Signs of Aging Brains and Alzheimer’s Disease: A Study on the Role of Defective Myelin
Alzheimer’s disease is a degenerative form of dementia that is considered the most common neurodegenerative disease globally. The primary risk factor for this disease is age, though why it occurs remains unclear. Myelin, which is the layer that insulates nerve cells in the brain, is known to degenerate with age. A new study conducted by the scientists of the Max Planck Institute for Multidisciplinary Sciences in Göttingen shows that defective myelin actively promotes Alzheimer’s-related changes. Reducing age-related myelin damage could open up new ways to prevent the disease or slow its progression in the future.
Aging and Alzheimer’s Disease
The aging brain naturally undergoes changes that may result in the onset of Alzheimer’s disease. Such changes include the formation of amyloid plaques, which are made up of certain proteins called amyloid beta peptides or Aβ peptides. In Alzheimer’s patients, these plaques form many years and even decades before the first symptoms appear. Over time, nerve cells die irreversibly, resulting in impaired information transmission in the brain. The risk of developing Alzheimer’s doubles every five years after the age of 65.
The Role of Myelin in Alzheimer’s Disease
The Max Planck Institute research team investigated the role of myelin, the lipid-rich insulating layer of nerve cell fibers in the brain, in Alzheimer’s disease. Myelin maintains and facilitates rapid communication between nerve cells while supporting their metabolism. The team showed that age-related changes in myelin promote pathological changes in Alzheimer’s disease. They explored the possible role of age-related myelin degradation in the development of the disease.
The scientists used different mouse models of Alzheimer’s that had amyloid plaques similar to those in Alzheimer’s patients. However, they also introduced myelin defects, which occur in the human brain at later ages, for the first time. The results show that myelin degradation accelerates the deposition of amyloid plaques in the brains of mice. It stresses nerve fibers, causing them to swell and produce more Aβ peptides. When confronted with both defective myelin and amyloid plaques, microglia, which are immune cells in the brain, primarily remove myelin debris while the plaques continue to accumulate. The researchers suspect that the microglia are “distracted” or overwhelmed by myelin damage, preventing them from responding adequately to the plaques.
Potential Therapeutic Approaches
According to Klaus-Armin Nave, MPI Director of Multidisciplinary Sciences, “The study results show, for the first time, that defective myelin in the aging brain increases the risk of Aβ peptide deposition. We hope this will lead to new therapies. If we can slow down age-related damage to myelin, this could also prevent or delay Alzheimer’s disease.” The scientists’ findings hint that reducing the damage to myelin may prevent the progression of Alzheimer’s disease. However, further research is required into impaired immune cells to understand how to slow the damage caused by aging.
Beyond the Role of Myelin: Exploring the Relationship Between Age and Alzheimer’s Disease
While aging is a significant risk factor for Alzheimer’s disease, research also suggests that some lifestyle factors may help reduce the chances of developing the disease. A few of the notable factors that may reduce the risk of Alzheimer’s disease are discussed below.
Diet: Several studies suggest that a Mediterranean-style diet, which emphasizes whole grains, legumes, fruits, and vegetables, may help prevent Alzheimer’s disease, given that the nutrients present in these foods contribute to overall health and well-being. Moreover, it is a low-fat, plant-based diet, which reduces the risk of chronic diseases like heart disease.
Exercise: Exercise is another factor that helps individuals maintain and improve their health and reduce their risk of developing Alzheimer’s disease. Engaging in routine physical activity helps improve heart health, promotes neuroplasticity, and reduces inflammation.
Mental Stimuli: Research suggests that keeping the brain active and stimulated may reduce the risk of developing Alzheimer’s. Activities like reading, writing, solving puzzles, or playing games help stimulate the brain and promote neuroplasticity, which helps reduce the risk of developing Alzheimer’s.
Conclusion
Alzheimer’s disease is the most common neurodegenerative disease worldwide, and the primary risk factor for its onset is age. Myelin, the insulating layer around nerve cells in the brain, degenerates with age, actively promoting Alzheimer’s-related changes. Researchers at the Max Planck Institute for Multidisciplinary Sciences in Göttingen conducted a study that shows how defective myelin in the aging brain increases the risk of Aβ deposition, potentially leading to new therapeutic approaches to the disease. Additionally, besides age, lifestyle factors like diet, exercise, and mental stimuli play a role in reducing the risk of developing Alzheimer’s disease. A healthy and active lifestyle can help reduce the chances of developing Alzheimer’s disease and improve overall health and well-being.
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Alzheimer’s disease, an irreversible form of dementia, is considered the most common neurodegenerative disease in the world. The main risk factor for Alzheimer’s disease is age, although it is not clear why. The insulating layer around nerve cells in the brain, called myelin, is known to degenerate with age. Researchers at the Max Planck Institute (MPI) for Multidisciplinary Sciences in Göttingen have now shown that such defective myelin actively promotes Alzheimer’s-related changes. Reducing age-related myelin damage could open up new ways to prevent the disease or slow its progression in the future.
What was he about to do? Where did I leave the keys? When was that date again? It begins with slight memory lapses, followed by increasing problems with orientation, following conversations, articulating, or performing simple tasks. In the final phase, patients are often care dependent. Alzheimer’s disease progresses gradually and mainly affects older people. The risk of developing Alzheimer’s doubles every five years after the age of 65.
Signs of aging in the brain.
“The underlying mechanisms that explain the correlation between age and Alzheimer’s disease remain to be elucidated,” says Klaus-Armin Nave, MPI Director of Multidisciplinary Sciences. with his team of Department of Neurogenetics, investigates the function of myelin, the lipid-rich insulating layer of nerve cell fibers in the brain. Myelin ensures rapid communication between nerve cells and supports their metabolism. “Intact myelin is essential for normal brain function. We have shown that age-related changes in myelin promote pathological changes in Alzheimer’s disease,” continues Nave.
In a new study now published in the scientific journal Nature, the scientists explored the possible role of age-related myelin degradation in the development of Alzheimer’s disease. Their work focused on a typical feature of the disease: “Alzheimer’s is characterized by the deposition of certain proteins in the brain, the so-called amyloid beta peptides, or Aꞵ peptides for short,” says Constanze Depp, one of the first two of the study. authors “Aꞵ peptides clump together to form amyloid plaques. In Alzheimer’s patients, these plaques form many years and even decades before the first symptoms appear.” In the course of the disease, nerve cells eventually die irreversibly and the transmission of information in the brain is disturbed.
Using imaging and biochemical methods, the scientists examined and compared different mouse models of Alzheimer’s in which amyloid plaques occur similar to those in Alzheimer’s patients. However, for the first time, they studied mice with Alzheimer’s that also had myelin defects, which also occur in the human brain at later ages.
Ting Sun, second first author of the study, describes the results: “We saw that myelin degradation accelerates the deposition of amyloid plaques in the brains of mice. The defective myelin stresses nerve fibers, causing them to swell and produce more Aꞵ peptides.”
Overwhelmed immune cells
At the same time, myelin defects attract the attention of immune cells in the brain called microglia. “These cells are very vigilant and monitor the brain for any signs of deterioration. They can pick up and destroy substances, such as dead cells or cell components,” adds Depp. Normally, microglia detect and remove amyloid plaques, keeping buildup at bay. However, when confronted with both defective myelin and amyloid plaques, microglia primarily remove myelin debris while the plaques continue to accumulate. The researchers suspect that the microglia are “distracted” or overwhelmed by myelin damage and therefore unable to respond adequately to the plaques.
A cornerstone for therapeutic approaches.
The study results show, for the first time, that defective myelin in the aging brain increases the risk of Aꞵ peptide deposition. “We hope this will lead to new therapies. If we can slow down age-related damage to myelin, this could also prevent or delay Alzheimer’s disease,” says Nave.
https://www.sciencedaily.com/releases/2023/06/230606111503.htm
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