Cancer: The Phenoptosis Concept Essay

Alzheimer disease (AD) is the most common cause of dementia in the elderly, accounting for 65–70% of all cases (Jellinger, Janetzky, Attems, & Kienzl, 2008). The other dementias are of the Parkinson 's group, the fronto-temporal group and the vascular group. The total worldwide yearly costs for the treatment and care of patients suffering from dementia are estimated to be around 250 billion US dollars. The lifetime risk for AD between the ages of 65 and 100 is 33% for men and 45% for women with an annual increase of 1–2% in the seventh decade to almost 60% in the 10th decade with doubling every 5 years (Jellinger et al., 2008). AD is incurable, and thus represents a major public health problem. AD represents a challenge to humanity due to its relatively recent discovery, progressive nature of the illness, and complex diagnosis.

The disease called Alzheimer’s is the fourth leading cause of death in the United States (Weiner, 1987). It is estimated that the elderly population will double between now and 2030. During this period, the number of elderly will grow by an average of 2.8% annually (U.S. Census Bureau, 2001). By 2050, the number of people with Alzheimer’s is estimated to range from 11.3 million to 16 million (Alzheimer’s Association, 2005). These startling numbers should prompt an examination into one of the leading causes of death among this group of people. Understanding what Alzheimer’s is and the known causes of the disease are a good starting point. For those who have aging family members, knowing the risk factors and warning

Alzheimer’s Disease is a disease of the future. With the growing aged population, this disease, which affects primarily the elderly, will become of increasing relevance to the medical profession. Also, the high frequency of Alzheimer’s, and the high cost in labor, money, and material of caring for its victims shall put considerable burden on the society as a whole. Here, however, these issues are not going to be debated. Instead the pathology of Alzheimer’s will be reviewed to the extent it is known today.

The length of the telomere indicates age-related diseases, unhealthy lifestyle, and longevity in the lifespan.

In Chapter 27 “The Secret to Immortality” of The Immortal Life of Henrietta Lacks Rebecca Skloot provided an explanation to why HeLa cells were “immortal” unlike other mortal cancer cells; the p53 tumor suppressor gene had been “turned off” by the Human Papilloma Virus Lacks had. She mentions how according to the Hayflick Limit, human cell’s were able to replicate an average of fifty times. In addition, she explains how telomeres in cells shrink slightly every time the cell divides. According to Aging Cell’s 2004 article “The Cellular Lifespan and Senescence Signalring in Embryonic Stem Cells,” tumor cells “have high telomerase activity” yet they are not immortal. HeLa cells, similarly to Embryonic Stem (ES) Cells have the tumor suppressor gene p53 turned off. This differentiates HeLa from other tumor cells; while other tumor cells will replicated more than the average cell and eventually reach senescence, HeLa continues to replicate to this day thanks to the HPV virus that turned off its

One of the most prominent and perhaps most feared condition associated with aging is dementia. The family of disorders can cause individuals to lose their mind, reducing one from being a complex, thinking, feeling human being to being confused and vegetative, unable to recognize their loved ones. Serious dementia affects nearly 37 million people globally, but predictions of how those numbers will change over the next few decades are conflicting (textbook). Although we know dementia as to do with damage to nerve cells in the brain, there are ongoing studies looking at correlations between other health issues and these types of diseases.

Most telomere are no more that the simple repetition of the DNA nucleotide sequence TTAGGG — two thymine bases, an adenine base, and three guanine bases. With a full length telomere containing more that 15,000 base pairs, telomeres can perform their functions of preventing chromosome from losing coding regions of the genome during replication for many replications before reaching what Dr. Jerry Shay describes as their “critical length” (Shay & Wright). When the telomeres of a cell reach this critical length and can no longer replicate without damaging the base pair sequences of the chromosomes themselves, programmed cell death occurs in the form of apoptosis. However, the length of a chromosome’s telomere is not only a linear function of erosion, but also a function of how often telomerase rebuilds the strands by adding the TTAGGG base pair sequence. It is this way to “cheat” the critical point that provides medicine with the possibility to extend our

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

More than five million are living with Alzheimer’s disease in the United States and the number is set to almost triple by the year 2050. It is common in the elderly and generally occurs in persons over 65 years of age, but early onset of Alzheimer’s has also been documented (“Alzheimer’s disease facts,” 2016, para. 1). It starts in the medial temporal area of the brain, usually in the hippocampus, and then spreads to other areas of the brain. Blows (2011) explains, “Alois Alzheimer was a German psychiatrist who in 1906 described a dementia with two specific changes found in the brain after death... these changes were the presence of extracellular plaques and intracellular neurofibrillary tangles and these became the hallmarks of this disease” (p. 286). Loss of neurons takes place and amyloid plaques form. This is due to build-up of non-functioning proteins and can be observed by imaging techniques (Radin, 2003, p. 41). There are many risk factors that increase the risk of Alzheimer’s disease. The greatest risk factor is family history, but other risk factors include diabetes, hypertension obesity, hyperlipidemia, smoking, depression, physical inactivity, low estrogen levels, and head trauma (Huether & McCance, 2014, p. 546). The actual cause of Alzheimer’s is unknown, but there are genes associated with it that make the disease heritable. What is clear is that

Alzheimer’s disease (AD), is a type of dementia that no one would ever want their grandmother or grandfather to suffer from, as it destroys memory and other important mental functions of its sufferer. Alzheimer's disease is currently ranked as the sixth leading cause of death in the United States. While the age 65 and older is its target age, it has consumed the lives of over 1.9 million people. The brain begins to show signs of damage in the hippocampus, the part of the brain essential in forming memories. As more neurons die, parts of the brain then begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain tissue has shrunk significantly. The idea that Alzheimer’s disease is related to age in 1974 was introduced

Alzheimer 's disease which chronically leads to Senile Dementia, is a horrific change in homeostasis for human beings. The most obvious change in homeostasis from Alzheimer 's is loss of memory. Memory loss can vary from short term to long term. Alzheimer 's disease has been occurring in humans for a long time. This is a disease that affects different body systems, and interrupts homeostasis to a significant point. As Alzheimer 's disease is further investigated, there are more discoveries with how it is caused, what it affects, and how to reduce the risk of developing it. Alzheimer 's disease is a frightening disease that is represented in humans. There are many concerns with this disease that are worth finding out for the future victims

The topics include: Alzheimer’s disease and what provokes it, amyloid-beta proteins, synapses, synaptic pruning, neurons, cognitive and microglial cells. Alzheimer’s disease affects mostly individuals in their mid-60s and is “a type of dementia that causes problems with memory, thinking and behavior” (Alzheimer 's Association). The articles reflect the discovery of the Alzheimer’s disease affects the brain by the destruction of the connection of the brain cells which causes damage in neurons and accelerate cognitive decline, and occasionally call it the earliest stage. Amyloid-beta is a term that refers to the plaques made by the proteins which interferes and cause the loss of synapses also known as synaptic pruning is the loss of connections between neurons caused microglia, that according with The Campbell Biology In Focus textbook, “microglia are immune cells that protect against pathogens” (Campbell.) The authors of the research support “microglia that prune excess synapses in development are inappropriately activated and mediate synapse loss in Alzheimer’s disease.” (Taub, 2016)

This paper will discuss the relationship between the aging process and key diseases associated with aging. Examples of aging-associated diseases include cancer, diabetes, cardiovascular disease, and neurodegenerative diseases (López-Otín, Blasco, Partridge, Serrano, & Kroemer, 2013, p. 1194). Of these, we will discuss in-depth recent studies that have linked aging with Alzheimer’s disease, cardiovascular disease, and diabetes. These diseases affect a significant proportion of the population over the age of 65 and place a considerable burden on the American health care system. Therefore, a better understanding of how they are related to aging and each other can result in the adoption of innovative treatments and declined risk for older adults.

Telomeres are directly correlated to the aging of a human body. Although some people might think that shorter telomere lengths are detrimental, the natural shortening of these telomeres are essential to healthy and normal aging. It is natural for cells to divide through mitosis, but each time cells are split telomeres are lost through the process. This is why the telomere maintenance system was evolved to protect the ends of chromosomes (Prescott, Kraft, & Chasman, 2011). Every time a cell is divided, its telomeres are weakened, and stress can accelerate this weakening, and biologically age the person. As a

These reactions will likely produce chronic inflammation, which is thought to contribute to many chronic, and terminal diseases such as alzheimer 's or cancer. This theory allows us to focus on the immune system, more specifically areas in which cells deteriorate or diversify too much. Once we are able to target which specific parts of the immune system causes it to deteriorate, cell repair potential is likely. If immune cell deterioration is due to diversification of human cells, one will one day be able to either slow the process or stop specific areas to allow the immune system to be strong and thus the likeliness of diseases such as alzheimer 's or diabetes will decrease. Another theory of aging is the Wear- and Tear Theory. This theory describes the aging process as the general deterioration of our body over time, whether it be environmental factors or just degeneration of our body 's structure and core. Like a car, over time we become less functional exposure to “radiation, toxins, and ultraviolet light can damage our genes,” as well as our own body 's functioning. Some nerve cells of the brain do not replicate or replace themselves as we age, so function will be lost as well. As our cells divide, it shortens the “telomeres of the chromosomes,” which will ultimately not be able to divide anymore as well. This theory allows one to understand the general