A new study reports that amyloid — a protein that signifies Alzheimer’s disease — can start building up in people as young as 20.
Researchers say this is the first study to show the development in young humans.
Changiz Geula, research professor at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University Feinberg School of Medicine, said the discovery is “unprecedented.”
“This is very significant,” Geula said. “We know that amyloid, when present for long periods of time, is bad for you.”
His study in Brain details how researchers evaluated basal forebrain cholinergic neurons.
They wanted to see how the neurons were impacted at an early age. The scientists also wanted to know why the neurons are among the first to die. The neurons are linked to memory and attention.
The team looked at the neurons from brains of deceased people in three groups.
The first group consisted of 13 cognitively normal young people ranging in age from 20 to 66. The second group had 16 nondemented older individuals who were 70 to 99 years old. The third group was comprised of 21 people with Alzheimer’s who ranged in age from 60 to 95.
The scientists found that amyloid molecules started to accumulate inside the neurons in young adulthood. The molecules created small toxic clumps called amyloid oligomers. The clumps were larger in older people with and without Alzheimer’s disease. Nerve cells in other areas of the brain did not have as much buildup.
Scientists already know that the clumps can cause calcium to leak into the cell and destroy it. Geula believes the accumulation of amyloid probably makes the cells vulnerable, damaging and eventually killing the neurons.
Geula said it’s also possible the clumps grow to a certain size and clog the cell. The clumps could also damage cells by secreting amyloid outside the cell, which leads to the large amyloid plaques seen in people with Alzheimer’s.
What’s Next in the Study of Amyloids?
In the future, Geula’s team wants to look at how amyloid damages the neurons.
Dr. Raj C. Shah, an associate professor at the Rush Alzheimer's Disease Center in Chicago, said that if the findings can be replicated, it leads him to consider two options.
“First, we need to explore if amyloid accumulation has a normal function in humans,” he said.
Second, if they find that amyloid accumulation is not a normal function in humans, Alzheimer's disease may need to be viewed as a lifelong condition — not just something that happens when we are older.
“General knowledge about the timing of exposure to a risk factor opens the window for exploring lifelong approaches to try to prevent the symptoms of Alzheimer's disease … symptoms that may occur many decades from the time of initial amyloid accumulation,” Shah said.
Dr. Richard Isaacson, director of the Alzheimer's Prevention Clinic within the Weill Cornell Memory Disorders Program, said that many people do not know that Alzheimer's disease starts in the brain decades before memory loss symptoms start.
“This study is interesting as it provides strikingly early evidence of amyloid accumulation in the brain,” Isaacson added.