Alzheimer’s Starts Much Sooner Than We Thought
Brains of old people with Alzheimer’s disease indicate characteristic irregular clusters of faulty protein known as amyloid. Now, for the initial time, researchers have identified amyloid can begin to build up in the brains of people as young as 20. The research outcome is surprising because it was considered amyloid only started to build up later in life.
The scientists, from Northwestern University, Evanston, IL, report their results in the journal Brain.
Lead investigator Changiz Geula, states that:
“Finding that amyloid starts to build up so early in life is unprecedented. This is really important. We understand that amyloid, when present for extensive periods of time, is not good for you.”
Around 5 million People in America are living with Alzheimer’s disease, the very common type of dementia. While it can occur earlier, it usually attacks individuals over the age of 60.
Even though our knowing of Alzheimer’s increases daily, we even now do not know what sets it off. We do know that individuals with Alzheimer’s disease have been identified to have irregular amounts of faulty protein in and around brain cells.
This research concerns by itself with amyloid identified inside brain cells. Amyloid is a common term for protein fragments that occur normally in the body. In a healthy brain, these fragments are taken away and removed. But in Alzheimer’s disease, they build up and clump together.
In their research, Prof. Geula and colleagues analyzed a particular group of brain cells identified as basal forebrain cholinergic neurons. These brain cells are closely engaged in memory and attention and are among the initial to die in normal aging and in Alzheimer’s disease.
They analyzed and compared these brain cells in 3 groups of deceased individuals: 13 individuals aged 20-66 who were cognitively normal when they died, 16 individuals aged 70-99 who didn’t have dementia when they died, and 21 individuals aged 60-95 who had Alzheimer’s condition when they died.
The team identified that amyloid protein started building up in these vulnerable neurons in young adulthood and carried on throughout the lifespan.
Neurons in other areas of the brain didn’t show the same amount of amyloid accumulation, they note.
Amyloid clusters within brain cells may play a role to amyloid plaques outside cells
The faulty proteins produced toxic clusters known as amyloid oligomers. The investigators identified the clusters were smaller in the younger, healthy people, and bigger in older people and those with Alzheimer’s.
Prof. Geula states that their finding provides one reason for the early death of the vulnerable neurons:
“The small clumps of amyloid could be a key reason. The lifelong build up of amyloid in these neurons probably leads to the susceptibility of these cells to pathology in aging and loss in Alzheimer’s.”
We previously know that subjecting brain cells to the amyloid clusters leads to an excessive amount calcium to leak into the cells, so they die. Therefore, the investigators recommend it is probably that as these clumps accumulate, they harm and then gradually kill the brain cells.
It could also be that the clumps or clusters turn into so big that the disposal mechanisms in the cells can’t deal with them, Prof. Geula adds.
There is also the chance that the build up of amyloid clusters within brain cells may lead to the development of amyloid plaques outside brain cells – another hallmark of Alzheimer’s, the team proposes.
The authors plan to research these mechanisms in more depth to establish accurately how amyloid damages brain cells.