Alzheimer's disease is the most common form of dementia that affects over 55 million people worldwide. Beta-amyloid plaques that are commonly found in Alzheimer's patients were thought to be the cause for the deterioration of memory and cognition that is characteristic of the disease.
But a lot of old people also accumulate amyloid plaques that do not go on to develop dementia. Researchers from Karolinska Institutet in Sweden propose another theory in a study that says Alzheimer's might be the result of the lack of soluble amyloid beta protein instead of insoluble plaques.
Insoluble Plaques in the Brain Might Not Be the Cause of Alzheimer's Disease, New Theory Suggests
History of Alzheimer's Disease
Psychiatrist and neuroanatomist Alois Alzheimer reported "a peculiar severe disease process of the cerebral cortex" during a gathering of psychiatrists in Tübingen, Germany in 1906.
The case was of a woman named Auguste Deter who starts finding it difficult to remember recent events and experienced changes in her behavior that she could not explain, such as having more problems in writing and speaking.
According to the Alzheimer Society of Canada, Auguste was only turning 50 in 1900 and was quite young for symptoms of dementia that were presumed to only affect adults aged 65 and over. She suffered from memory loss, delusions, hallucinations, aggression, and confusion that worsened until her untimely death five years later.
Alzheimer requests Auguste's brain and medical records to examine her brain. He noted that it shrunk in certain areas and has distinctive plaques on her brain.
He concluded that Auguste suffered from a rare form of dementia that affects people below 65 years old, theorizing that these abnormal plaques in the woman's brain are related to the disease. His study paved way for more research and related disease and until today, these clumps of beta-amyloid plaques are considered to be the cause of Alzheimer's disease.
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New Theory Explains the Cause of Alzheimer's Disease
Although Dr. Alzheimer's study has opened the doors to more research about the disease, the theorized cause of it has two major problems. Firstly, it fails to explain why even people with beta-amyloid plaques do not develop the disease. Secondly, clinical trials that reduce plaques have been unsuccessful.
The original soluble form of the amyloid-beta protein that performs important functions in the brain is consumed and lost when they form into insoluble plaques, Science Alert reported. Previous studies have also shown that reduced levels of soluble amyloid-beta 42 led to worse clinical outcomes.
The new study titled "High Soluble Amyloid-β42 Predicts Normal Cognition in Amyloid-Positive Individuals with Alzheimer's Disease-Causing Mutations" that was published in the Journal of Alzheimer's Disease investigated whether the amount of plaques in the brain or the amount of remaining amyloid-beta 42 is more important in the progression of Alzheimer's disease.
They studied the data on a group of people who have inherited a rare inherited gene mutation that increases their risk of developing the disease. The team found that the depletion of amyloid-beta 42 is more harmful than the number of insoluble plaques in the brain.
Participants with high levels of amyloid-beta 42 in their cerebrospinal fluid were protected and preserved their cognition over the course of the study. Regardless of the number of insoluble plaques in their brain, they remained cognitively normal. The findings support previous studies that showed the important functions of amyloid-beta 42 in memory and cognition.
Researchers also noted that inherited forms of Alzheimer's disease can cause dementia in those with low amyloid-beta 42 even without any detectable plaques, suggesting that the latter are not the cause of dementia but rather the low levels of the former.
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