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One third of amyloid disease is hereditary, in which case there is normally an early age of onset. [19] Half of amyloid-related diseases are sporadic and have a late age of onset – in these cases, the protein aggregation may be associated with aging-related decline in protein regulation.
Familial amyloid polyneuropathy, also called transthyretin-related hereditary amyloidosis, transthyretin amyloidosis abbreviated also as ATTR (hereditary form), or Corino de Andrade's disease, [1] is an autosomal dominant [2] neurodegenerative disease. It is a form of amyloidosis, and was first identified and described by Portuguese neurologist ...
An immune system disorder but not an autoimmune disease. Amyloidosis: No consistent evidence of association with autoimmunity. Amyotrophic lateral sclerosis: No consistent evidence of association with autoimmunity. Anti-tubular basement membrane nephritis: No consistent evidence of association with autoimmunity. Atopic allergy: A hypersensitivity.
AL amyloidosis is caused by the deposition of abnormal antibody free light chains. The abnormal light chains are produced by monoclonal plasma cells, and, although AL amyloidosis can occur without diagnosis of another disorder, it is often associated with other plasma cell disorders, such as multiple myeloma and Waldenström's macroglobulinemia. [6]
Heredofamilial amyloidosis, also known as hereditary amyloidosis, or familial amyloidosis, is an inherited condition that may be characterized by systemic or localized deposition of amyloid in body tissues. [1]: 522 [2]
To date, 37 human proteins have been found to form amyloid in pathology and be associated with well-defined diseases. [2] The International Society of Amyloidosis classifies amyloid fibrils and their associated diseases based upon associated proteins (for example ATTR is the group of diseases and associated fibrils formed by TTR). [3]
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