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.
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.