Washington, March 2:
The risk of developing Alzheimer’s later in life begins as early as age 20 in some people — a much younger age than scientists ever imagined. Amyloid – an abnormal protein whose accumulation in the brain is a hallmark of Alzheimer’s disease – starts accumulating inside neurons of young humans brains.
It is already established that amyloid accumulates and forms clumps of plaque outside neurons in ageing adults and in Alzheimer’s.
“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,” said lead investigator Changiz Geula from Northwestern University’s Feinberg School of Medicine.
In the study, scientists examined basal forebrain cholinergic neurons to try to understand why they are damaged early. These vulnerable neurons are closely involved in memory and attention.
Geula and colleagues examined these neurons from the brains of three groups of deceased individuals. Scientists found amyloid molecules began accumulating inside these neurons in young adulthood and continued throughout the lifespan.
Nerve cells in other areas of the brain did not show the same extent of amyloid accumulation. The amyloid molecules in these cells formed small toxic clumps, amyloid oligomers, which were present even in individuals in their 20’s and other normal young individuals.
The size of the clumps grew larger in older individuals and those with Alzheimer’s. This points to why these neurons die early.
“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 ageing and loss in Alzheimer’s,” the authors wrote.
“It is also possible that the clumps get so large, the degradation machinery in the cell cannot get rid of them and they clog it up,” Geula noted. The team now plans to investigate how the internal amyloid damages the neurons in future research.
The study was published in the journal Brain. IANS