Alzheimer's: An Irreversible Brain Degeneration Leading to Death - Research Paper

Introduction

Alzheimer's disease is an irreversible degeneration of the brain, causing disruptions to the personality, memory, cognition, and other critical functions that could result in complete brain failure leading to death. Alzheimer's disease is amongst the most common forms of dementia, and Alzheimer's disease hallmarks include the accumulation of beta-amyloid plaques between neurons in the neurofibrillary tangles and brain. Some of the environmental and genetic factors contributing to the risk of Alzheimer's disease include diabetes, smoking, traumatic brain injury, diet, among other factors. Correspondingly, Parkinson's disease (PD) before Dr. Alois Alzheimer described the AD, James Parkinson described Parkinson's disease as the "shaking palsy." According to James Parkinson, the condition is diagnosed in an even an individual who depicts at least three of the following symptoms; muscle rigidity, tremor, and bradykinesia (slowed movement). Also, other associated symptoms to Parkinson's disease include cramped writing, shuffling gait, swallowing difficulties, quiet speech, expressionless face, among other signs resulting from the malfunction of specific nerve cells in the brain.

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Besides the details of Alzheimer's and Parkinson's disease, both conditions affect individuals physically and cognitively. In Parkinson's disease, it causes muscles to become rigid and tighten, which makes it difficult to do physical activities. At different extents, Parkinson's disease is defined as a movement disorder. On the other hand, individuals with Parkinson's disease may experience memory loss or dementia, among other cognitive problems. In Alzheimer's disease, physical changes are a result of brain change, which affects the physical function and increases vulnerability to other more health problems (Vemuri et al. 405). The cognitive effects of Alzheimer's disease are due to the clusters and plaques that appear in the brain in charge of behaviors that affects cognition. In different cases, the symptoms of Alzheimer's and Parkinson's disease can be managed following a series of interventions. Thus, this paper will give evidence-based research indicating that Alzheimer's and Parkinson's disease would dramatically change an individual's life, affecting not only the person but the entire family as well. Also, it will offer details concerning the different methods of managing diseases.

Methods

Based on the differences in diagnostic criteria, study populations, and methodology is different studies, the epidemiological numbers vary significantly. For instance, the prevalence of PD and AD in community-based studies has been estimated at 30% - 40%; however, the figures range from 10% - 80% of individuals with Parkinson's disease (Vemuri et al. 405). Within the methods, research on both AD and PD is based on the pathological features and the shared mechanisms.

Genes

Despite Alzheimer's and Parkinson's disease is clinically different, there are possibilities of pathological overlap. For instance, Alzheimer's and Parkinson's disease have been hypothesized to shared common gene determinants. According to various genome-wide association (GWA) studies, they suggest that the idiopathic forms of Alzheimer's and Parkinson's disease have an identified number of loci containing genetic variants that increase the risk of the two conditions (Moskvina et al. 1268). The role of the PON1 gene in Alzheimer's and Parkinson's disease is essential because of the biological functions in the oxidation stress, inflammation, pesticide metabolism, and other mechanisms in the pathogenesis of the conditions.

In case-control studies about the PON1 gene variants in PD and AD, they reveal a positive albeit association with PON1-coding polymorphisms: Q192R (rs662) and L55 M (rs854560). The Glutathione S-transferase omega-1 and glutathione S-transferase omega-2 genes (GSTO1 and GSTO2) in Alzheimer's and Parkinson's disease accommodate functions like the moderation of oxidative stress, and most cases cause the pathophysiology of the disorders (Wingo et al. 204). The evidence-based studies imply that GSTO and PON1 genes define that PD and AD have common genetic mechanisms.

a-Synuclein (a-SN)

The a-Synuclein (a-SN) is a 140-amino acid protein encoded by single genes comprising of seven exons borne by chromosomes. In different studies, they imply that a-Synuclein has various associations with PD and AD. In different extents, a-SN has been suggested to be associated with the formation of the aberrant synapse in the AD patients' brains. Within the early detection and stage of AD, a-Synuclein can be seen at the presynaptic location, implying that abnormal deposits could be a first event in the AD pathogenesis. According to a report, it found a-Synuclein in the plaques in the brain suggesting that a full-length a-Synuclein given by the neurons could result in neuronal degeneration or loss of life (Borghi et al. 65). From recent reports from the Alzheimer's Disease Neuroimaging Initiative, it found that increased a-Synuclein in patients AD, which means that a-Synuclein takes part in the AD mechanism. Also, statements on the availability of Lewy bodies imply that a-Synuclein is a contributing factor to PD pathophysiology as well.

Tau Protein

Tau Proteins are microtubule-associated phosphoprotein whose levels are regulated by phosphatases and tau kinase. In their role, the tau protein is critical in the maintenance of neuronal viability, dynamics, and microtubule stability. The abnormal phosphorylation of tau results in the creation of neurofibrillary tangles (NFTs) produced by the actions of tau protein resulting in loss of synapse, neurons, and later to dementia. It means that tau protein may get involved in Alzheimer's disease mechanisms.

Additionally, tau is also involved in Parkinson's disease. In a study by Herbert et al., they determined the diagnostic value of cerebrospinal fluid (CSF) and tau proteins in Parkinson's disease. In their results, they implied that the combination of DJ-1 and tau protein improved discrimination to identify Parkinson's disease (Herbert et al. 112-115). The finding highlighted the benefits of a combination of DI-1 and tau as biomarkers for differential diagnosis of Parkinson's disease.

Iron

In different studies, iron is found in metals such as copper, aluminum, and zinc, suffer progressive changes in advance of neurodegeneration, implying that the imbalances could be involved with the decline of cognitive functions. In the pathogenesis of Alzheimer's disease, molecular mass fractions of iron play a significant role. The different pathological features of the neurodegenerative condition Alzheimer's and Herbert Parkinson's disease are associated with dysregulation of iron in parts of the brain where pathology is highly expressed (Raven et al. 130).

Locus Coeruleus

The Locus Coeruleus (LC) released norepinephrine, which produces effects based on the adrenoreceptor (AR) acted on (Zarow et al. 340). Often, the LC has greatly affected Alzheimer's and Parkinson's disease in different ways. In Alzheimer's and Parkinson's disease, they share a significant neuropathological iteration, which involves a reduction in LC noradrenergic neurons (Szot 61). This LC reduction occurs in the progression of both AD and PD.

Nicotinic Receptors

Nicotinic Receptors are in the Cys-loop superfamily of pentameric ligand-gated ion channels that are associated with AD and PD. In the central nervous system (CNS), the nicotinic receptors help in modulating presynaptic, and extrasynaptic signaling found in CNS disorders such as AD and PD.

In summary, evidence suggests that a high risk of Parkinson's disease is involved with pesticides while a high risk of Alzheimer's disease is involved with hypertension and high cholesterol level in middle age, pesticides, smoking, depression, traumatic brain injury, and hyperhomocysteinemia. Correspondingly, weak evidence suggests that PD is associated with high iron intake, chronic anemia, traumatic brain injury, and high consumption of milk while AD is associated with exposure to electromagnetic fields, excess alcohol, high aluminum intake, among others.

Results

Stimulation Exacerbating the Symptoms

Stimulation that exacerbates the symptoms and cognitive impairments of AD and PD include the deep brain stimulation. In Parkinson's disease, the motor symptoms involved follow the degeneration of neurons in the substantia nigra. With the application of deep brain stimulation (DBS), it helps in mitigating or treating some of the parkinsonian symptoms like rigidity and tremor. Even though the mechanisms by which DBS exacerbates the symptoms are difficult to study in patients, there is an indication that the DBS helps in worsening the symptoms. The deep brain stimulation has delivered success in treating symptoms of PD. Also, the development of DBS for the individual suffering from PD has been motivated by failures seen from the pharmacological interventions, particularly in the later stages of the condition (King et al. 130).

As for Alzheimer's disease, there is a significant translational gap between the understanding of AD etiology, affected brain parts, and the ability to offer therapeutic means that could influence the disease symptoms. In the exacerbating of AD symptoms and cognitive impairments, brain stimulation does not provide the expected results (King et al. 130). As such, there is extensive literature on noninvasive brain stimulation in AD patients using transcranial magnetic stimulation, vagal nerve stimulation, and the direct current stimulation. More so, assessing the specific affected brain regions remains difficult.

Cognitive Impairments of AD and PD

Cognitive impairment is disabling comorbidity for PD patients as it represents challenges for the caregivers, physicians, and the health care system at large. Some of the involved features in PD cognitive impairment involve visuospatial reasoning, memory and language function, paranoia, visual hallucinations, and attention fluctuations. Executive deficits and visuospatial primarily mark Parkinson's disease compared to Alzheimer's disease, which is predominated by memory impairments. In PD, cognitive impairment encompasses a spectrum of severity from mild symptoms to the end-stage, which could include dementia. Overall, the prevalence of PD associated with memory loss is 25% to 30% of the total Parkinson's disease cases, which could dramatically increase with age (Vemuri et al. 405).

Effects of Cognitive Impairments of PD and AD on Caregivers

Often, the primary concern on Parkinson's and Alzheimer's disease is based on cognitive impairment. According to different longitudinal studies, they reveal that cognitive impairment affects around 20% - 50% of individuals suffering from PD, and 80% of the patients are affected by dementia (Perry et al. 420). When an individual with PD or AD experiences a high cognitive impairment such as motor difficulties, neuropsychiatric symptoms, dementia, and other cognitive declines, the health-related quality decreases while the burden mounted on the caregiver increases. Majorly, increased caregiver strain has been linked to very high mortality. When an individual lack cognition, it means that they cannot undertake most of the functions as required of them (Perry et al. 420). Such an occurrence pushes for the need for a caregiver.

As the cognitive impairments increase, more stress is placed on the caregiver since he or she must take care of the individual regardless of the age. In most of the cases, the caregiver faces significant stresses as they strive to deal with the patients of AD and PD. The event of constant caregiving could result in immense pressure and later lead to caregiver burnout. This can negatively affect the caregiver and the individual as well...