What are Amyloid Plaques? - Definition & Significance

Instructor: Robin Harley

Robin has a PhD in health psychology. She has taught undergraduate and graduate psychology, health science, and health education.

Amyloid plaques are clumps of beta-amyloids, which destroy connections between nerve cells. They are found in the brains of patients with Alzheimer's disease, an incurable dementia that impacts thinking, memory and behavior.

Alzheimer's Disease

It's likely that you know someone who has suffered from Alzheimer's disease. It's the most common type of dementia that negatively impacts a person's thinking, memory and behavior. This genetic disease has affected approximately 5.3 million Americans in 2015. Most of these people are over the age of 65, and it is estimated that 700,000 people will die from Alzheimer's this year. There is no cure at present, but research has produced some promising treatments. People with this disease have large amounts of amyloid plaques and neurofibrillary tangles in their brains. In this lesson, we will discuss both, but will focus on the formation and structure of amyloid plaques.

Amyloid Plaques

Amyloid plaques are clumps of protein fragments called beta-amyloids. These single-molecule beta-amyloids are toxic to nerve cells, also called neurons, and their connections. These connections, called synapses, are the points of contact between one neuron and another that allow for communication throughout the brain and body. While beta-amyloids begin as a single molecule, they tend to clump up into clusters that can move freely throughout the brain. As they begin to bunch up, beta-amyloids can bind easily to receptors on neurons. Receptors are naturally-occurring proteins that exist on neurons and receive chemical messages from other neurons.

Beta-Amyloid Plaque
Beta-Amyloid Plaque

Once the beta-amyloids bind to neurons, they bring about the destruction of the synapses. Synapses serve important functions in the nervous system. Because they allow one cell to communicate with another, they can increase in number as we learn new things, form new memories, process emotions and engage in thought and planning. These connections can evolve as we experience new things. They make our brains adaptable. The degradation of these synapses can lead to impairments in memory, thinking, planning and emotional regulation. The beta-amyloid clusters eventually form into larger plaques, but research is now showing that neuronal damage can occur before they reach this stage.

How do these beta-amyloids destroy synapses? A Stanford University experiment with mice has illustrated this well. In this study, mice were genetically-engineered to be susceptible to Alzheimer's disease. The researchers located a receptor that exists near the synapses on neurons called PirB. This receptor plays a role in weakening synapses. This is not always a bad thing, because too much flexibility in synapse strength can lead to problems like epilepsy. PirB has a high affinity for beta-amyloids. The researchers found that mice who had the PirB receptors also had increased activity of an enzyme called cofilin. Cofilin breaks down the structure of synapses. When beta-amyloids bind to the PirB receptors, cofilin increases its destruction.

Amyloid Plaques in the Human Brain
Amyloid Plaques

Some people can develop amyloid plaques as they grow older. However, people who have Alzheimer's disease have higher concentrations of plaques in areas of the brain responsible for memory, like the hippocampus. Other abnormal structures found in Alzheimer's patients' brains are called neurofibrillary tangles. These form when tau, a protein that supports the structure of neurons, becomes twisted. This can lead to a collapse of part of the neuron's structure. As the disease progresses, neurons and their connections are destroyed. Let's look at how medication and other treatments can slow this process.

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