Alzheimer’s Disease (AD) is a progressive neurological disorder that involves the deterioration of brain cells. It is common among the elderly, rare among young people, and is characterized initially by memory impairment, which later leads to more serious symptoms such as difficulty in reasoning, planning, perception, and language. Symptoms may vary in terms of severity. The commonness of the disease is equally serious – for every 66 seconds in the United States, a person develops the disease.
The prevalence of Alzheimer’s is alarming. The costs of long-term health care have now surpassed a quarter of a trillion dollars this year. Funds have been poured into research, but to this day, no definitive answer about its cause has been found. Despite this, several theories posit that the disease could come from either neurological or genetic mutation or disturbance. The most widely discussed theory is known as the Amyloid Cascade hypothesis.
The Amyloid Cascade Hypothesis
Researchers feel like this hypothesis, proposed amidst several unanswered questions, could best explain the nature of the disease. It asserts that the amyloid precursor protein (APP) forms the amyloid-beta. Special enzymes severe the protein at certain places, forming what is called the amyloid-beta peptide. These clump together as oligomers, which are said to be toxic to brain cells. The accumulation of oligomers is then asserted as the direct factors of the disease’s symptoms.
Although this hypothesis is popularly accepted among researchers, the challenge appears in the fact that amyloid-beta accumulating in plaques also happens in normal aging; thus, the “no definite cause” status of the disease.
Other possible factors
Another considered theory is called the Mitochondrial Cascade hypothesis, which asserts gene inheritance as what defines a person’s mitochondrial function at the base. Mitochondrial function then experiences changes at different rates over time, eventually influencing the start of an Alzheimer’s Disease chronology.
Accumulation of tau plaques and tangles have also been considered as prime suspects in cell death and tissue loss. Tau primarily helps the transport system in healthy areas, but where tangles are forming, twisted tau strands significantly destabilize the system. In the process, nutrients can no longer move through cells, causing death.
Two other categories linked to genetics are proposed by the Alzheimer’s Association, which identifies risk genes and deterministic genes as potential factors. Basically, there are two types of the disease – early onset and late onset. Both types are known to have a genetic component. Risk genes may increase the chances of developing AD but do not actually guarantee it. Deterministic genes, on the other hand, guarantee that anyone will develop AD if one gene is inherited.
Both define what is known as “Familial Alzheimer’s,” and although rare, provide significant clues as to how AD potentially develops.
Some scientists posit that age-related neurological changes may have the ability to harm nerve cells, which then may contribute to the disease. These changes are known as cerebral atrophy (shrinking of certain brain parts), breakdown of energy-producing cells, inflammation (by injury or another disease), and free radicals.
Other theories also explore nutrition as a cause. Global malnutrition and a lack or absence of specific vitamins have been found in people diagnosed with AD, although there is no clear evidence that successfully determines whether poor diet is a cause or effect of cognitive decline.
Other areas of research gather other surprisingly possible causes of the disease:
- Anti-anxiety medication – New science deduced from a 6-year British Medical Journal study following 1,797 diagnosed Canadians pointed out that benzodiazepines (a class of medications used to treat anxiety), was associated with a 51% increase in the disease.
- Sleep deprivation – Being regularly sleep-deprived is common among people of all ages. A Temple University in Philadelphia found via mice experiment that tau accumulation increased by letting mice sleep for only four hours a night. Chronic sleep deprivation is known to cause mental and physical stress, which hastens harmful processes that eventually lead to AD.
- Cerebral diabetes – According to Brown University neuroscientist Suzanne de la Monte, Alzheimer’s Disease is metabolic. She emphasized the natural ability of insulin as the prompter of brain cells to contract glucose from the blood. Her insight however, was that brains could form insulin resistance, paving the way for harmful protein buildups in the brain.
It can be difficult to make sense of the all the theories that point towards Alzheimer’s. Experts then tell us to view it as a disease that can be developed by a variety of ways. Research is still in the midst of finding out brain physiology and anatomy, which unfortunately provides us several indefinites for now. However, prevention may be done by way of developing a brain-healthy lifestyle.
Meredith Rogers is a blogger, health writer, and a nurse. She is currently editor-in-chief for GeriatricNursing.org, a nursing blog about various nursing issues related to older adults.