Addressing Myelin Degradation: A Potential Breakthrough in the Fight against Alzheimer’s Disease
New research has unveiled a promising approach to combating Alzheimer’s disease by targeting the degradation of myelin, a protective sheath surrounding nerve cells in the brain.
Alzheimer’s disease, a progressive form of dementia, is the most prevalent neurodegenerative disorder worldwide. While age is a major risk factor, the underlying causes remain incompletely understood. However, it is widely recognized that myelin, which deteriorates as we age, plays a crucial role.
A recent study conducted by scientists at the Max Planck Institute for Multidisciplinary Sciences in Göttingen has shed light on the direct contribution of compromised myelin to the observed changes in Alzheimer’s disease. These findings suggest that preventing or slowing down myelin degeneration associated with aging could offer new avenues for tackling the disease.
The onset of Alzheimer’s disease is marked by subtle memory lapses, misplaced objects, forgotten appointments, and difficulty with simple tasks. As the disease progresses, patients often become dependent on care due to a decline in cognitive abilities.
Alzheimer’s disease advances gradually and primarily affects the elderly population. The risk of developing Alzheimer’s doubles every five years after the age of 65.
Unraveling the Aging Brain
“The mechanisms underlying the connection between age and Alzheimer’s disease have yet to be fully elucidated,” explains Klaus-Armin Nave, director at the MPI for Multidisciplinary Sciences.
Nave and his team from the Department of Neurogenetics are investigating the role of myelin, a lipid-rich insulating layer surrounding nerve fibers in the brain. Myelin plays a critical role in facilitating rapid communication between nerve cells and supporting their overall metabolism.
“Maintaining healthy myelin is essential for normal brain function. Our research has shown that age-related changes in myelin contribute to the pathological alterations observed in Alzheimer’s disease,” adds Nave.
In a recently published study in the journal Nature, the scientists explored the potential involvement of age-related myelin degradation in the development of Alzheimer’s.
The study focused on a distinctive characteristic of the disease: the accumulation of specific proteins, known as amyloid beta peptides or Aβ peptides, in the brain. Constanze Depp, one of the study’s lead authors, explains, “Alzheimer’s is characterized by the formation of amyloid plaques, which are aggregates of Aβ peptides. These plaques begin to form many years, even decades, before the onset of symptoms in Alzheimer’s patients.” As the disease progresses, nerve cells undergo irreversible damage, disrupting information transmission in the brain.
Using imaging and biochemical techniques, the researchers studied various mouse models of Alzheimer’s that exhibited amyloid plaques similar to those seen in human patients. For the first time, they examined Alzheimer’s mice with concurrent myelin defects, which commonly occur in the aging human brain.
Ting Sun, another lead author of the study, describes the results: “We observed that myelin degradation accelerates the deposition of amyloid plaques in the brains of mice. The damaged myelin places stress on nerve fibers, leading to swelling and increased production of Aβ peptides.”
Overwhelmed Defense Cells
Simultaneously, the myelin defects attract microglia, immune cells responsible for monitoring the brain for signs of impairment. “These cells are highly vigilant and capable of detecting and eliminating substances such as dead cells or cellular components,” adds Depp. Under normal circumstances, microglia recognize and clear amyloid plaques, preventing their excessive accumulation.
However, when confronted with both defective myelin and amyloid plaques, microglia primarily target the remnants of myelin, allowing the plaques to persist. The researchers suspect that the myelin damage overwhelms or distracts the microglia, hindering their appropriate response to the plaques.
For the first time, this study demonstrates that defective myelin in the aging brain heightens the risk of Aβ peptide deposition. Nave remarks, “We are hopeful that this discovery will lead to new therapeutic approaches. If we can effectively slow down age-related myelin damage, it may also help prevent or decelerate the progression of Alzheimer’s disease.”
Reference: Depp, C., Sun, T., Sasmita, A.O., Spieth, L., Berghoff, S.A., Nazarenko, T., Overhoff, K., Steixner-Kumar, A.A., Subramanian, S., Arinrad, S., Ruhwedel, T., Möbius, W., Göbbels, S., Saher, G., Werner, H.B., Damkou, A., Zampar, S., Wirths, O., Thalmann, M., Simons, M., Saito, T., Saido, T., Krueger-Burg, D., Kawaguchi, R., Willem, M., Haass, C., Geschwind, D., Ehrenreich, H., Stassart, R., & Nave, K.A. (2023). Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease. Nature. DOI: 10.1038/s41586-023-06120-6
Frequently Asked Questions (FAQs) about Alzheimer’s disease prevention
What is Alzheimer’s disease?
Alzheimer’s disease is a prevalent neurodegenerative disorder characterized by progressive cognitive decline and memory loss. It is the most common form of dementia and primarily affects the elderly population.
What is the role of myelin in Alzheimer’s disease?
Myelin is the protective sheath around nerve cells in the brain. Age-related degradation of myelin has been found to contribute to the changes observed in Alzheimer’s disease. Impaired myelin can accelerate the deposition of amyloid plaques, which are a hallmark of the disease.
How does myelin degradation affect Alzheimer’s progression?
When myelin deteriorates, it causes stress on nerve fibers, leading to increased production and accumulation of amyloid beta peptides (Aβ peptides) in the brain. Additionally, the presence of myelin defects may overwhelm the brain’s immune cells, impairing their ability to clear amyloid plaques effectively.
Can preventing myelin degradation help in Alzheimer’s prevention?
Research suggests that curbing age-related myelin damage could offer new opportunities for preventing or slowing down Alzheimer’s disease. By preserving healthy myelin, it may be possible to reduce the risk of Aβ peptide deposition and potentially delay disease progression.
What are the signs of Alzheimer’s disease?
Early signs of Alzheimer’s may include memory lapses, difficulty with orientation, following conversations, articulating thoughts, and performing simple tasks. As the disease advances, patients often become increasingly dependent on care due to cognitive decline.
Is there a correlation between age and Alzheimer’s disease?
Age is the primary risk factor for Alzheimer’s disease. The risk of developing the disease doubles every five years after the age of 65. The mechanisms linking age and Alzheimer’s disease are still not fully understood, but age-related myelin degradation may play a role in disease progression.
What are amyloid plaques?
Amyloid plaques are clusters of amyloid beta peptides that accumulate in the brain of individuals with Alzheimer’s disease. These plaques form years or even decades before the onset of symptoms and are associated with the irreversible damage to nerve cells and disrupted information transmission in the brain.
More about Alzheimer’s disease prevention
- Max Planck Institute for Multidisciplinary Sciences: Link
- Nature Journal: Link
- Alzheimer’s Association: Link