Recent years have seen numerous major conflicts in the search for a cure for Alzheimer’s disease, making the field more competitive and acrimonious than ever before.
Science magazine revealed in July 2022 that a seminal 2006 scientific paper published in the esteemed journal Nature that linked a specific type of brain protein called beta-amyloid to Alzheimer’s disease may have been based on faked data.
Although the evidence supporting the use of aducanumab, an antibody targeting beta-amyloid, as a treatment for Alzheimer’s disease was incomplete and conflicting, the FDA authorised it as a treatment for the disease a year earlier, in June 2021. It has been debated by medical professionals whether aducanumab should have been approved at all.
There are millions of individuals in need of treatment, so why are scientists stumbling around in the dark trying to find a solution to what could be called one of the most significant health problems humanity faces today?
Escaping the Beta-Amyloid rut
For a long time now, researchers have been attempting to find ways to cure Alzheimer’s disease by stopping the protein beta-amyloid from aggregating into harmful plaques in the brain. In reality, we scientists have gotten ourselves into an intellectual rut by focusing almost solely on one method, often dismissing or rejecting other possible explanations.
Beta-amyloid is designed to defend brain cells from invading bacteria, but it assaults the brain cells it is supposed to protect because the membranes of both bacteria and brain cells are made of fat molecules that are remarkably similar to one another.
This is because our immune system fails to distinguish between germs and brain cells, resulting in a gradual and continuous loss of brain cell function that can only end in dementia.
When Alzheimer’s is seen as the brain’s immune system mistakenly attacking the same organ it is designed to defend, we can see it as an autoimmune illness. Autoimmune illnesses, such as rheumatoid arthritis, are characterised by the presence of autoantibodies and are often treated successfully with steroid-based therapy. On the other hand, Alzheimer’s disease is immune to these treatments.
The brain is a one-of-a-kind organ widely acknowledged to be the universe’s most complex structure. We propose a model of Alzheimer’s disease in which beta-amyloid serves a protective and supportive function for the immune system while also playing a key part in the autoimmune process that may underlie the disease’s onset.
We hope that targeting alternative immune-regulating pathways in the brain will lead us to novel and effective treatment options for Alzheimer’s, even though medications traditionally employed in the treatment of autoimmune diseases may not be effective against the disease.
Other theories of the Disease
This autoimmune theory of Alzheimer’s is only one of many novel and diverse hypotheses currently gaining traction. For instance, some researchers have hypothesised that Alzheimer’s is caused by damage to the brain’s mitochondria. The energy needed for learning and memory comes from mitochondria, which use oxygen and glucose from the food we ingest to create ATP.
As the final stage of a specific brain infection, this theory holds that oral bacteria are to blame. Others argue that a defect in the brain’s processing of metals like zinc, copper, and iron may be at the root of the disorder.
It’s encouraging to see fresh ideas being applied to this age-old problem. Every three seconds, someone somewhere in the world receives a diagnosis of dementia, which today affects over 50 million people. Alzheimer’s patients often lose the ability to recognise even close family members, including spouses of more than 50 years.
Alzheimer’s disease is a major public health concern that requires new approaches. We need a better understanding of Alzheimer’s, its causes, and what we can do to treat it and help people and families living with it for their well-being as well as for the socioeconomic impact on our already strained health-care system dealing with the ever-increasing costs and demands of dementia.
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