Table of ContentsView AllTable of ContentsGenetic Risk FactorsLife ExpectancySymptomsDiagnosisTreatmentSupportive CareResearchNext in hATTR Amyloidosis GuideSigns and Symptoms of hATTR Amyloidosis
Table of ContentsView All
View All
Table of Contents
Genetic Risk Factors
Life Expectancy
Symptoms
Diagnosis
Treatment
Supportive Care
Research
Next in hATTR Amyloidosis Guide
This article reviews the role of genetics in developing hATTR amyloidosis. An overview of the symptoms,diagnosis,treatment, and outlook of hATTR amyloidosis will also be discussed.
Luis Alvarez / Getty Images
Hereditary ATTR Amyloidosis and Genetic Risk Factors
Genes are composed ofDNA, which is the blueprint for a person’s appearance and how their body works. A child inherits half of their genes from one biological parent and half from the other.
Most genes code for proteins, which are molecules that carry out vital functions in the body. If a gene is faulty ormutated, the coded protein can be structurally and functionally abnormal, leading to disease.
Transthyretin ProteinThe transthyretin protein is made in the liver and normally functions to transport thyroid hormone (thyroxine) and retinol (vitamin A).
Transthyretin Protein
The transthyretin protein is made in the liver and normally functions to transport thyroid hormone (thyroxine) and retinol (vitamin A).
In hereditary ATTR amyloidosis, the abnormal transthyretin protein forms clumps called “amyloid fibrils,” which deposit themselves within different tissues and organs throughout the body, causing harm and toxicity.
Hereditary ATTR amyloidosis isautosomal dominantly inherited, meaning if either parent has the disease, their child has a 50% risk of inheriting the faulty TTR gene.
That said, it’s important to understand that inheriting a TTR gene mutation does not always mean a person will develop symptoms or that the disease will severely affect them.
Currently, over 130 TTR gene mutations are linked to hereditary ATTR amyloidosis. Symptoms and disease impact vary depending on the TTR gene mutation inherited.
hATTR Amyloidosis and Life Expectancy
Symptoms of hATTR amyloidosis begin in adulthood and are progressive, meaning they worsen over time. If not treated, hATTR amyloidosis has an irreversible course and, on average, becomes fatal seven to 10 years after the onset of symptoms.
Diagnosis and Genetic Testing for hATTR Amyloidosis
Progressive hATTR Amyloidosis Symptoms
Symptoms of hATTR amyloidosis arise from the buildup of abnormal protein within various organs throughout the body. The protein buildup damages the organs, interfering with their normal functioning.
The most common sites of amyloid deposition are theperipheral nervous systemand the heart. Other organs, namely the gut, kidneys, eyes, and brain, may also be involved.
Peripheral Nervous System
The peripheral nervous system consists of nerves that communicate information between a person’s brain and spinal cord and the rest of their body (e.g., their limbs and internal organs).
Damage or inflammation of peripheral nerves (peripheral neuropathy) from amyloid deposits may cause prickling or burning pain, reduced temperature sensitivity, and tingling and numbness (paresthesia), often starting in the feet and lower limbs.
As the disease advances, symptoms, including muscle weakness, progress to the arms and trunk, and walking becomes impaired.
Theautonomic nervous system (ANS), which regulates body functions out of a person’s control (e.g., heartbeat and digestion), is also part of the peripheral nervous system and is commonly affected in hereditary ATTR amyloidosis.
Symptoms and signs of autonomic nervous system dysfunction include:
Heart
Amyloid deposits in the heart are mainly associated withpalpitationsand abnormal heart rhythms (arrhythmias), especiallyatrial fibrillation.
Restrictive cardiomyopathy—stiffening of the heart due to amyloid fibrils infiltrating the heart muscle—is also common in hereditary amyloidosis.
Amyloid cardiomyopathy can eventually lead to heart failure, causing symptoms like:
Comprehensive Guide to Cardiac Amyloidosis
Other Organs
Other potential symptoms of hereditary ATTR amyloidosis based on organ involvement include:
Types of Amyloidosis Symptoms
hATTR Amyloidosis Testing and Diagnosis
Several tests are performed to diagnose hATTR.
First,urine and/or blood testsare often ordered to check for amyloid protein.
Next, anabdominal fat pad biopsyis usually performed to confirm the presence of amyloid deposits.
Abdominal Fat Pad BiopsyThis procedure involves removing a small piece of fatty tissue below a person’s belly button. The tissue sample is sent to a laboratory where a Congo red stain is applied to identify amyloid material.
Abdominal Fat Pad Biopsy
This procedure involves removing a small piece of fatty tissue below a person’s belly button. The tissue sample is sent to a laboratory where a Congo red stain is applied to identify amyloid material.
Imaging or other diagnostic testsmay also support the diagnosis of hATTR amyloidosis and evaluate for specific organ involvement. Examples of such tests include:
Lastly, agenetic blood testis performed to analyze the DNA sequence of the mutated TTR gene. The specific TTR gene mutation provides vital clues about which organs will likely be affected and, in some cases, how well a person may respond to a particular therapy.
Overall, identifying the exact TTR gene mutation is crucial in helping healthcare providers devise an individualized treatment plan.
Treatment for Neuropathy and Other hATTR Amyloidosis Symptoms
Hereditary amyloidosis is still considered an incurable disease, although various disease-modifying therapies are available to slow or potentially stop amyloid buildup within the body.
Gene-Silencing Therapies
TTR Stabilizers
Another TTR stabilizer—acoramidis—is currently being studied for the treatment of hATTR amyloidosis-related heart and nerve disease.
Organ Transplantation
Because the liver is the primary source of amyloid production, aliver transplantis another potential (albeit less favorable) treatment for hATTR amyloidosis.
The cells of the new liver have the donor’s genetic makeup without the mutated gene. Replacing a person’s liver with a new one removes the source of the mutated TTR protein, allowing for a significant reduction of amyloid in the body.
A liver transplant is a significant undertaking, and studies of its benefits are mixed. Research on people with hATTR amyloidosis has found an 85% survival rate (percentage of people alive) five years after a liver transplant and 73% 10 years after a transplant.
Lastly, depending on amyloid-related damage to the heart, aheart transplantalone (or in combination with a liver) may also be considered.
Management and Supportive Care
Besides disease-modifying therapies, there is a vast array of supportive treatments that can improve the quality of life and symptoms in individuals living with hATTR amyloidosis.
For example, nerve pain associated with hATTR amyloidosis can be eased with prescription medication, such as:
In some cases, depending on the organ involved, surgery might be considered. For instance, avitrectomy(removal of the liquid gel that fills the eye cavity) can be performed in people with eye floaters related to amyloidosis.
Adopting specific eating patterns (e.g., avoiding fatty foods and eating small, frequent meals) can be helpful for digestive symptoms, such as diarrhea or early satiety.
Research Advancements and Future Directions
Besides gene-silencing therapies and TTR stabilizers, a therapeutic strategy being studied is usingmonoclonal antibodiesto remove amyloid deposits. The antibodies target pre-existing amyloid deposits, potentially allowing for the recovery of the involved organ.
Summary
hATTR amyloidosis is autosomal dominantly inherited, so a child has a 50% chance of inheriting the mutated TTR gene if either biological parent carries it. Besides genetic testing to detect the mutated TTR gene, tissue biopsies and urine, blood, and imaging tests can confirm the diagnosis.
Treatment of hATTR amyloidosis involves a combination of supportive therapies to manage symptoms and disease-modifying therapies to slow or stop the buildup of amyloid protein. Clinical trials of monoclonal antibodies to remove amyloid fibrils as well as gene-editing technologies to correct the faulty TTR gene are underway.
19 SourcesVerywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Finsterer J, Iglseder S, Wanschitz J, et al.Hereditary transthyretin-related amyloidosis.Acta Neurol Scand. 2019;139(2):92-105. doi:10.1111/ane.13035Amyloidosis Foundation.Hereditary amyloidosis.Adams D, Koike H, Slama M, Coelho T.Hereditary transthyretin amyloidosis: a model of medical progress for a fatal disease.Nat Rev Neurol. 2019;15(7):387-404. doi:10.1038/s41582-019-0210-4Manganelli F, Fabrizi GM, Luigetti M, et al.Hereditary transthyretin amyloidosis overview.Neurol Sci. 2022;43(Suppl 2):595-604. doi:10.1007/s10072-020-04889-2Tozza S, Severi D, Spina E, et al.The neuropathy in hereditary transthyretin amyloidosis: a narrative review.J Peripher Nerv Syst. 2021;26(2):155-159. doi:10.1111/jns.12451Barroso FA, Coelho T, Dispenzieri A, et al.Characteristics of patients with autonomic dysfunction in the Transthyretin Amyloidosis Outcomes Survey (THAOS).Amyloid. 2022 Sep;29(3):175-183. doi:10.1080/13506129.2022.2043270Juarez M, Del Rio-Pertuz G, Parmar K, et al.A case of early hereditary transthyretin amyloid cardiomyopathy recognition with genetic screening: a case report.J Prim Care Community Health. 2022;13:21501319211062682. doi:10.1177/21501319211062682Obici L, Suhr OB.Diagnosis and treatment of gastrointestinal dysfunction in hereditary TTR amyloidosis.Clin Auton Res. 2019;29(Suppl 1):55-63. doi:10.1007/s10286-019-00628-6Solignac J, Delmont E, Fortanier E, et al.Kidney involvement in hereditary transthyretin amyloidosis: a cohort study of 103 patients.Clin Kidney J. 2022;15(9):1747-1754. doi:10.1093/ckj/sfac118Abramowitz C, Chin EK, Almeida DRP.Retrolenticular vitreous opacities as a diagnostic indicator of systemic amyloidosis.J Vitreoretin Dis. 2022;6(5):405-408. doi:10.1177/24741264221079718Luigetti M, Romano A, Di Paolantonio A, et al.Diagnosis and treatment of hereditary transthyretin amyloidosis (hATTR) polyneuropathy: current perspectives on improving patient care.Ther Clin Risk Manag. 2020;16:109-123. doi:10.2147/TCRM.S219979Paulsson Rokke H, Sadat Gousheh N, Westermark P, et al.Abdominal fat pad biopsies exhibit good diagnostic accuracy in patients with suspected transthyretin amyloidosis.Orphanet J Rare Dis. 2020;15(1):278. doi:10.1186/s13023-020-01565-8Carroll A, Dyck PJ, de Carvalho M, et al.Novel approaches to diagnosis and management of hereditary transthyretin amyloidosis.J Neurol Neurosurg Psychiatry. 2022;93(6):668-678. doi:10.1136/jnnp-2021-327909Damy T, Garcia-Pavia P, Hanna M, et al.Efficacy and safety of tafamidis doses in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT) and long-term extension study.Eur J Heart Fail. 2021;23(2):277-285. doi:10.1002/ejhf.2027Gillmore JD, Judge DP, Cappelli F, et al.Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy.N Engl J Med. 2024;390(2):132-142. doi:10.1056/NEJMoa2305434Amyloidosis Research Consortium.Hereditary transthyretin amyloidosis.Kakihara S, Hirano T, Imai A, et al.Small gauge vitrectomy for vitreous amyloidosis and subsequent management of secondary glaucoma in patients with hereditary transthyretin amyloidosis.Sci Rep. 2020;10(1):5574. doi:10.1038/s41598-020-62559-xEmdin M, Morfino P, Crosta L, et al.Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.Eur Heart J Suppl. 2023;25(Suppl B):B79-B84. doi:10.1093/eurheartjsupp/suad079Sethi Y, Mahtani AU, Khehra N, et al.Gene editing as the future of cardiac amyloidosis therapeutics.Curr Probl Cardiol. 2023;48(8):101741. doi:10.1016/j.cpcardiol.2023.101741
19 Sources
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.Finsterer J, Iglseder S, Wanschitz J, et al.Hereditary transthyretin-related amyloidosis.Acta Neurol Scand. 2019;139(2):92-105. doi:10.1111/ane.13035Amyloidosis Foundation.Hereditary amyloidosis.Adams D, Koike H, Slama M, Coelho T.Hereditary transthyretin amyloidosis: a model of medical progress for a fatal disease.Nat Rev Neurol. 2019;15(7):387-404. doi:10.1038/s41582-019-0210-4Manganelli F, Fabrizi GM, Luigetti M, et al.Hereditary transthyretin amyloidosis overview.Neurol Sci. 2022;43(Suppl 2):595-604. doi:10.1007/s10072-020-04889-2Tozza S, Severi D, Spina E, et al.The neuropathy in hereditary transthyretin amyloidosis: a narrative review.J Peripher Nerv Syst. 2021;26(2):155-159. doi:10.1111/jns.12451Barroso FA, Coelho T, Dispenzieri A, et al.Characteristics of patients with autonomic dysfunction in the Transthyretin Amyloidosis Outcomes Survey (THAOS).Amyloid. 2022 Sep;29(3):175-183. doi:10.1080/13506129.2022.2043270Juarez M, Del Rio-Pertuz G, Parmar K, et al.A case of early hereditary transthyretin amyloid cardiomyopathy recognition with genetic screening: a case report.J Prim Care Community Health. 2022;13:21501319211062682. doi:10.1177/21501319211062682Obici L, Suhr OB.Diagnosis and treatment of gastrointestinal dysfunction in hereditary TTR amyloidosis.Clin Auton Res. 2019;29(Suppl 1):55-63. doi:10.1007/s10286-019-00628-6Solignac J, Delmont E, Fortanier E, et al.Kidney involvement in hereditary transthyretin amyloidosis: a cohort study of 103 patients.Clin Kidney J. 2022;15(9):1747-1754. doi:10.1093/ckj/sfac118Abramowitz C, Chin EK, Almeida DRP.Retrolenticular vitreous opacities as a diagnostic indicator of systemic amyloidosis.J Vitreoretin Dis. 2022;6(5):405-408. doi:10.1177/24741264221079718Luigetti M, Romano A, Di Paolantonio A, et al.Diagnosis and treatment of hereditary transthyretin amyloidosis (hATTR) polyneuropathy: current perspectives on improving patient care.Ther Clin Risk Manag. 2020;16:109-123. doi:10.2147/TCRM.S219979Paulsson Rokke H, Sadat Gousheh N, Westermark P, et al.Abdominal fat pad biopsies exhibit good diagnostic accuracy in patients with suspected transthyretin amyloidosis.Orphanet J Rare Dis. 2020;15(1):278. doi:10.1186/s13023-020-01565-8Carroll A, Dyck PJ, de Carvalho M, et al.Novel approaches to diagnosis and management of hereditary transthyretin amyloidosis.J Neurol Neurosurg Psychiatry. 2022;93(6):668-678. doi:10.1136/jnnp-2021-327909Damy T, Garcia-Pavia P, Hanna M, et al.Efficacy and safety of tafamidis doses in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT) and long-term extension study.Eur J Heart Fail. 2021;23(2):277-285. doi:10.1002/ejhf.2027Gillmore JD, Judge DP, Cappelli F, et al.Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy.N Engl J Med. 2024;390(2):132-142. doi:10.1056/NEJMoa2305434Amyloidosis Research Consortium.Hereditary transthyretin amyloidosis.Kakihara S, Hirano T, Imai A, et al.Small gauge vitrectomy for vitreous amyloidosis and subsequent management of secondary glaucoma in patients with hereditary transthyretin amyloidosis.Sci Rep. 2020;10(1):5574. doi:10.1038/s41598-020-62559-xEmdin M, Morfino P, Crosta L, et al.Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.Eur Heart J Suppl. 2023;25(Suppl B):B79-B84. doi:10.1093/eurheartjsupp/suad079Sethi Y, Mahtani AU, Khehra N, et al.Gene editing as the future of cardiac amyloidosis therapeutics.Curr Probl Cardiol. 2023;48(8):101741. doi:10.1016/j.cpcardiol.2023.101741
Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read oureditorial processto learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Finsterer J, Iglseder S, Wanschitz J, et al.Hereditary transthyretin-related amyloidosis.Acta Neurol Scand. 2019;139(2):92-105. doi:10.1111/ane.13035Amyloidosis Foundation.Hereditary amyloidosis.Adams D, Koike H, Slama M, Coelho T.Hereditary transthyretin amyloidosis: a model of medical progress for a fatal disease.Nat Rev Neurol. 2019;15(7):387-404. doi:10.1038/s41582-019-0210-4Manganelli F, Fabrizi GM, Luigetti M, et al.Hereditary transthyretin amyloidosis overview.Neurol Sci. 2022;43(Suppl 2):595-604. doi:10.1007/s10072-020-04889-2Tozza S, Severi D, Spina E, et al.The neuropathy in hereditary transthyretin amyloidosis: a narrative review.J Peripher Nerv Syst. 2021;26(2):155-159. doi:10.1111/jns.12451Barroso FA, Coelho T, Dispenzieri A, et al.Characteristics of patients with autonomic dysfunction in the Transthyretin Amyloidosis Outcomes Survey (THAOS).Amyloid. 2022 Sep;29(3):175-183. doi:10.1080/13506129.2022.2043270Juarez M, Del Rio-Pertuz G, Parmar K, et al.A case of early hereditary transthyretin amyloid cardiomyopathy recognition with genetic screening: a case report.J Prim Care Community Health. 2022;13:21501319211062682. doi:10.1177/21501319211062682Obici L, Suhr OB.Diagnosis and treatment of gastrointestinal dysfunction in hereditary TTR amyloidosis.Clin Auton Res. 2019;29(Suppl 1):55-63. doi:10.1007/s10286-019-00628-6Solignac J, Delmont E, Fortanier E, et al.Kidney involvement in hereditary transthyretin amyloidosis: a cohort study of 103 patients.Clin Kidney J. 2022;15(9):1747-1754. doi:10.1093/ckj/sfac118Abramowitz C, Chin EK, Almeida DRP.Retrolenticular vitreous opacities as a diagnostic indicator of systemic amyloidosis.J Vitreoretin Dis. 2022;6(5):405-408. doi:10.1177/24741264221079718Luigetti M, Romano A, Di Paolantonio A, et al.Diagnosis and treatment of hereditary transthyretin amyloidosis (hATTR) polyneuropathy: current perspectives on improving patient care.Ther Clin Risk Manag. 2020;16:109-123. doi:10.2147/TCRM.S219979Paulsson Rokke H, Sadat Gousheh N, Westermark P, et al.Abdominal fat pad biopsies exhibit good diagnostic accuracy in patients with suspected transthyretin amyloidosis.Orphanet J Rare Dis. 2020;15(1):278. doi:10.1186/s13023-020-01565-8Carroll A, Dyck PJ, de Carvalho M, et al.Novel approaches to diagnosis and management of hereditary transthyretin amyloidosis.J Neurol Neurosurg Psychiatry. 2022;93(6):668-678. doi:10.1136/jnnp-2021-327909Damy T, Garcia-Pavia P, Hanna M, et al.Efficacy and safety of tafamidis doses in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT) and long-term extension study.Eur J Heart Fail. 2021;23(2):277-285. doi:10.1002/ejhf.2027Gillmore JD, Judge DP, Cappelli F, et al.Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy.N Engl J Med. 2024;390(2):132-142. doi:10.1056/NEJMoa2305434Amyloidosis Research Consortium.Hereditary transthyretin amyloidosis.Kakihara S, Hirano T, Imai A, et al.Small gauge vitrectomy for vitreous amyloidosis and subsequent management of secondary glaucoma in patients with hereditary transthyretin amyloidosis.Sci Rep. 2020;10(1):5574. doi:10.1038/s41598-020-62559-xEmdin M, Morfino P, Crosta L, et al.Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.Eur Heart J Suppl. 2023;25(Suppl B):B79-B84. doi:10.1093/eurheartjsupp/suad079Sethi Y, Mahtani AU, Khehra N, et al.Gene editing as the future of cardiac amyloidosis therapeutics.Curr Probl Cardiol. 2023;48(8):101741. doi:10.1016/j.cpcardiol.2023.101741
Finsterer J, Iglseder S, Wanschitz J, et al.Hereditary transthyretin-related amyloidosis.Acta Neurol Scand. 2019;139(2):92-105. doi:10.1111/ane.13035
Amyloidosis Foundation.Hereditary amyloidosis.
Adams D, Koike H, Slama M, Coelho T.Hereditary transthyretin amyloidosis: a model of medical progress for a fatal disease.Nat Rev Neurol. 2019;15(7):387-404. doi:10.1038/s41582-019-0210-4
Manganelli F, Fabrizi GM, Luigetti M, et al.Hereditary transthyretin amyloidosis overview.Neurol Sci. 2022;43(Suppl 2):595-604. doi:10.1007/s10072-020-04889-2
Tozza S, Severi D, Spina E, et al.The neuropathy in hereditary transthyretin amyloidosis: a narrative review.J Peripher Nerv Syst. 2021;26(2):155-159. doi:10.1111/jns.12451
Barroso FA, Coelho T, Dispenzieri A, et al.Characteristics of patients with autonomic dysfunction in the Transthyretin Amyloidosis Outcomes Survey (THAOS).Amyloid. 2022 Sep;29(3):175-183. doi:10.1080/13506129.2022.2043270
Juarez M, Del Rio-Pertuz G, Parmar K, et al.A case of early hereditary transthyretin amyloid cardiomyopathy recognition with genetic screening: a case report.J Prim Care Community Health. 2022;13:21501319211062682. doi:10.1177/21501319211062682
Obici L, Suhr OB.Diagnosis and treatment of gastrointestinal dysfunction in hereditary TTR amyloidosis.Clin Auton Res. 2019;29(Suppl 1):55-63. doi:10.1007/s10286-019-00628-6
Solignac J, Delmont E, Fortanier E, et al.Kidney involvement in hereditary transthyretin amyloidosis: a cohort study of 103 patients.Clin Kidney J. 2022;15(9):1747-1754. doi:10.1093/ckj/sfac118
Abramowitz C, Chin EK, Almeida DRP.Retrolenticular vitreous opacities as a diagnostic indicator of systemic amyloidosis.J Vitreoretin Dis. 2022;6(5):405-408. doi:10.1177/24741264221079718
Luigetti M, Romano A, Di Paolantonio A, et al.Diagnosis and treatment of hereditary transthyretin amyloidosis (hATTR) polyneuropathy: current perspectives on improving patient care.Ther Clin Risk Manag. 2020;16:109-123. doi:10.2147/TCRM.S219979
Paulsson Rokke H, Sadat Gousheh N, Westermark P, et al.Abdominal fat pad biopsies exhibit good diagnostic accuracy in patients with suspected transthyretin amyloidosis.Orphanet J Rare Dis. 2020;15(1):278. doi:10.1186/s13023-020-01565-8
Carroll A, Dyck PJ, de Carvalho M, et al.Novel approaches to diagnosis and management of hereditary transthyretin amyloidosis.J Neurol Neurosurg Psychiatry. 2022;93(6):668-678. doi:10.1136/jnnp-2021-327909
Damy T, Garcia-Pavia P, Hanna M, et al.Efficacy and safety of tafamidis doses in the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT) and long-term extension study.Eur J Heart Fail. 2021;23(2):277-285. doi:10.1002/ejhf.2027
Gillmore JD, Judge DP, Cappelli F, et al.Efficacy and safety of acoramidis in transthyretin amyloid cardiomyopathy.N Engl J Med. 2024;390(2):132-142. doi:10.1056/NEJMoa2305434
Amyloidosis Research Consortium.Hereditary transthyretin amyloidosis.
Kakihara S, Hirano T, Imai A, et al.Small gauge vitrectomy for vitreous amyloidosis and subsequent management of secondary glaucoma in patients with hereditary transthyretin amyloidosis.Sci Rep. 2020;10(1):5574. doi:10.1038/s41598-020-62559-x
Emdin M, Morfino P, Crosta L, et al.Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.Eur Heart J Suppl. 2023;25(Suppl B):B79-B84. doi:10.1093/eurheartjsupp/suad079
Sethi Y, Mahtani AU, Khehra N, et al.Gene editing as the future of cardiac amyloidosis therapeutics.Curr Probl Cardiol. 2023;48(8):101741. doi:10.1016/j.cpcardiol.2023.101741
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