Even 20-Year-Old Brains May Show Signs Of Future Alzheimer's From Amyloid Clumps
Scientists are continually learning about the causes of Alzheimer's disease, the most common form of dementia. Statistics show that more than 5 million in the United States alone are living with the neurodegenerative health issue, which is the 6th leading cause of death in the country.
New findings published in the journal Brain now show that amyloids, the abnormal proteins found in accumulation in the brain that are a hallmark of the health issue, can be found in individuals as young as 20 years old.
Previous studies have shown accumulated clumps of plaque outside neurons in older individuals. Yet for the first time, Northwestern Medicine research shows evidence of amyloid accumulation in the brains of very young individuals.
"Discovering that amyloid begins to accumulate so early in life is unprecedented," said lead investigator Changiz Geula, research professor at the Cognitive Neurology and Alzheimer's Disease Center at Northwestern University Feinberg School of Medicine, in a news release. "This is very significant. We know that amyloid, when present for long periods of time, is bad for you."
For the study, researchers examined basal forebrain cholinergic neurons in the hopes of better understanding why they are damaged so early on and are among the first neurons to die in normal aging in Alzheimer's. These neurons are also closely associated with memory and attention.
During the process, they examined the neurons from the brains of three groups of deceased individuals: 13 cognitively normal young individuals, ages 20 to 66; 16 non-demented old individuals, ages 70 to 99; and 21 individuals with Alzheimer's ages 60 to 95.
Study results showed that amyloid molecules began accumulating inside the neurons during young adulthood and continued throughout lifespan. However, other nerve cells in separate parts of the brain did not show the same extend of amyloid accumulation. Instead, these cells of amyloid molecules formed toxic clumps, amyloid oligomers, which are present even in individuals during their 20s and other normal young individuals. The size of the clumps grew larger with age and for those with Alzheimer's.
With advancing years, the clumps contribute to the damage of neurons and eventually kill them. As neurons are exposed to numerous clumps, they also trigger an excess of calcium leaking into the cell that causes their death.
"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," Geula said.
In future studies, researchers hope to further investigate how the amyloids damage neurons and how they contribute to the problem at such an early age.
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