Researchers at Northwestern University have recently reported in the journal Brain that the amyloid plaques characteristic of Alzheimer’s disease can be found in young adult brains. The study is entitled “Neuronal amyloid-β accumulation within cholinergic basal forebrain in aging and Alzheimer’s disease.”
Alzheimer’s disease is an age-related, neurodegenerative disorder characterized by cognitive and behavioral problems. Individuals with the disease initially experience memory loss and confusion that gradually leads to behavior and personality changes, a decline in cognitive abilities, and ultimately to severe loss of mental function. Alzheimer’s disease is characterized by brain formation of amyloid plaques (composed of beta-amyloid proteins, remnants of neurons and other nerve cells and proteins), and the loss of the connection between neurons that are responsible for memory and learning leading to their eventual death. As neurons die, the affected regions of the brain begin to shrink.
It is well-known that in Alzheimer’s, amyloid proteins accumulate, forming amyloid plaques outside neurons in aging adult brains. Researchers have now made the surprising discovery that amyloid molecules actually start accumulating within neurons in people as young as 20.
“Discovering that amyloid begins to accumulate so early in life is unprecedented,” said the study’s senior author Dr. Changiz Geula in a news release. “This is very significant. We know that amyloid, when present for long periods of time, is bad for you.”
Researchers analyzed the basal forebrain cholinergic neurons, known to be involved in memory and attention, to determine the reason why they are injured early, since they are among the first neurons to die in either a normal aging brain or in Alzheimer’s. Three groups of deceased individuals were analyzed: 13 were cognitively normal between 20 to 66 years, 16 were non-demented elderly individuals aged 70 to 99, and 21 had Alzheimer’s, aged 60 to 95.
Researchers found that amyloid proteins started accumulating inside these particular neurons during young adulthood and continued throughout the lifespan of the individual. Other nerve cells examined did not exhibit the same extent of amyloid accumulation. The amyloid molecules in the basal forebrain cholinergic neurons produced small toxic clumps — amyloid oligomers — which were identified in individuals in their 20’s and other normal young individuals. In the elderly and individuals with Alzheimer’s, the size of the clumps was greater.
“This points to why these neurons die early,” noted Dr. Geula. “The small clumps of amyloid may be a key reason. 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 is thought that these growing clumps most likely harm and eventually kill the neurons, possibly by triggering an excess of calcium leakage, leading to their death; by secretion of amyloid to the outside of the cell contributing to the generation of large amyloid plaques. Alternatively, “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,” suggested Dr. Geula. The research team plans to further study how internal amyloid can injure neurons.
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