Protein build-up in the brain and cognitive decline
In Alzheimer’s disease, abnormal amyloid-beta protein can accumulate in the brain and may be associated with disruption of nerve cell communication, inflammation and cognitive decline.
Amyloid is a term for certain proteins that can fold in an unusual way and clump together. These clumps can build up in different tissues throughout the body. In Alzheimer’s disease, the key amyloid type is amyloid‑beta, a protein fragment that can build up in the brain, particularly between nerve cells.
When amyloid‑beta builds up, it can form amyloid plaques (protein clumps in the brain). Amyloid plaques are one of the biological changes associated with Alzheimer’s disease.
Importantly, some people can have amyloid in the brain without having noticeable memory or thinking symptoms, especially early on.
Why is amyloid important in Alzheimer's disease?
Amyloid accumulation may be associated with:
- activation of inflammatory responses
- cognitive decline
- damage to brain networks
- impaired communication between nerve cells
- memory changes.
Amyloid changes may occur before noticeable symptoms develop in some people.
Related topics
- Alpha-synuclein
- Tau protein and neurofibrillary tangles.
Common patient questions
Amyloid is strongly associated with Alzheimer's disease and is thought to play a key role in triggering the disease process. However, Alzheimer's involves multiple biological changes, including tau abnormalities and brain cell dysfunction.
How these processes interact is still an active area of research.
Amyloid is most strongly linked with Alzheimer's disease, but dementia has many causes, and amyloid's role differs across these conditions.
Not everyone with amyloid accumulation develops the same symptoms, and not all dementias involve amyloid accumulation.
Yes, an amyloid PET scan is a specialised brain imaging test that can detect amyloid accumulation in the brain. It may help doctors assess whether Alzheimer’s disease-related amyloid changes are present in selected patients.
In Australia, there are now TGA-approved disease-modifying therapies for some people with early Alzheimer's disease. These treatments are designed to target amyloid in the brain and may be suitable only for carefully selected patients following specialist assessment.
Access, eligibility criteria, risks, benefits and costs should be discussed with a neurologist or other specialist involved in dementia care. Currently, these therapies are not listed on the Pharmaceutical Benefits Scheme (PBS) and involve out-of-pocket costs.