Brains of older people with Alzheimer’s disease show characteristic abnormal clusters of faulty protein called amyloid. Now, for the first time, scientists have discovered amyloid can begin to accumulate in the brains of people as young as 20. The finding is surprising because it was thought amyloid only began to accumulate later in life.
The researchers, from Northwestern University, Evanston, IL, report their findings in the journal Brain.
Lead investigator Changiz Geula, a research professor at Northwestern University Feinberg School of Medicine’s Cognitive Neurology and Alzheimer’s Disease Center, says:
“Discovering that amyloid begins to accumulate so early in life is unprecedented. This is very significant. We know that amyloid, when present for long periods of time, is bad for you.”
As many as 5 million Americans are living with Alzheimer’s disease, the most common form of dementia. While it can occur earlier, it most often strikes people over the age of 60.
Although our understanding of Alzheimer’s increases every day, we still do not know what sets it off. We do know that people with Alzheimer’s disease have been found to have abnormal amounts of faulty protein in and around brain cells.
- Alzheimer’s disease affects parts of the brain that control thought, memory and language
- Changes in the brain can begin years before the first symptoms appear
- By 2050, the number of Americans living with Alzheimer’s is projected to rise to 14 million.
This study concerns itself with amyloid found inside brain cells. Amyloid is a general term for protein fragments that occur naturally in the body. In a healthy brain, these fragments are carried away and disposed of. But in Alzheimer’s disease, they accumulate and clump together.
In their study, Prof. Geula and colleagues examined a specific group of brain cells known as basal forebrain cholinergic neurons. These brain cells are closely involved in memory and attention and are among the first to die in normal aging and in Alzheimer’s disease.
They examined and compared these brain cells in three groups of deceased people: 13 people aged 20-66 who were cognitively normal when they died, 16 people aged 70-99 who did not have dementia when they died, and 21 people aged 60-95 who had Alzheimer’s disease when they died.
The team found that amyloid protein began accumulating in these vulnerable neurons in young adulthood and continued throughout the lifespan.
Neurons in other parts of the brain did not show the same extent of amyloid accumulation, they note.
The faulty proteins formed toxic clusters called amyloid oligomers. The researchers found the clusters were small in the younger, healthy individuals, and larger in older individuals and those with Alzheimer’s.
Prof. Geula says their finding offers one reason for the early death of the vulnerable neurons:
“The small clumps of amyloid may be a key reason. The lifelong accumulation of amyloid in these neurons likely contributes to the vulnerability of these cells to pathology in aging and loss in Alzheimer’s.”
We already know that exposing brain cells to the amyloid clusters causes too much calcium to leak into the cells, so they die. Therefore, the researchers suggest it is likely that as these clumps accumulate, they damage and then eventually kill the brain cells.
It could also be that the clumps or clusters become so big that the disposal mechanisms in the cells cannot cope with them, Prof. Geula adds.
There is also the possibility that the accumulation of amyloid clusters inside brain cells may contribute to the formation of amyloid plaques outside brain cells – another hallmark of Alzheimer’s, the team suggests.
The authors plan to study these mechanisms in more detail to establish exactly how amyloid damages brain cells.
Meanwhile, Medical News Today recently learned how a team of researchers from the UK and Sweden has discovered a key inhibitor molecule that can interrupt an important stage in the development of Alzheimer’s disease. The molecule sticks to amyloid fibrils and stops them clumping into toxic clusters.