Alzheimer’s disease is caused due to weak insulate nerve cells in old age 

Summary : Researchers have established that damaged myelin in Alzheimer’s disease actively promotes illness-related alterations.

Source : Max Planck Gesellschaft

The most prevalent neurodegenerative condition in the world is thought to be Alzheimer’s disease, an irreversible type of dementia. Age is the greatest risk factor for Alzheimer’s, yet the reason why is still a mystery. Myelin, the insulating covering that surrounds nerve cells in the brain, is known to deteriorate with age. Now, studies from the Max Planck Institute (MPI) for Multidisciplinary Sciences in Göttingen have demonstrated how such damaged myelin actively encourages the occurrence of disease-related alterations in Alzheimer’s. Future methods of illness prevention or disease progression may be slowed by slowing age-related myelin degradation.

He was about to do what? What happened to his keys? Once more, when was that appointment? It begins with little memory lapses, then gets worse while trying to go around, follow conversations, speak clearly, or do simple jobs. Patients are most frequently care-dependent in the latter stage. Alzheimer’s disease steadily worsens and primarily impacts the elderly. After the age of 65, the chance of having Alzheimer’s doubles every five years.

Age-related changes in the brain

According to Klaus-Armin Nave, head of the MPI for Multidisciplinary Sciences, the underlying mechanisms that explain the correlation between age and Alzheimer’s disease have not yet been elucidated. He studies the role of myelin, the lipid-rich insulating coat of the nerve cell fibers in the brain, along with his team from the Department of Neurogenetics. The metabolism of nerve cells is supported, and quick communication between them is ensured by myelin. Normal brain function depends on intact myelin. Nave has demonstrated that pathological alterations in Alzheimer’s disease are promoted by age-related changes in myelin.  

The scientists investigated the potential contribution of age-related myelin breakdown to the onset of Alzheimer’s in a recent study. That has just been published in the academic journal Nature. Their research concentrated on the following traits of illness: According to Constanze Depp, one of the study’s two initial authors, Alzheimer’s is characterized by the deposition of specific proteins in the brain, the so-called amyloid beta peptides, or A peptides for short. Amyloid plaques are made up of the A peptides clumping together. These plaques develop in Alzheimer’s patients years, perhaps even decades, before any symptoms do. As the illness progresses, nerve cells eventually experience irreversible death, disrupting information flow in the brain.

The Researchers on Alzheimer’s disease

The researchers looked at and contrasted various mouse models of Alzheimer’s disease in which amyloid plaques develop similarly to those in Alzheimer’s patients. Using imaging and biochemical techniques. They did, however, study Alzheimer’s mice for the first time that also have myelin abnormalities, which also develop in the human brain with aging.

They observed that myelin deterioration increases the development of amyloid plaques in the mouse brains, according to Ting Sun however, the nerve fibers are under stress from the damaged myelin, which makes them enlarge and release more A peptides.

A surplus of immune cells

The immune cells known as microglia in the brain are also drawn to the myelin abnormalities. These cells constantly scan the brain for indications of dysfunction however, they have the ability to pick up and annihilate things, like dead cells or biological parts, Depp continues. Amyloid plaques are often found and removed by microglia, preventing their accumulation. However, when faced with both damaged myelin and amyloid plaques, microglia largely eliminate the myelin fragments while the plaques persist. The myelin damage may “distract” or overpower the microglia, which prevents them from responding to plaques as they should.

A tenet of therapeutic strategies

The study’s findings demonstrate for the first time that the danger of A-peptide deposition is increased by damaged myelin in the aging brain however, Nave believes If they can slow down age-related myelin degradation, they may be able to prevent or delay Alzheimer’s disease,”