Alzheimer’s disease is a widely known and irreversible form of dementia.
As individuals age, their chances of developing Alzheimer’s increase, though the reasons behind this remain elusive.
However, recent findings from the Max Planck Institute (MPI) for Multidisciplinary Sciences reveal that degenerating myelin—a protective layer around brain nerve cells—could actively accelerate Alzheimer’s.
By understanding and decelerating the deterioration of myelin with age, it might be possible to halt or at least delay the progression of Alzheimer’s.
Symptoms of Alzheimer’s
Starting off with mild memory lapses, Alzheimer’s gradually develops into a severe condition where individuals often require constant care. For those aged 65 and above, the risk of Alzheimer’s doubles every subsequent five years.
A Closer Look at Myelin
Myelin is a lipid-rich substance that envelopes the brain’s nerve cell fibers, ensuring swift communication between these cells while also supporting their metabolic functions.
According to Klaus-Armin Nave, the director at MPI, changes in myelin due to aging can trigger pathological shifts characteristic of Alzheimer’s.
The researchers centered their investigations on the role of deteriorating myelin in Alzheimer’s development. A hallmark feature of this disease is the accumulation of proteins known as amyloid beta peptides (Aꞵ peptides) in the brain.
These peptides form amyloid plaques that manifest long before Alzheimer’s symptoms appear. As the disease progresses, these plaques disrupt communication between nerve cells.
To comprehend the connection between myelin and Alzheimer’s, researchers examined Alzheimer’s mouse models with similar amyloid plaque formations as seen in human patients.
For the first time, they incorporated mice with myelin defects similar to those found in older humans.
Myelin Degradation and Aꞵ Peptides: It was observed that the mice with myelin defects exhibited accelerated amyloid plaque formation in their brains. The compromised myelin stressed the nerve fibers, leading them to produce more Aꞵ peptides.
The Role of Microglia: These brain immune cells are responsible for maintaining brain health by eliminating harmful substances. They usually detect and remove amyloid plaques.
But when these microglia encounter both damaged myelin and plaques, they primarily focus on removing myelin remnants, allowing the plaques to proliferate.
This suggests that the presence of defective myelin might hinder the microglia’s ability to combat the accumulation of plaques.
Potential Implications: This groundbreaking study underscores the critical role that defective myelin might play in the development and progression of Alzheimer’s.
By addressing the age-related degradation of myelin, there’s hope for novel therapeutic avenues to either prevent or slow down the advance of Alzheimer’s.
If you care about brain health, please read studies about vitamin D deficiency linked to Alzheimer’s and vascular dementia, and blood pressure problems at night may increase Alzheimer’s risk.
For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and epilepsy drugs may help treat Alzheimer’s disease.
The study was published in Nature.
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