Dementia and Alzheimers disease have a profound adverse impact on affected individuals and their families. People who have been diagnosed with these neurological problems are mostly prone to isolation and marginalization and are even being misunderstood by the family members (Wortman, 2012). Dementia and Alzheimers disease contribute significantly to global health challenges due to associated cost, impact and size, particularly among the senior population. The 2010 statistical approximations reveal there were more than 35.6 million people who have Alzheimers disease and other forms of dementia (Wortmann, 2012). It is projected that by 2030 there will be approximately 66 million people suffering from different forms of dementia, and figures are likely to stand at 115 million at the end of 2050 (Wortmann, 2012). Diagnosis of specific neurodegenerative disorder is not an easy task due to overlapping symptoms and complexity of microscopic pathological developments. Aging process has been cited as a factor in the emergence of these neurodegenerative disorders. Although there are many contemporary biological theories, none of them has given comprehensive physiological and pathological changes which underlie neurodegenerative disorders and other forms of cellular degradation with advancing age (Jin, 2010). However, biological theories have been found to provide essential information regarding aging process in an integral manner.
Aging is a natural biological process that takes place as people grow old. It is a complicated process, and no single theoretical approach has been able to explain it. However, it is the interaction of all biological theories that can be able to elucidate the process of aging. Aging has been examined and scrutinized for a long time to establish whether anti-aging remedies can be synthesized. This paper aims to explore modern biological theories that explain the aging process and describe dementia and Alzheimers disease, with their associated pathology and symptoms.
Current Biological Aging Theories
In spite of the tremendous advancement in molecular science and technology, the factors that influence human lifespan remain inconclusive. There are two broad categories of modern biological theories, namely programmed and error theories, which have been advanced to explain the process of aging; however, none of these approaches provides a satisfactory explanation (Jin, 2010). Nevertheless, it is acceptable that these theories interact in a sophisticated manner, thereby influencing the aging process. The programmed theories postulate that the aging process follows a biological timetable which probably controls the childhood growth and development. The programmed biological theories involve the regulation that is mediated by gene expressions which affect the mechanism for repair, maintenance, and response. The error or damage theories posit that environmental assaults can induce cumulative damage at various levels to organisms which cause aging (Jin, 2010).
Programmed theories are grounded on the concept that living for an extended period leads to evolutionary disadvantage. Thus, organisms tend to develop a suicide mechanism that limits their lifespans beyond a certain age, taking into account species. These theories have their foundation on the proposition that the evolutionary benefits survival reduces with age and facilitates benefits for the population. The programmed theories are divided into three subgroups which include programmed longevity, endocrine theory, and immunological theory (Jin, 2010). Programmed longevity involves switching on and off of particular genes during aging, while defining senescence as a stage during which there is a manifestation of age-related deficits. The endocrine theory demonstrates that biological clock works via hormones to influence the pace of aging. Studies have confirmed that the aging process is under hormonal control, and evolutionarily conserved insulin has been identified a key facilitator that affects aging (Jin, 2010). The immunological theory is associated with a reduction in the functionality of the immune system over time that leads to increased vulnerability to infections. The effectiveness of the immune systems is at peak during puberty, but it declines as the age advances. The immune system is impaired in an advancing age and may not be effective in combating disease; this has been associated with cellular stress which leads to eventual death (Jin, 2010).
The error theories include wear and tear theory, the rate of living, cross-linking, free radicals, and somatic DNA damage theories (Jin, 2010). The wear and tear theory sheds light on structural and functional changes that occur during aging as result of use and pressures. The rate of living theory states that an organism contains particular amounts of vital substance, and when such substance gets depleted, the organism dies. Thus, according to this theory, the organism with a high rate of basal oxygen metabolism will have a short lifespan. The rate of living theory cannot adequately total maximum lifespan. According to cross-linking theory, the aging process in an organism is dependent on the formation of casual chemical bonds between protein molecules. However, the repair enzymes are unable to dissolve chemical bonds that aggregate proteins. The accumulation of cross-linked proteins leads to cellular and tissue damage, thereby slowing body physiological processes which cause aging. The free-radical theory posits that the inborn aging process is induced by cumulative oxidative damage by free radicals which are generated during aerobic respiration. Free radicals are molecules which have single unpaired electrons; they are highly unstable and reactive, and they will likely react with nearby molecules in a bid to gain electrons that facilitate stability (Liochev, 2013). Jin (2010) observes that macromolecules which include nucleic acids, sugars, lipids, and proteins are vulnerable to free radicals attack. Finally, somatic DNA damage is one of the theories associated with aging. One of meta-analysis studies identified an increased accumulation of damaged DNA which was linked with advanced ages (Soares et al., 2014).
Brain Changes Associated with Aging
One of the areas affected by aging process is the brain. Physiological and anatomical changes that occur with age are complex, and no single theory can be used to explain them. It is rather a sophisticated interaction of several theories that may include DNA damage, wear and tear, endocrine, immunological, free-radicals, cross-linking, and programmed longevity biological theories that can provide some explanation. In fact, age-related changes have led to the emergence of health issues which include Alzheimer's disease and dementia that affect people who are mostly at advanced ages. These multiple aging theories can explain pathological brain changes. There has been a focus on brain changes that are linked to aging. Several studies have shown the impact of aging on neuroimaging parameters of tissue properties such as brain volume reduction, cortical thickness changes, brain density shifts, and regional brain changes relating to tissue microstructure which is measured by use of diffusion tensor imaging (Salat et al., 2009). Salat et al. (2009) further posit that fewer studies have reported changes in tissue signal properties such as spin-lattice relaxation time and signal intensity. In fact, the prolongation of spin-lattice relaxation time has been identified in temporal lobe white matter and is linked to increasing age. In addition to spin-lattice relaxation time prolongation, there has been a reduction in the differentiation of gray and white matter spin-lattice, and this correlates with cognitive performance. Alterations of signal properties with reduction of gray/white matter contrast have been observed in the regions measured in relation to aging. It is postulated that signal properties may be affected by tissue changes in the microstructural aspect that precede macrostructural effect of white tissue degradation or cortical atrophy. These observations show that particular brain tissue change that alters the imaging properties of brain structures.
The increasing age has been linked to a reduction in cortical thickness. Salat et al. (2009) findings showed a phenomenon of a reduction of cortical thickness in the pre-central, post-central, occipital regions, cuneus, parietal cortex, superior frontal, and superior temporal. However, cortical thickening with increasing age was observed in medial frontal regions. Apparently, brain image properties tend to get altered during the adult-age lifespan. The pattern of change is regionally specific, and this can be used as a metric for neural aging and age-related neurological diseases.
The age-related brain tissue changes are regionally specific in the cortical area. However, the changes, in contrast, were significant in frontal regions whereby the white matter is mostly affected (Jin, 2010). There is the difference between cortical thinning and contrasts in advancing age; this may be linked to histological or pathological variation. It is possible that the changes in the cortical thickness may lead to contrast changes.
Aging is a risk factor for neurological problems. Alzheimers disease is diagnosed in persons who are above 65 years (Jin, 2010). Identification of molecular basis for neurological disorders pathology may help in understanding the aging process. The common symptom identifiable with Alzheimers disease in its early stage is the lack of ability to acquire new memories.
It is important to understand how biological aging theories explain abnormalities underlying dementia and Alzheimers disease. The adult brain hippocampus has endogenous neural stem cells that have been identified to play an essential role in memory functioning. The neural stem cells functionality is consistently decreasing with increasing age, while proper explanation of this phenomenon remains elusive (Jin, 2010). Telomeres maintenance helps the stem cells functionality in organs which have high cellular turnover, but telomere division usually decreases as age increases. It has been observed that there is DNA damage associated with shortening of the telomeres, and oxygen free radicals mostly elicit the damage. Thus, there is an interaction of two theories, i.e. free-radicals theory and somatic DNA damage; the ultimate results involve impaired brain functioning. According to telomere theory, when telomere achieved a particular length, the cell stops replicating and dies, leading to the eventual death of the whole organism. Telomere theory is still a form of DNA damage theory; thus, the damage to telomeres or reduction in their functionality causes an impaired memory due to reduced cell division in the hippocampus region. The cross-linking theory can explain the presence of Lewy bodies which cause brain damage, and this observation is evidenced by the presence of Lewy bodies in dementia (Dementia with Lewy bodies) and identification of proteins strangle, plaques and tangles in the case of Alzheimer's disease. The existence of alpha-synuclein proteins deposits in case of Parkinson's disease dementia is a precise testimony that cross-linking biological theory of aging is valid; it can explain pathological brain changes that are associated with neurodegenerative disorders.
Dementia means a decline in mental ability which interferes adversely in daily life. It is a progressive but not specific disease. Its wide range of symptoms associated with mental decline is sufficient to make an individual unable to cope with life activities (Hooyman, Kawamoto, & Kiyak, 2014). Some of the symptoms that validate the diagnosis of dementia include impaired functioning associated with memory, language and communication as well as lack of focus and attention, visual perception, reasoning and judgment. Dementia is a general term describing different conditions which can be classified as types of dementia. The various forms of dementia include vascular dementia, dementia with Lewy bodies, Alzheimers disease, mixed dementia, and Parkinsons disease dementia, amongst others.
Alzheimers disease is the most prevalent type of dementia. Its symptoms include difficulties in remembering recent events, names and conversations, and apathy and depression; these are early signs. The British Broadcasting Corporation (2016) indicated that people who had increasing symptoms of depression were at greater risk of dementia. The symptoms at advanced stages include poor judgment, confusion, disorientation, impaired communication and difficulties associated with walking, speaking and swallowing. The brain in a patient diagnosed with Alzheimers disease has a particular pathology. It is characterized by the deposition of protein fragment beta-amyloid or plagues, the presence of twisted proteins strands and evidence of nerve damage and death.
Vascular dementia tends to occur after a stroke. However, it is a less common form of dementia. Some of its key symptoms include impaired judgment and ability to make decisions, and difficulties associated with planning and organizing are the most likely signs at initial stages. Memory loss is not an initial symptom in vascular dementia, as opposed to Alzheimers disease. Blood vessels can get blocked or damaged, leading to infarcts or stroke. The extent of harm will influence an individual's levels of physical functioning and thinking. Brain blood vessels abnormalities can be identified through imaging, which can act as diagnostic confirmation of vascular dementia. Changes in thinking and skills can occur after a stroke that causes blockage of major brain blood vessels. However, it must be noted that vascular dementia can coexist with other forms of dementia, including Alzheimer's disease and dementia with Lewy bodies.
Dementia with Lewy bodies is characterized by memory loss and thinking problems which are also common to Alzheimer's disease. However, it is dissimilar symptomatically to Alzheimers disease by comprising such symptoms as rigidity of muscles, well-informed visual hallucinations, gait imbalance, sleep disturbances and slowness at its early stage. Dementia with Lewy bodies is associated with brain abnormality whereby there is the aggregation of protein alpha-synuclein (Jones & O'Brien, 2014). Dementia occurs when the aggregation of such proteins occurs in the cortex. Alpha-synuclein aggregation also occurs in people diagnosed with Parkinson's disease, but the aggregated pattern is different from the one observed in dementia with Lewy bodies (Breitve et al., 2014).
Lewy proteins can also be identified in persons with Alzheimer's disease and Parkinson's disease. Furthermore, it can be observed that many patients with dementia with Lewy bodies and Parkinson's dementia have protein tangles and plaques which are common in Alzheimer's disease. Thus, it is possible that these disorders are linked to a common abnormality associated with the processing of alpha-synuclein in the brain (Jones & O'Brien, 2014).
The essential differences between Alzheimers disease and dementia with Lewy bodies (DLB) can include prominence of early memory loss in Alzheimers disease, but advanced DLB can also cause memory concerns, in addition to its typical characteristics of visual perception, planning, and judgment. Alzheimers disease can elicit problems related to walking and balancing as it progresses from moderate to severe forms. However, movement symptoms are the core causatives of disability in DLB, as opposed to Alzheimers disease. The autonomic nervous system is likely to be affected more in dementia with Lewy bodies than Alzheimers disease; this can decrease blood pressure and induce dizziness, urinary incontinence and falls, which are likely to be more prevalent in people with DLB than Alzheimers disease. The inability to recognize familiar people, hallucinations and delusions are more frequent during dementia with Lewy bodies than Alzheimer's disease. Finally, the rapid eye movement (REM) disorder is more prevalent in DLB patients than the ones with Alzheimer's disease (Breitve et al., 2014).
Mixed dementia has more than one form of dementia. The commonest mixed form of dementia involves the presence of tangles and plaques which are found in Alzheimer's disease and blood vessels abnormalities that are present in vascular dementia. Frequently, the plaques and tangles in Alzheimer's disease coexist with Lewy bodies. Thus, a person may have brain changes that are associated with Alzheimer's disease, DLB and vascular dementia (Jones & O'Brien, 2014).
Parkinson's disease dementia is another form of dementia that affects the motor area in the brain. On microscopic brain examination, persons diagnosed with this disease will have deposits of alpha-synuclein proteins, whereas the functions of these proteins remain unknown. The patients with Parkinson's disease dementia usually present with poor memory, impaired judgment and concentration, difficulties in the interpretation of visual information, sleep disturbance, irritability, anxiety, visual hallucination, depression, and muffled speech (Dominguez & Burli, 2010).
Is There Any Difference between Dementia and Alzheimers Disease?
Dementia is a general or umbrella term that covers a wide range of symptoms associated with neurodegenerative disorders. Dementia is not a disease, but it is a syndrome. Alzheimer's disease is a particular neurodegenerative disorder, and it falls under dementia (Brettschneider et al., 2015). Thus, Alzheimers disease is a type of dementia. Dementia describes a set of symptoms that are indicative of brain damage. These symptoms include difficulties in thinking, problem-solving, communication and memory. Alzheimers disease causes brain damage, leading to dementia. However, there are some differences between dementia and Alzheimer's disease. An individual with dementia is diagnosed taking into consideration merely symptoms, without considering the concepts underlying those symptoms. In regard to Alzheimer's disease, the precise cause is known. Finally, Alzheimers disease is irreversible, whereas some form of dementia such as those caused by drug interaction and nutritional issues can be reversed.
Neurological Disorder Case
The patient reported with complaints relating to visual hallucination, sweating, muscle rigidity, repeated falls, sleep disturbances movement problems and short span of attention. Taking into account these symptoms, the diagnosis is dementia with Lewy bodies. The reason is that the signs exhibited by the patient are Lewy body symptoms.
Aging is a gradual, continuous process that commences in early adulthood. During middle age, body physiological functions tend to decline with time. Modern biological theories do not adequately explain the aging process. However, the given theories can explain the aging process in one way or another. Although many aging issues remained unanswered, some neurodegenerative disorders have been linked to aging. The brain changes have been cited as some of the key causes of reduction in cognitive power, memory and motor skills.
I was assigned a paper that I felt would be almost impossible to complete myself. Not only did the writer of supremewritingservice.com complete the assignment successfully. He also returned my paper to me early so that I could review it in time to ask for a couple of small adjustments. I wasn’t charged anything at all for the rewrites! I have had a great experience with supremewritingservice.com and definitely plan to come back the next time I have an assignment that I can’t write. Thank you so much!
I was assigned a paper that I felt would be almost impossible to complete myself. Not only did the writer of Supremewritingservice.com complete the assignment successfully. He also returned my paper to me early so that I could review it in time to ask for a couple of small adjustments. I wasn't charged anything at all for the rewrites!
My assignment was too hard to handle! I didn’t know what I was going to do until someone suggested using the services of supremewritingservice.com. After I placed my order, I didn't have to worry about a thing. The paper was completed for me in just a couple of days and I got an A+ on it! Thanks, supremewritingservice.com!
Let’s earn with us!
Get 10% from your friends’ orders!