Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds. Alzheimer’s is a public health crisis in need of innovative ideas and fresh directions, but the pursuit of a cure for the dreaded disease is proving to be elusive, with theories being formulated and discarded. However, one has persistently hung on and monopolized the lion’s share of resources: the study of a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s.
In June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment, even though the data supporting its use were incomplete and contradictory. Some physicians believe aducanumab never should have been approved, while others maintain it should be given a chance.
With millions of people needing an effective treatment, why are researchers still fumbling in this quest for a cure for what is arguably one of the most important diseases confronting humankind?
For years, scientists have been focused 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.
But now some believe that scientists have unjustifiably concentrated almost exclusively on this approach, often neglecting, or even ignoring other possible explanations.
The need for a new “out-of-the-clump” way of thinking about Alzheimer’s is emerging as a top priority in brain science and other theories are being considered with more urgency.
A laboratory at the Krembil Brain Institute, part of the University Health Network in Toronto, is formulating a new theory of Alzheimer’s disease.
Based on the past 30 years of research, they no longer think of Alzheimer’s as primarily a disease of the brain. Rather, they believe that Alzheimer’s is principally a disorder of the immune system within 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 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 head trauma, the brain’s immune system kicks into gear to help repair. When bacteria are present in the brain, the immune system is there to fight back.
The new theory posits that beta-amyloid is not an abnormally produced protein in the brain, but rather is a normally occurring molecule that is part of the brain’s immune system. It is supposed to be there.
When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain’s comprehensive immune response. And this is where the problem begins.
Because of striking similarities between the fat molecules that make up both the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks the very brain cells it is supposed to be protecting.
This leads to a chronic, progressive loss of brain cell function, which ultimately culminates in dementia – all because our body’s immune system cannot differentiate between bacteria and brain cells.
When regarded as a misdirected attack by the brain’s immune system on the very organ it is supposed to be defending, Alzheimer’s disease emerges as an autoimmune disease.
There are other theories also being considered, but this is the alternative frontrunner in the race to find a cure for the disease that is affecting a population that thanks to medical advances, is living longer and longer—and therefore becoming more vulnerable to Alzheimer’s disease.
