Alzheimer’s is a perplexing disease. Scientists have not been able to find the underlying cause of the condition but are beginning to understand many aspects of Alzheimer’s, such as how the disease may spread in the brain.
A recent clinical research study discovered that the “waste-disposal system” in a brain cell may be responsible for spreading harmful protein aggregates between cells in Alzheimer’s. Learn more about the research, which could lead to the development of new drugs to stop the progression of the disease.
Alzheimer’s eventually robs senior loved ones of their ability to perform necessary activities of daily living (ADLs), their ability to recognize familiar people and places, as well as their memory. Scientists are making advancements in Alzheimer’s research every day, but are still unfortunately unable to pinpoint what causes this assault on the brain.
The most widespread theory is that Alzheimer’s can be attributed to several underlying causes, including:
Amyloid plaques are clumps of abnormal protein fragments. The medical term for the abnormal protein accumulation is “beta-amyloid.” Beta-amyloid is toxic to brain cells and its synapses, as it binds itself to the nerve receptors and subsequently causes the nerve cells in the brain to die. The brain eventually shrinks from the loss of neurons and ceases to function properly.
Most people accumulate some amyloid in their brain as they age. However, those with Alzheimer’s have more amyloid, particularly in areas of the brain involving memory (such as the hippocampus). Other abnormal structures found in the brains of people with the disease include tau tangles, also called neurofibrillary tangles. Tau is a protein that supports the structure of nerve cells and it can become twisted, leading to a collapse of part of the neuron structure. As Alzheimer’s progresses in the brain, amyloid plaques and tau tangles cause more neurons to be destroyed.
When old, worn-out parts are in the cell, the lysosome (the part of the cell that can engulf substances) forms a membrane bubble around them. The lysosome then breaks these large parts down into small molecules that are small enough to be transported through the cell’s membrane — to be recycled.
Scientists at Linköping University, in Sweden, have discovered that this recycling does, in fact, have an impact on the symptoms of Alzheimer’s in the brain. A recent study showed that exosomes are a part of this recycling and removal system and that they both carry beta-amyloid and spread toxic proteins to brain cells.
“The spread of the disease follows the way in which parts of the brain are anatomically connected. It seems reasonable to assume that the disease is spread through the connections in the brain and there has long been speculation about how this spread takes place at the cellular level,” states Associate Professor, Martin Hallbeck, in the Department of Clinical and Experimental Medicine at Linköping University.
Scientists in the study examined the exosomes collected from the brain tissue of deceased persons. The research team found a much higher level of beta-amyloid in the exposomes from brains with Alzheimer’s than from the brain tissue of the control group — the group without the disease.
Perhaps one of the most intriguing aspects of the study was that the researchers were able to prevent exosomes from being formed, released and then absorbed by other cells — reducing the spread of beta-amyloid between the nerve cells.
More research is needed before the study findings can be put to practical use in developing new drugs or treatment modalities for people with Alzheimer’s, but it certainly opens the door to new possibilities.
“Our study demonstrates that it is possible to influence this pathway and possibly develop drugs that could prevent the spreading. The findings also open up the possibility of diagnosing Alzheimer’s in new ways, by measuring the exosomes,” says Hallbeck.
Were you aware of Alzheimer’s impact on — or progression in — the brain? We’d like to hear from you in the comments below.