Early Life Stages Of Aging Essay

     Going back forty-five years is not an easy task to complete because I can’t remember some of the finer details of my childhood. I know I was born on a hot August afternoon in Birth Year at Place Of Birth in City ands State. My mother was just twenty-two at the time and was already the mother of two, I was her third child. My father was twenty-one and already a workaholic, I know because my mother would constantly remind me not to be like that. My mother and father were good parents and they tried to give us the best upbringing they could. My father was the kind of person that believed he should provide and protect his family, and he did a very good job of doing that.

Q has reached maximum body growth and biological aging or senescence has begun. Biological ageing is “genetically influenced declines in the functioning of organs and systems that are universal in all members of our species” (Berk, 2010, p. 432). Q exercises daily but he admits that he doesn’t eat a healthy diet all the time. “Regular moderate to

Later adulthood is the time in life when changes in marriage, families, and peer relationships are affected the most by the loss of someone close to that person. “Most people 70 years of age or older are widowed, divorced, or single” (Zastrow & Kirst-Ashman, 2010, p.619). Losing a spouse or close friend can create a sense of loneliness, which causes depression, anxiety and the emptiness feeling can become overwhelming. Depression also leads to psychological effects that will deteriorate a person’s health causing the chance for a terminal disease to become much higher. The weaker appearance of older adults causes family and remaining peers to step up in the role of making sure the person’s wellbeing is being met. (Zastrow & Kirst-Ashman, 2010). Living accommodations and healthcare needs

In contrast, mitochondrial dysfunction accelerates premature aging. Recent studies of mitochondria, mitochondrial DNA and free radical production has found an increased accumulation of mitochondrial DNA defect, increased production of ROS and decrease in mitochondrial function in brain tissues of aged rodents and humans relative to young ones giving an indication that increase in mitochondrial DNA defect is involved in aging. Data from studies in mice with mutations in mitochondrial DNA suggests that increase in mitochondrial DNA mutations that arise during development may lead to an increase in ROS , deregulated stem cell homeostasis and premature aging by affecting mitochondrial bioenergetics. Aberrant mitochondrial biogenesis and secondary changes in mitochondrial energy production may leads to loss in accuracy of biochemical events involved in mitochondrial ETC subsequently leading to an electron leakage of 0.5 – 5% and increased production of

For the Adult Development and Aging class projects, interviewed three people of different ages about their work, social, relationships, and stress. Information was collected by student interviews. The data sample consisted of 96 participants, with 32 in each age group. The three age groups include early adults, middle-aged adults, and older adults. The mean age for each age group include 28 years old for early adults, 53 for middle-aged adults, and 75 for older adults. There were significantly more women than men in the study. The young adults were less likely to be married and a vast majority of the young adults had no children. Constantly, most middle-age and older adult had

Remmen, H. V., & Richardson, A. (2001). Oxidative damage to mitochondria and aging. Experimental Gerontology, 36(7), 957-968. doi: https://doi-org.uws.idm.oclc.org/10.1016/S0531-5565(01)00093-6.

For instance, young mitochondrial cells produce a lot of energy in the form of ATP. With this energy production, we are also creating free radicals which damage our cells. Young mitochondrial cells produce a lot of energy and few free radicals. They are also better at containing the free radicals not allowing them to escape from the mitochondria. For the ones that do escape there are scavenger molecules that capture and destroy them. In young cells the rate at which the cells are replaced and DNA repaired is much higher than the production of free radicals. However, as we age telomeres shorten and gene expression changes causing changes to occur. Older mitochondria become less efficient at producing energy while creating more free radicals. This occurs because aging cells lose their ability to supply the mitochondria with the needed proteins. Which causes the mitochondria to fail. As we age, mitochondria lose their ability to contain the free radicals within their membrane. Allowing for more free radicals to escape causing even more damage. With age, mitochondrial scavenger molecules begin to fail, so we aren’t able to capture and destroy them as well. Lastly, as we age the rate at which cells are turned over decreases. With these changes in gene expression there are more free radicals being produced causing more damage to cells. Since the rate at which these damaged cells are replaced/repaired slows down, we start to have more damaged cells than functioning ones. Due to the decrease in turnover rate damage begins to accumulate within the cells. The rate at which the molecules are replaced can’t keep up with the rate at which the molecules become damaged. Which eventually leads to cells becoming dysfunctional and no longer able

If your cells were subjected to oxidative damage, this can result in premature aging (the signs of aging will show early on your skin and organs) and you’ll be at higher risks to diseases.

Aging causes structural and functional changes in brain. As aging population has become a burden, it is essential to study aging brain aiming to maintain cognitive integrity. Previous studies indicated that young blood improves the function of stem cells in organs including brain by heterochronic parabiosis model. However, data is lacking whether regeneration or beyond occurs by this model. The authors Villeda et al., hypothesized that aged animal exposed to young blood can counteract aging process and rejuvenate brain cognitive function. Therefore, the authors conducted research to examine within molecular, structural, functional, and cognitive aspects.

The implication that protein degradation pathways are dysregulated by hyperoxia is especially important given that not only is it implicated in aging within the lung, but that the mitochondrial dysregulation not only seen at work within this body of literature, but also the right ventricles used in this study would suggest that protein degradation could play a role in the right ventricular dysfunction found after exposure to post-natal hyperoxia (Goss, 2017).

Some hypotheses for aging involve the body’s natural process of metabolism. We are constantly metabolizing the food we eat, the air we breathe and other vital functions, and some biochemical byproducts of our metabolism, such as free radicals, can affect our health. Free

Aging, also known as Senescence, is a natural process, “beginning at reproductive fitness and culminating in death,” Observed in most living organisms, senescence is characterized by a gradual reduction in “reserve capacity of organ systems”, (Heydari). Supporting research by U. of Florida’s Aging Biochemistry Laboratory indicates an increased apoptotic rate of cardiomyocytes, T-lymphocytes, and neurons, as age advances (Leeuwenburgh, par. 3.1). These factors manifest the classic signs of aging as well as many age-associated diseases, such as reduced cardiac function, susceptibility to illness and

Old age brings many diseases and disabilities such as diabetes, Alzheimer’s, and heart failure, which are caused by the accumulation of damage in the mammal’s cells over time (Bolotnikova, 2017). Nicotinamide adenine dinucleotide, NAD, is a coenzyme that is used by all cells in every living mammal’s body produced by the powerhouse of the cell, the mitochondria (Stipp, 2015). Proven by many studies, the decay of the mitochondria, the more mammals age and eventually die (Stipp, 2015). Knowing this, scientists have been looking at a bigger picture of increasing the levels of NAD in the cells to prevent aging.

theories of why we age, the physical and mental changes we undergo as we age,

Ageing is a natural and inevitable consequence of human life. Once born, there is no scope for a man from old age. Old age brings both physical infirmity and social predicament. The Major social problem of older people is their adjustment to their surrounding social world in general and their immediate families in particular. In foreseeable era, old peoples were taken care of in a joint family structure. In the sub-continental societies, old peoples were used to get honor and admiration from the society at large. And their family treated them humanely and with care and sympathy. Advent of industrialization and urbanization has drastically changed social and family life. The joint family has disappeared people in the society are becoming more and more individualistic. In this situation, the old people are facing the