The life expectancy for transthyretin (ATTR) amyloidosis varies from person to person. Your age, overall health, and primary symptoms all play a role.

Transthyretin amyloidosis (ATTR) is a rare condition in which amyloid proteins build up in the body, damaging tissues and affecting their function.

There are two main types:

  • Hereditary transthyretin amyloidosis (hATTR): This occurs due to genetic variants in the transthyretin (TTR) gene that make the TTR protein unstable and lead it to misfold (lose its usual shape) and form amyloid deposits.
  • Wild-type ATTR (ATTRwt): This occurs from age-related changes that gradually destabilize the TTR protein, leading it to misfold and form amyloids.

Both types are progressive conditions that can affect life expectancy.

On average, life expectancy in ATTR amyloidosis ranges from about 3 to 15 years after symptoms begin, but many factors influence your outlook.

Where symptoms start plays a role. People with primary symptoms in the peripheral nervous system (polyneuropathy) often live longer than those with symptoms that primarily affect the heart (cardiomyopathy).

In hATTR, the most common genetic variants lead to peripheral nervous system involvement or a “mixed-type” that affects both the nerves and the heart. ATTRwt is usually present with primary heart symptoms. As a result, life expectancy in ATTRwt is often, but not always, lower than in hATTR.

The age at diagnosis also matters. People diagnosed before the age of 50 may live about 10 to 20 years after symptoms begin, compared with about 7 years for those diagnosed later in life.

Other factors that may affect life expectancy include:

  • a family history of disease severity and progression
  • the stage of disease at time of diagnosis
  • coexisting health conditions
  • lifestyle factors such as diet, exercise, or substance use
  • early treatment and treatment adherence

ATTR amyloidosis is a progressive condition linked to genetics or aging. Without treatment, the TTR protein keeps misfolding and forming amyloid deposits.

Unlike other misfolded proteins, amyloid bundles are difficult for the body to break down. Instead of being cleared, they stay where they’re deposited and continue to buildup.

As more amyloid collects, it causes more tissue damage and greater loss of function.

Symptoms of ATTR amyloidosis can appear gradually as amyloid plaques buildup. The specific signs depend on whether the condition affects the nerves (polyneuropathy), the heart (cardiomyopathy), or both.

Progressive symptoms of ATTR with polyneuropathy (ATTR-PN):

Early

  • tingling or burning sensations in the hands and feet
  • numbness in the hands and feet
  • loss of temperature and pain sensation
  • carpal tunnel syndrome in both wrists (often the first symptom)

Progressive

  • muscle weakness and wasting
  • major loss of physical sensations
  • dizziness
  • erectile dysfunction (ED)
  • digestive problems
  • trouble walking
  • incontinence
  • eventually total loss of mobility

According to a 2025 study, many people with polyneuropathy experience trouble walking within 3 years of symptom onset and require wheelchair assistance within 4 to 7 years.

Progressive symptoms of ATTR amyloidosis with cardiomyopathy (ATTR-CM):

Early

  • heart palpitations
  • fatigue
  • carpal tunnel syndrome in both wrists

Progressive

  • shortness of breath
  • swelling (edema) in the legs and ankles
  • severe heartbeat irregularities
  • fainting
  • muscle wasting
  • heart failure

People diagnosed with mixed-type ATTR may experience symptoms from both polyneuropathy and cardiomyopathy.

For some people, treatment can slow or even halt the progression of ATTR amyloidosis.

Treatment for hATTR may include therapies that lower the amount of dysfunctional TTR in the body, such as:

  • gene silencing drugs (patisiran, vutrisiran)
  • TTR stabilizers (acoramidis, tafamidis)

Other options include anti-fibril drugs, such as coramitug CM and AT-02 (pan-amyloid) CM, that help break down amyloid deposits.

In some cases, a liver transplant can stop the progression of hATTR. Because the hereditary form of this condition produces dysfunctional TTR in the liver, replacing it with a donor liver allows the body to make typical TTR.

ATTRwt progression

Treatment for ATTRwt looks different. Because ATTRwt isn’t linked to a genetic mutation, gene silencing therapies aren’t typically used. Instead, TTR stabilizers like tafamidis may be prescribed to help the protein keep its structure and prevent misfolding.

Tafamidis and acoramidis are currently the only therapies with approval from the Food and Drug Administration (FDA) for ATTRwt with cardiomyopathy.

Liver transplants aren’t used in ATTRwt since the TTR made by the liver is functional but destabilizes with age.

Although ATTRwt is linked to aging, not everyone develops this condition. Risk varies from person to person, and some are more likely to form amyloid deposits than others.

Factors that may contribute include oxidative stress, inflammation, hormone changes, and age-related declines in how the body processes proteins. ATTRwt is also more common in men than in women.

Transthyretin (ATTR) amyloidosis occurs when amyloid protein deposits build up in the body and affect organ function. It may be caused by a hereditary genetic mutation or by age-related changes that destabilize the TTR protein.

Although ATTR amyloidosis is progressive, early treatment can slow or even stop its course. Treatment options may include TTR stabilizers, gene silencing therapies, anti-fibril drugs, or in some cases, a liver transplant.

On average, the life expectancy of someone with the condition ranges from about 3 to 15 years after symptoms develop. With early diagnosis, new therapies, and ongoing care, many people are living longer and maintaining a better quality of life.