Why do old people get dementia
Why the elderly are more prone to Alzheimer's
The likelihood of developing Alzheimer's increases with age. How exactly older brains are more likely to be affected by this disease, however, has so far been unclear.
Susanne Wegmann, scientist at the German Center for Neurodegenerative Diseases (DZNE) in Berlin, together with colleagues uncovered a possible cause for this connection: Certain proteins involved in Alzheimer's disease - so-called tau proteins - can spread better in the aging brain . This is shown by laboratory tests.
Changes in the brain
The current study was carried out in collaboration with Harvard Medical School and Massachusetts General Hospital. The results were recently published in the journal "Science Advances".
Alzheimer's disease usually begins with impaired memory and later affects other cognitive abilities. Two different protein deposits in the patient's brain are involved: "amyloid beta plaques" and "tau neurofibrils".
The appearance of tau neurofibrils reflects the course of the disease quite precisely: They first appear in the memory centers of the brain and then appear in other areas as the disease progresses. Presumably, tau proteins or their aggregates migrate along nerve tracts and thus contribute to the disease spreading in the brain.
Faster protein diffusion
What role does age play in these spreading processes? If dew spreads more easily in older brains, that could explain why older people are more prone to Alzheimer's disease. Wegmann and her colleagues pursued this hypothesis.
Using a "gene ferry" - a tailor-made virus - the scientists smuggled the blueprint for the human tau protein into the brains of mice. Individual cells then began to produce the protein. Twelve weeks later, the researchers examined how far the tau protein had moved from the production site. "The human tau proteins spread about twice as fast in older mice as in younger ones," says Wegmann, summarizing the results.
The experimental approach also enabled the scientists to analyze more precisely how dew spreads. This protein is found in a healthy, soluble form in all nerve cells in the brain. In Alzheimer's disease, however, it can change pathologically by changing its shape and then clumping into so-called fibrils.
"For a long time it was assumed that pathological tau protein is primarily passed on from one nerve cell to the next. However, our results show that the healthy form of the protein is also passed on in the brain, and that this process increases with age. Cells can They are also damaged by the fact that they receive and accumulate a great deal of healthy tau protein, "says Wegmann.
The findings from the study raise a number of new questions, which Wegmann will now investigate with her working group at the DZNE: What processes are the basis of the increased spread of tau in the aging brain? Is too much tau protein produced or too little defective protein broken down? Answering these questions could open up new therapeutic possibilities in the long term. (red. 10/7/2019)
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