Alzheimer’s may not actually be a brain disease, experts say : ScienceAlert

finding a cure for Alzheimer’s The disease is becoming an increasingly competitive and controversial discovery with many significant controversies in recent years.

In July 2022, science magazine reported that a key 2006 research paper, published in reputed journal Naturewho identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s may have been based on fabricated data.

A year ago, in June 2021, Educanumab was approved by the US Food and Drug AdministrationAn antibody-targeted beta-amyloid as a treatment for Alzheimer’s, even though the data supporting its use were incomplete and conflicting.

Some physicians believe that aducanumab should never have been approved, while others say it should be given a chance.

With millions in need of an effective treatment, why are researchers still faltering in the search for a cure for one of the most important diseases facing mankind?

Avoiding the Beta-Amyloid Root

For years, scientists have been focusing on trying to come up with new treatments for Alzheimer’s. By preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid.

In fact, we scientists have arguably thrown ourselves into an intellectual rut, focusing almost exclusively on this approach, often ignoring or ignoring other possible explanations.

Sadly, this dedication to studying abnormal protein clumps has not translated into a useful drug or therapy. The need for a new “out-of-the-clump” way of thinking about Alzheimer’s is emerging as a top priority in brain science.

My lab at the Crembill Brain Institute, part of the University Health Network in Toronto, is preparing New theory of Alzheimer’s disease,

Based on our last 30 years of research, we no longer think of Alzheimer’s as primarily a disease of the brain. Rather, we believe that Alzheimer’s is primarily a disorder of the immune system within the brain,

The immune system, found in every organ of the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect against foreign invaders.

When a person trips and falls, the immune system helps repair damaged tissue. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.

Exactly the same processes exist in the brain. When a head trauma occurs, the brain’s immune system kicks into gear to help repair it. When bacteria are present in the brain, the immune system is there to fight back.

Alzheimer’s as an autoimmune disease

We believe that beta-amyloid is not an abnormally produced protein, but a commonly found molecule that is part of the brain’s immune system. It should be there.

When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is an important contributor to the broader immune response of the brain. And this is where the problem starts.

Because of the striking similarity between the fat molecules that make up the bacterial membrane and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks brain cells that are believed to is to protect.

This leads to a chronic, progressive loss of brain cell function, which eventually results in dementia—all because our body’s immune system cannot differentiate between bacteria and brain cells.

When perceived by the brain’s immune system as a misdirected attack on the same organ it is supposed to defend, Alzheimer’s disease emerges as an autoimmune disease.

There are several types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play an important role in the development of the disease, and for which steroid-based treatments may be effective. But these treatments will not work against Alzheimer’s disease.

The brain is a very special and specialized organ, which is recognized as the most complex structure in the universe, In our model of Alzheimer’s, beta-amyloid helps protect and strengthen our immune system, but unfortunately, it also plays a central role in the autoimmune process that, we believe, can lead to the development of Alzheimer’s. .

Although drugs traditionally used in the treatment of autoimmune diseases may not work against Alzheimer’s, we strongly believe that targeting other immune-regulating pathways in the brain may help us find new and effective treatments for the disease. Ways to go.

Other theories of disease

In addition to this autoimmune theory of Alzheimer’s, many other new and diverse theories are beginning to emerge. For example, some scientists believe that Alzheimer’s is a disease of a tiny cellular structure called the mitochondria Energy factories in every cell of the brain.

Mitochondria convert oxygen from the air we breathe and glucose from the food we eat into the energy needed to remember and think.

Some say it is a . is the end result of special brain infectionwith Bacteria from the mouth are often being suggested as the culprit., Still others suggest that the disease may arise from a abnormal conduction of metals within the brainPossibly zinc, copper, or iron.

glad to see it New thinking about this age-old disease, Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds. Often, people with Alzheimer’s disease do not recognize their own children or even their spouses over the age of 50.

Alzheimer’s is a public health crisis that requires innovative ideas and new directions.

To deal with the increasing costs and demands of dementia, for the well-being of people and families living with dementia, and the socioeconomic impact on our already stressed health care system, we need a better understanding of Alzheimer’s, its causes. , and what we can do to treat it and to help the people and families living with it.Conversation

donald weaverProfessor of Chemistry and Director of the Crembill Research Institute, University Health Network, University of Toronto

This article is republished from Conversation Under Creative Commons license. read the original article,

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