Amyloid plaques appear in neurons already in youth
Researchers at Northwestern University (Evanston, Illinois), working under the leadership of Professor Changiz Geula, have demonstrated that the abnormal protein beta-amyloid, which is the hallmark of Alzheimer's disease, begins to accumulate in people's neurons already at the age of 20, that is, much earlier than was commonly believed before until now.
During their work, the authors tried to understand the causes of damage to cholinergic neurons of the basal forebrain, which die among the first in both normal aging and Alzheimer's disease. These neurons play an important role in the mechanisms of memory and attention.
The researchers analyzed the state of this population of neurons in the brains of three groups of dead people. One group included 13 adults aged 20-66 years with normal cognitive abilities, the second – 15 elderly people aged 70-99 years who did not suffer from dementia, and the third – 21 people aged 60-95 years with Alzheimer's disease.
The obtained data demonstrated that beta-amyloid molecules begin to accumulate in the cholinergic neurons of the basal forebrain at an early young age and this process continues throughout life. Inside these neurons, beta-amyloid molecules form small toxic clots known as amyloid oligomers, which are detected even in the brain tissue of 20-year-olds with normal cognitive functions. These clots were larger in the brain cells of elderly people and patients with Alzheimer's disease. In nerve cells of other regions of the brain, the accumulation of beta-amyloid was less pronounced.
It is known that intracellular aggregates of beta-amyloid trigger the influx of excessive amounts of calcium ions into cells, which can lead to their death. Therefore, it can be assumed that an increase in the size of these aggregates as the disease ages or progresses eventually destroys nerve cells. According to another assumption of the authors, over time, intracellular amyloid aggregates acquire such dimensions that they disable the mechanisms of self-purification of neurons.
It is also possible that amyloid aggregates damage the brain by secreting beta-amyloid into the extracellular space, where it forms larger amyloid plaques, which are a characteristic feature of Alzheimer's disease.
The authors plan to devote their further work to a detailed study of the mechanisms of the destructive action of beta-amyloid accumulating inside nerve cells.
Article by Alaina Baker-Nigh et al. Neuronal amyloid-beta accumulation within cholinergic basal forebrain in aging and Alzheimer's disease is published in the journal Brain.
Portal "Eternal youth" http://vechnayamolodost.ru Northwestern University:
Alzheimer Amyloid Clumps Found in Young Adult Brains.