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In mammals, serum amyloid A (SAA) is a 10 kDa (10-15 kDa) apolipoprotein composed of two identical chains. It is mainly synthesized in the liver and is involved in cholesterol metabolism. It also has anti-inflammatory and anti-oxidant activities. Deficiency of SAA causes familial AA amyloidosis characterized by deposition of SAA amyloid fibrils in major organs, including the kidney, heart, and liver. The SAA is a precursor of amyloid fibrils isolated from dialysate from patients with end-stage renal failure. However, SAA did not form amyloid fibrils in vitro in this study. A mechanism for the pathophysiology of AA amyloidosis may be related to the carbohydrate moiety of SAA, whereas the amino acid sequence of the protein is not directly involved in the process. Amyloidosis is the deposition of insoluble protein fibrils in tissue. The protein fibrils are deposits of insoluble protein aggregates. One such protein is amyloid A, which is produced by the liver. This can lead to the death of cells, and in this case, ultimately, the entire organ.
Amyloidosis refers to diseases in which proteins are deposited in the extracellular space in the form of insoluble fibrils. The most common disorders of this type are systemic amyloidoses, which are characterized by the deposition of fibrils of serum amyloid A (SAA). The deposition of amyloid is a major factor in the pathogenesis of most systemic amyloidoses, and has been associated with a number of other disease states, including Alzheimer disease (AD), organ transplants, and prion disease. Progressive amyloidosis is a rare complication of familial amyloidosis, with a prevalence of 0.5% in the general population, and up to 10% in the liver transplantation (LT) population. In hereditary amyloidosis, mutations in the amyloid precursor protein (APP) and the transthyretin (TTR) gene cause fibril formation and deposition of amyloid in the tissues and organs. These mutant proteins are a crucial component of the amyloid fibrils.
The SAA-derived peptide was found to have no sequence homology with AA fibrils and to be the smallest fragment that has the capability of forming amyloid fibrils. Identification of the domains of SAA involved in fibril formation may help to understand the molecular mechanism of amyloidogenesis and to design drugs against amyloid diseases. This study may be the first step towards the development of drugs for the treatment of amyloid diseases.
Voices of Recovery was designed to honor friends, families, and fellows who have made significant contributions to SAA. It is a way to express appreciation, to acknowledge the gift of recovery, and to promote healing and hope for all.
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