The search for a cure for Alzheimer disease it is becoming an increasingly competitive and contentious search with recent years witnessing several major controversies.
In July 2022, the journal Science reported that a key research article from 2006, published in the prestigious journal Nature, which identified a brain protein subtype called beta-amyloid as the cause of Alzheimer’s, may have been based on fabricated data.
A year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, a antibody– target amyloid-beta as a treatment for Alzheimer’s, despite incomplete and conflicting data supporting its use. Some doctors believe aducanumab should never have been approved, while others say it should be given a chance.
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With millions of people in need of effective treatment, why do researchers keep fumbling for a cure for what is arguably one of the most important diseases facing humanity?
Escape beta-amyloid rutin
For years, scientists have focused on trying to find new treatments for Alzheimer’s by preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid. In fact, it could be said that we scientists have gotten into an intellectual rut by concentrating almost exclusively on this approach, often neglecting or even ignoring other possible explanations.
Unfortunately, this dedication to studying abnormal groups of proteins has not translated into a useful drug or therapy. The need for a new way of thinking about Alzheimer’s is emerging as a top priority in brain science.
My lab at the Krembil Brain Institute, part of the University Health Network in Toronto, is devising a 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 immune system inside the brain.
The immune system, found in every organ in the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect from foreign invaders. When a person trips and falls, the immune system helps repair damaged tissues. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.
The exact same processes are present in the brain. When there is a head injury, the brain’s immune system kicks in 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 rather a normally produced molecule that is part of the brain’s immune system. It’s supposed to be there. When brain When trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain’s overall immune response. And this is where the problem starts.
Because of the striking similarities between the fat molecules that make up the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between the invading bacteria and the host. brain and mistakenly attacks the very brain cells it is supposed to protect.
This leads to a chronic and progressive loss of brain cell function, eventually culminating in dementia, all because our body’s immune system cannot tell the difference between bacteria and brain cells.
When it is considered as a misdirected attack by the brain immune system in the very organ it is supposed to defend, Alzheimer’s emerges as an autoimmune disease. There are many types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play a crucial role in the development of the disease and for which steroid-based therapies can be effective. But these therapies will not work against Alzheimer’s disease.
The brain is a very special and distinctive organ, recognized as the most complex structure in the universe. In our model of Alzheimer’s, beta-amyloid helps protect and support 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 disease.
Although drugs conventionally used in the treatment of autoimmune diseases may not work against Alzheimer’s, we strongly believe that targeting other pathways of immune regulation in the brain will lead to new and effective treatment approaches for the illness.
Other theories of the disease
In addition to this autoimmune theory of Alzheimer’s, many other new and varied theories are beginning to appear. For example, some scientists believe that Alzheimer’s is a disease of tiny cellular structures called mitochondria, the energy factories in every brain cell. conversion of mitochondria oxygen from the air we breathe and glucose from the food we eat into the energy needed to remember and think.
Some argue that it is the end result of a particular brain infection, and it is often suggested that bacteria from the mouth are to blame. Still others suggest that the disease may arise from abnormal handling of metals within the brain, possibly zinc, copper or iron.
It is gratifying to see new ideas about this ancient disease. Dementia currently affects more than 50 million people worldwide, and a new diagnosis is made every three seconds. People living with Alzheimer’s disease often cannot recognize their own children or even their spouse over 50 years of age.
Alzheimer’s is a public health crisis that needs innovative ideas and new directions. For the well-being of individuals and families living with dementia, and for the socioeconomic impact on our already overburdened health care system facing the ever-increasing costs and demands of dementiaWe need a better understanding of Alzheimer’s disease, its causes, and what we can do to treat it and help the individuals and families living with it.
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