A Look at Alzheimer’s Disease as New Clues Emerge

the changing state of matter provides insight into degenerative diseases

By Jonny Lupsha, Wondrium Staff Writer

A process called phase transition offers new insight into degenerative diseases, NPR reported. Phase transition involves matter changing from one state to another, and when brain cells can’t do so, it can cause toxins to build up in the brain. How does it relate to Alzheimer’s?

Blue brain on dark background concept
Scientific research confirms that “phase transition” inside neurons of the brain occurs in degenerative diseases such as Alzheimer’s disease. Photo by Doitforfun / Shutterstock

According to NPR, a process of physics that most students learn about in grade school may play a part in degenerative disease. “The process, known as phase transition, is what allows water vapor to condense into liquid water, or even freeze into solid ice,” the article said. “That same sort of process allows brain cells to constantly reorganize their inner machinery. But in degenerative diseases that include amyotrophic lateral sclerosis, frontotemporal dementia, and Alzheimer’s, the phase transitions inside neurons seem to go awry.”

The article goes on to state that cell interiors become too viscous, clogging up and allowing toxins to build up in and around them, leading to malfunction. This theory is the latest chapter in the book of Alzheimer’s disease, the leading cause of dementia.

Discovering Alzheimer’s

Dr. Thad A. Polk, an Arthur F. Thurnau Professor in the Department of Psychology and the Department of Electrical Engineering and Computer Science at the University of Michigan, said that Alzheimer’s disease is named after German psychiatrist Dr. Alois Alzheimer, who first identified the disease in the early 1900s.

“Alzheimer followed [the patient’s] case closely for five years,” Dr. Polk said. “After she died in 1906, he carefully examined her brain, and when he looked at her brain under a microscope, Alzheimer found two significant abnormalities that are now considered to be the defining features of Alzheimer’s disease.”

The first of those abnormalities was a series of abnormal clumps of protein fragments between neurons. Those clumps are now known as amyloid plaques. The second abnormality is the presence of neurofibrillary tangles, which are a result of misfolded tau proteins. Unfortunately, the only way to definitively diagnose Alzheimer’s disease is to examine a deceased patient’s brain for these abnormalities—the typical symptoms of forgetfulness and misidentifying people and objects are found in several kinds of dementia.

Treating Alzheimer’s

Alzheimer’s remains incurable and no treatments slow the actual progression of the disease. However, some treatments can temporarily relieve symptoms and improve cognitive function in patients.

“The drug donepezil is often prescribed, especially during the early and middle stages of the disease,” Dr. Polk said. “Donepezil inhibits the breakdown of the neurotransmitter acetylcholine and therefore tends to increase the levels of this neurotransmitter in the brain. Acetylcholine is a crucial neurotransmitter in the motor system, in the hippocampus, and in the cerebral cortex, and it plays an important role in memory, in attention, in sleep, and in mood.”

Dr. Polk said that Alzheimer’s causes acetylcholine levels to drop, which is why donepezil can help alleviate symptoms temporarily. Another commonly prescribed medicine for Alzheimer’s is called memantine, which works differently from donepezil.

“This drug works by reducing the activity of the excitatory neurotransmitter glutamate in the brain,” he said. “Too much glutamate activity can sometimes lead to neuron death in a process called excitotoxicity, and so scientists decided to try memantine in order to reduce glutamate activity. And they found that it did improve cognitive function in some moderate to severe Alzheimer’s patients.

“Again it’s not a cure, and it doesn’t work for everyone, but it does often help and is therefore commonly prescribed in the moderate and severe stages of the disease.”

Dr. Thad A. Polk contributed to this article. Dr. Polk is an Arthur F. Thurnau Professor in the Department of Psychology and the Department of Electrical Engineering and Computer Science at the University of Michigan. He received a BA in Mathematics from the University of Virginia and an interdisciplinary PhD in Computer Science and Psychology from Carnegie Mellon University.