A Hallmark of Alzheimer's Can Show Up In Young People Too
We all worry about Alzheimer's disease from time-to-time, especially if we've had the unfortunate experience of watching a loved one suffer from it late in life. Now new research has revealed that a key hallmark of the encroaching disease, the accumulation of an abnormal protein in the brain, can start in people as young as 20 years old - younger than scientists ever imagined.
That's at least according to a study recently published in the journal Brain, which details how accumulation of the protein amyloid may be a strong cue for people at greater risk for developing the neural degradative disease.
It's long been known that amyloid accumulates and forms clumps of plaque outside neurons in aging adults and in Alzheimer's patients, but "discovering that amyloid begins to accumulate so early in life is unprecedented," lead investigator Changiz Geula, a researcher at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University, said in a statement.
The discovery was made after Geula and his colleagues looked specifically at basal neurons in the forebrain called cholinergic cells, as they are often the first to die in both normal aging and Alzheimer's patients. Tied to memory and attention, the researchers wanted to know what exactly was making them so vulnerable.
Data was collected on three groups of people whose brains were analyzed after they died: 13 people aged 20-66 who were mentally healthy 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 at the time of their death.
They found that the harmful protein accumulates even in 20-year-old brains, and the size of the amyloid clumps grew notably larger in the older Alzheimer's brains.
"This is very significant," Geula said. "We know that amyloid, when present for long periods of time, is bad for you... 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."
"It's also possible that the clumps get so large, the degradation machinery in the cell can't get rid of them, and they clog it up," he added.
The next step, the researchers explain, is to understand exactly how amyloid causes its damage, potentially opening up new treatment and even preventative options in the future.
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