Alzheimer disease is caused due to weak insulation of nerve cells in old age.

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

Alzheimer disease, an irreversible type of dementia, is considered the most prevalent neurodegenerative condition in the world. Age is the greatest risk factor for Alzheimer, yet the reason why is still a mystery. As people age, myelin, the insulating covering around nerve cells in the brain, deteriorates. Studies from the Max Planck Institute show that damaged myelin actively promotes disease-related changes in Alzheimer. Slowing age-related myelin degradation could help prevent illnesses or slow disease progression in the future.

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 disease steadily worsens and primarily impacts the elderly. After the age of 65, the chance of having Alzheimer doubles every five years.

How Age-Related Brain Changes Contribute to Alzheimer disease

Klaus-Armin Nave, head of the MPI for Multidisciplinary Sciences, notes that researchers have not yet elucidated the mechanisms linking age to Alzheimer disease. 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. Myelin supports nerve cell metabolism and ensures quick communication between them. Normal brain function depends on intact myelin. Nave has shown that age-related changes in myelin promote pathological alterations in Alzheimer’s disease.  

The scientists investigated the potential contribution of age-related myelin breakdown to the onset of Alzheimer in a recent study. The academic journal Nature has just published that. Their research focused on specific traits of the illness. Constanze Depp, one of the study’s initial authors, explained that Alzheimer features the deposition of amyloid beta peptides, or A peptides, in the brain. These A peptides clump together to form amyloid plaques. 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 disease

The researchers looked at and contrasted various mouse models of Alzheimer disease in which amyloid plaques develop similarly to those in Alzheimer patients. Using imaging and biochemical techniques. They did, however, study Alzheimer 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

Myelin abnormalities also attract immune cells known as microglia in the brain. 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,”