Animal brains can help test hypotheses about the cause of disease.
Alzheimer's disease is considered the most common form of dementia. According to the World Health Organization, in 2015 there were almost 30 million people with this diagnosis in the world. Brain changes like those that indicate Alzheimer's are not found only in humans. For example, a study of the genes of the gray mouse lemur helped to reveal some of the features of the influence of Alu DNA repeats on the risk of developing the disease.
The authors of the new study, accepted for publication in the journal Neurobiology of Aging, first discovered signs of Alzheimer's disease in the brain of chimpanzees. To do this, they posthumously analyzed the brains of 20 elderly monkeys aged 37 to 62 years. On average, in the wild, chimpanzees live up to 33–37 years, in captivity they can live up to 70.
The key features of the disease in humans are the appearance of amyloid plaques and neurofibrillary tangles in the brain tissues.
Amyloid plaques form when clumps of Aβ42 peptide form flat beta-folds. Neurofibrillary tangles are composed of overphosphorylated tau protein. This protein is associated with the work of intracellular microtubules. Excessive phosphorylation makes the protein insoluble, and it can no longer perform its tasks. With the proliferation of amyloid plaques and neurofibrillary tangles, fewer brain cells are able to function normally.
Both plaques and structures that precede the formation of neurofibrillary tangles were found in the brains of 12 of 20 monkeys. At the same time, as in humans, with age, the brain accumulates more and more manifestations of the disease. The researchers examined several regions of each monkey's brain: the prefrontal cortex (Brodman fields 9 and 10), the middle temporal gyrus (field 21), and the CA1 and CA3 hippocampus regions.
Scientists are not convinced that these manifestations affect the cognitive abilities of monkeys in the same way as in humans. During the life of these chimpanzees, no special tests were performed. However, this and further studies of animal brains may help to confirm or refute the hypothesis that amyloid plaques and neurofibrillary tangles are not a cause, but a “side effect” of the disease.
Natalia Pelezneva
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