Using powerful imaging technology, Swiss researchers recently observed the rapid spread of proteins associated with the development of Alzheimer’s disease. It is believed that the accumulation of these proteins in the brain may be linked to the development of dementia and are known as “superspreaders”. Researchers hope to learn why these abnormal clumps of amyloid beta proteins increase as dementia progresses.
A Better Understanding of Superspreader Proteins
The results of the study have brought the team another step closer to gaining a better understanding of how amyloid beta proteins spread in the brain tissue of patients diagnosed with dementia. Scientists are still struggling to figure out exactly what causes the brain damage linked to Alzheimer’s, because the organ is such a complex tangle of molecules. For one, they are still unsure if amyloid beta proteins cause neurological damage or if they are one of its symptoms. However, no evidence of brain cell damage directly linked to these proteins has been established in laboratory studies. Additionally, treatments targeting these proteins have also proven ineffective.
A study published in 2024 suggested that the plaques themselves were not directly responsible for dementia, but became entangled with other molecules, subsequently resulting in neuron damage. Nevertheless, more effective treatments could still potentially emerge through a better understanding of the mechanisms that drive amyloid protein growth. Using powerful imaging technology, the team could observe how these proteins joined together to form the long strands that ultimately became entangled clumps. The activity was observed in a salt solution, which emulates the brain’s natural environment better than traditional imaging laboratory conditions. Conventional techniques can potentially alter the morphology, making it impossible to analyze them in their naturally occurring form.
The Atomic Force Microscope
The team spent around 250 hours observing the proteins using an atomic force microscope. They found that certain amyloid beta proteins folded in a manner that made their edges extra reactive. This increases their ability to accumulate additional building blocks, resulting in long strands of fibrils that are capable of growing faster than other amyloid beta proteins. It was this population of proteins, amyloid beta 42, that were subsequently referred to as the “superspreaders”. It is only after an initial amyloid beta fibril has developed that the superspreaders form as secondary structures.
For now, the team has been able to learn much about the size and shape of the clumps. However, there is much about their structure that is yet to be uncovered. For example, they are yet to learn how amyloid beta 42 differs in chemical structure from other amyloid beta proteins. The chemical mechanisms that drive secondary structure growth are likewise yet to be revealed. Previous studies revealed that an individual’s dementia symptoms increase as these proteins accumulate in the brain. These symptoms include anxiety, impulsive behavior, and memory loss. However, the direct mechanisms that result in dementia-related brain damage are still somewhat of a mystery.
The Bottom Line on Amyloid Beta Proteins and Dementia
These observations have taken us a step closer to unraveling the complexities of the mechanisms behind dementia and other diseases. Using cutting-edge imaging techniques, the Swiss team of researchers has managed to observe how these proteins develop. This has provided new insights into how they potentially contribute to neurological damage. However, this is just the beginning of their journey. There is still much to learn about the unique chemical makeup of these proteins and the mechanisms responsible for the development of dementia and other neurological conditions.