis (INN, or Fx-1006A, trade name Vyndaqel) is a drug for the amelioration of transthyretin-related hereditary amyloidosis (also familial amyloid polyneuropathy, or FAP), a rare but deadly neurodegenerative disease.

The marketed drug, a meglumine salt, has completed an 18 month placebo controlled phase II/III clinical trial, and an 18 month extension study which provides evidence that tafamidis slows progression of Familial amyloid polyneuropathy.

Tafamidis is currently being considered for approval by the United States Food and Drug Administration (FDA) for the treatment of early stage transthyretin-related hereditary amyloidosis or familial amyloid polyneuropathy or FAP.

This drug, now called Tafamidis or Vyndaqel, slowed the progression of familial amyloid polyneuropathy in an 18 month placebo controlled trial and in an 18 month extension study sponsored by FoldRx Pharmaceuticals (acquired by Pfizer in 2010).

Recently, the European Medicines Agency approved the drug Tafamidis or Vyndaqel to slow the progression of familial amyloid polyneuropathy, a related disease caused by TTR aggregation that first presents as an autonomic and/or peripheral neuropathy (later progressing to a cardiomyopathy).

Kinetic Stabilization of tetrameric transthyretin in familial amyloid polyneuropathy patients provides the first pharmacologic evidence that the process of amyloid fibril formation causes this disease, as treatment with tafamidis dramatically slows the process of amyloid fibril formation and the degeneration of post-mitotic tissue.

The familial amyloid neuropathies (or familial amyloidotic neuropathies, neuropathic heredofamilial amyloidosis, familial amyloid polyneuropathy) are a rare group of autosomal dominant diseases wherein the autonomic nervous system and/or other nerves are compromised by protein aggregation and/or amyloid fibril formation.