First process is the build-up of a protein called amyloid beta. Amyloid beta is produced inside everyone’s brain. In healthy people, it is removed by the body before it can cause harm. But in the brains of people with AD, amyloid beta clumps together in bigger and bigger clusters known as plaques. As time goes on, plaques begin to form in different parts of the brain, including those areas responsible for learning, memory, and other tasks. The build-up of amyloid beta can begin up to 20 years before symptoms appear.1-2
The second process involves tau protein and may begin about 15 years before symptoms are apparent. Tau normally plays a helpful role in the brain. In people with AD, however, tau becomes altered – possibly as a downstream result of amyloid beta build-up – and forms tangles within nerve cells.1-2
Eventually, these two processes can damage nerve cells. As more regions of the brain are affected, this leads to the appearance of symptoms including short-term memory loss, short attention span, impulsivity, poor sense of direction, difficulty completing tasks, and others. By the time these symptoms become apparent, the underlying processes of the disease have been at work for up to 20 years.1-2
This understanding of the underlying mechanisms of AD highlights the importance of early detection and diagnosis as a central factor in improving patient care.3
Speaker 1 (00:05):
Many people, as they get older, may notice changes in memory and thinking abilities. At first, these changes may be so subtle that they’re easy to explain away as normal aging, and they may be. However, it's also possible that they're the earlier symptoms of Alzheimer’s disease. Alzheimer’s disease, or AD, is the most common form of dementia and accounts for 60% to 80% of all cases of dementia. In the United States alone, it is thought that one person develops AD every 66 seconds on average. In the early stages, people with AD may notice everyday tasks becoming more difficult to perform than before. Some typical early symptoms of AD you may notice include facing increased problems with memory, struggling to find the right words for things, becoming confused about time or place, having trouble managing money or paying bills, experiencing changes in mood, personality, or judgment, misplacing or being unable to find things.
Speaker 1 (1:13):
The symptoms of AD arise because of slow, ongoing injury to different parts of the brain. This injury, which affects nerve cells, is believed to be the result of two different processes that occur in the brains of people with AD. One involves a protein called amyloid beta, or A-beta, and the other involves a protein named tau. In the first of these processes, A-beta starts to collect inside the brain. This may begin as many as 20 years before the first signs of AD appear. A-beta is produced inside the brains of all people, but in healthy people, it is removed by the body before it can cause harm. In the brains of people with AD, A-beta clumps together in bigger and bigger groups and forms clusters known as plaques.
Speaker 1 (02:05):
As time goes on, plaques begin to form in more and more parts of the brain, which are responsible for learning, memory and other tasks. The second process, involving tau protein, begins about 15 years before the first signs of AD appear. Tau normally plays a helpful role in the brain. However, in people with AD, tau becomes altered and forms tangles within nerve cells. Eventually, the processes involving A-beta and tau can injure nerve cells. As this injury affects one brain region after another, it leads to the appearance of symptoms you may recognize. AD is a disease that progresses over time, leading to worsening symptoms, and can ultimately cause death.
Identifying the early signs and symptoms of Alzheimer’s disease is key to better patient outcomes.
1. Jack CR, Bennet DA, Blennow K, et al. NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease. Alzheimers Dement 2018;14:535–562.
2. Bateman RJ, Xiong C, Benzinger TLS, et al. Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease. N Engl J Med 2012;367:795–804.
3. Petersen RC. Mild cognitive impairment. Continuum (Minneap Minn). 2016;22(2):404-418.