Wild-Type (Senile) ATTR Amyloidosis
Wild-type (senile) ATTR amyloidosis is similar to familial ATTR amyloidosis, except the protein that is deposited is the normal, non-mutated transthyretin protein. The normal transthyretin protein is less prone to forming amyloid deposits than the mutated form.
As a result, patients only develop the disease in older age, usually at 65 years of age or older. Because amyloid deposits accumulate slowly in this form of the disease, the prognosis is generally better than AL (primary) amyloidosis and familial ATTR amyloidosis.
Treatment options
Treatment is generally aimed at the symptoms of wild-type (senile) ATTR amyloidosis, such as treating amyloid deposits in the heart. Because the heart is the most commonly affected organ, your disease will be monitored and treated by a cardiologist.
For some patients with severe wild-type (senile) ATTR amyloidosis, a heart transplant may be the best option. Stanford is one of the world's leading centers for heart transplantation for amyloidosis.
New treatment methods are under research and development. Learn more about the clinical trial Safety and Efficacy of Tafamidis in Patients with Transthyretin Cardiomyopathy.
