In 1901, a young German psychiatrist was called to an asylum to see a new patient. Auguste D., a woman, was experiencing increased confusion, paranoia and delusion. What was most fascinating about her case was her age. At 51, she was hardly old enough to begin experiencing what were once thought of as standard “effects of old age.” Even more interesting, her condition was worsening much faster than what normally occurs. After her hospitalization, the young psychiatrist moved on, but never truly forgot the case. Five years later, Auguste D. died. Then older, the psychologist, Alois Alzheimer, requested that he be allowed to study her brain. It was sent to him in Munich where it was dissected and he published the results of his research a year later.
In his writing, Alzheimer described finding extracellular structures later known as “plaques,” as well as fiber-like bundles known as “tangles” in the brain of Auguste D. that were uncommon in the brains of healthy adults her age. He concluded that her early onset symptoms were due to the formation of plaques and tangles that rarely result from the typical aging process. His observations led to the recognition that dementia was an illness and not a part of the normal phenomenon of aging. In 1910, the dementing disorder was named “Alzheimer’s Disease” in recognition of his work.
Today, Alzheimer’s disease affects nearly 5.8 million people in the United States and is the sixth leading cause of death. It is not the only form of dementia, but the most common – others include Lewy Body, frontotemporal disorders and vascular dementia. Alzheimer’s disease is an irreversible, progressive brain disorder that destroys memory, thinking skills and eventually, the ability to continue biological processes. The main cause of Alzheimer’s symptoms is the interruption of integral chemical processes in and outside of neurons, the nerve cells of the brain. These interruptions bring about loss of cell function and cell death. Over time, as neurons continue to die, cognitive capabilities decline until loss of all mental capability. There is no known cure for Alzheimer’s disease.
How is the Brain Affected?
The brain is constructed of a tightly-knit network of over 100 billion neurons. A neuron is a type of cell whose primary function is to process and transmit messages. The neuron consists of three parts: a cell body; a long, tail-like axon, and dendrites. Information transmissions are known as nerve impulses and they have both a chemical and electrical component. Roughly speaking, when stimulated, an electrical signal travels through the cell body along the axon. When the signal finds the ends of the axon, known as the terminal buttons, a neurotransmitter is released into a gap between neurons called a synapse. The neurotransmitters travel through the synapse to the waiting dendrites of the next neuron. The impulse then moves through the dendrites and cell body of the next neuron as an electrical signal and the process continues. The function and survival of a neuron depends upon this communication process remaining constant, as well as standard cell metabolism and constant maintenance and repair. Neurons are supported by glial cells – the most common cell type in the brain. Glial cells protect neurons from physical and chemical damage, and act as the brain’s “janitor” by clearing it of foreign substances and cellular debris. Alzheimer’s disease damages the brain by interrupting the processes that maintain neuron health causing millions of neurons to systematically “die.” Evidence of this lies in the presence of “plaques” and “tangles.”
In an Alzheimer’s brain, abnormal levels of the naturally-occurring protein called beta-amyloid 42 clump together to form plaques between neurons. The plaques disrupt cell function by retarding intra-cellular communication and interrupting cell maintenance and repair.
Neurofibrillary tangles are an abnormal accumulation of proteins inside the neuron called tau. In normal cellular function, nutrients and other essential materials are transported inside the cell through tracks called microtubules. Normal tau proteins function by supporting microtubules. In an Alzheimer’s brain, tau proteins clump and twist together, causing microtubules to break down. The neuron begins to degenerate and eventually, dies.
Today, Alzheimer’s disease affects nearly 5.8 million people in the United States and is the sixth leading cause of death.
When plaques and tangles begin to form, they generally begin in the hippocampus (the brain’s memory center) – thus, the first major symptom of Alzheimer’s: memory loss. From there, tangles spread quickly throughout the rest of the brain, affecting memory, then thought-processing and finally, bodily function.
It is still unknown what causes abnormal levels of tau or beta-amyloid proteins. It is also unknown whether plaques and tangles are the main causes of Alzheimer’s disease or merely symptoms. Emerging evidence does point to plaques and tangles as one of the main causes of loss of brain function, but it is also emerging that more factors are in play, such as chronic inflammation due to a buildup and loss of function of the brain’s glial cells, and vascular problems (blood flow interruptions).
There are several theories as to the true cause of Alzheimer’s. Each one is currently being studied in labs, but scientists are beginning to believe that the cause of the disease may be a chimera with multiple factors working together.
- The Amyloid Cascade Hypothesis proposes that the over-abundance and action of beta- amyloid triggers the formation of plaques and tangles. However, this hypothesis has not yet been proven in the lab. The most encouraging source of evidence for the theory are the findings in gene research that link amyloid-related gene problems to early- onset Alzheimer’s.
- Some scientists believe that the problem lies in the malfunction of the tau protein inside the cell which causes the tangles. Tangles spread as if an infection by rapidly moving from cell to cell in a connected line. Tangles influence the progress of the disease.
- Lack of adequate blood flow to the brain such as in advanced vascular disease, is known to cause the presence of plaques through lack of oxygen to the brain. Vascular disease being the primary cause of Alzheimer’s seems unlikely. It may play a part, however.
- Porphyromonas Gingivalis is the bacteria that produces gum disease. It produces protein-degrading enzymes called “gingipains” and in one study, scientists have found abnormal levels of gingipains in 90% of Alzheimer’s patient’s brains. A vaccine for P. Gingivalis is currently being developed as scientists look more closely.
The Timeline of Alzheimer’s Disease
Alzheimers progresses in three stages. In the mild stage, one will begin to forget material recently read and may have trouble planning or organizing. In this stage, the person is still able to care for himself/herself. As more and more brain cells continue to be destroyed, the afflicted individual eventually enters the moderate stage. In this stage, the person begins to feel “moody” or “withdrawn.” They begin to forget important information such as their home address, phone number or Social Security number. The personality will typically change, along with an increased threat of wandering or becoming “lost” in their own neighborhood. Finally, in the severe stage of the disease, the individual begins to lose awareness of their surroundings, physical abilities and communication. They can no longer care for themselves and must rely upon a caregiver.
Risk Factors
The number one risk factor for the disease is age. This can be compounded by a family history of the disease and genetic markers. Head injuries can play a major role in the development of the disease as these injuries can cause the development of plaques and tangles in even a young, healthy brain. Other risk factors include chronic vascular disease and poor nutrition.
Prevention
There is no cure for Alzheimer’s Disease. In order to decrease an individual’s chances of getting the disease, they should focus on the six categories of prevention.
- Regular exercise can reduce risk of Alzheimer’s by 50%. Aim for close to 150 minutes of exercise per week and make sure to include some strength and balance work.
- Continued social engagement can ward off Alzheimer’s disease. If you are feeling isolated, make sure to find ways to volunteer with an organization or join a social group.
- Maintain a healthy diet by cutting back on sugar and avoiding trans fats. It is recommended to consume more fruits, vegetables, beans, whole grains and fish.
- Never stop learning. Mental stimulation is key to maintaining a healthy brain. Take a class, challenge yourself with trivia and riddles, or simply find a new way to get somewhere.
- Set a regular sleep schedule and stick with it. Plan your naps so that you will be able to fall asleep at your designated time. Remove all distractions (television) from your bedroom.
- Manage stress and take some time for yourself. Relax, have fun and keep your sense of humor.
Alzheimer’s disease presents a scary future and the best way to avoid that future is prevention. When the disease does affect a person you know and love, remember that they are not at fault for the things they may say or do. They may not recognize who you are, but you will always know who they are and what they mean to you.
References
Bowron, C. (2019). The latest theories in Alzheimer’s research. Nextavenue.org. Retrieved from nextavenue.org/surprising-theories-alzheimers-research/
Ellison, J. (2019). Possible causes of Alzheimer’s disease. Bright Focus Foundation. Retrieved from brightfocus.org/alzheimers/article/possible-causes-alzheimers-disease
National Institute on Aging. (2019). What happens to the brain in Alzheimer’s disease? NIH. Retrieved from nia.nih.gov/health/what-happens-brain-alzheimers-disease
Smith, M., Robinson, L. & Segal, J. (2019). Preventing Alzheimer’s Disease. Help Guide. Retrieved from helpguide.org/articles/alzheimers-dementia-aging/preventing-alzheimers-disease.htm
