Introduction
An Analytical Study on Parkinson’s Disease. The study of neurodegenerative diseases is an important branch of biophysical and biomedical research. In particular, the research on Parkinson’s Disease (PD) and Alzheimer Disease (AD) disorders is very essential because they are the most common diseases being faced by people throughout the world. However, the exact factors inducing the disease are not yet understood. As a result, much research is required to address the problem. Though PD is more common, there are no medical treatments to cure this debilitating disease. Currently, the disease is treated by controlling the physical and mental symptoms. Due to the non-availability of proper treatment options and the increasing lifestyle factors, the disease is causing more impact on the patients. In the present research, we are using the K-S test and entropy to differentiate the control and PD patients. The K-S test is a simple, powerful, and non-parametric test used to compare the difference between the two probability distributions. The entropy is the degree of randomness that occurs in the signal. In the case of medical sciences, the value of entropy is inversely proportional to the complexity of the signal. The low value of entropy represents very less complexity in the signal and vice versa.
Definition and Background about Parkinson’s Disease
Parkinson’s disease is defined as an illness that results in a loss of nerve cells within a specific area of the brain (nigral system). The condition is notably characterized by trembling and stiffness of the limbs and also by shakiness of the face. Parkinson’s disease is progressive and unfortunately is currently incurable. Generally, onset occurs in late middle age and affects between 0.5% and 1% of patients aged between 40 and 70. Susceptibility is slightly higher in men than women. Idiopathic Parkinson’s disease refers to 75% of sufferers, while the remaining fraction carries a genetic origin. Symptoms of the disease are prevalent in the lack of muscle control department and have been found to have a connection with dopamine deficiencies because all the symptoms are associated with its release.
Parkinson’s disease is a movement disturbance syndrome with neurally degenerative characteristics that are clinically characterized by parkinsonian symptoms and signs. The disease is collectively referred to as the group of diseases with similar symptoms and causes. In idiopathic Parkinson’s disease, there is cell death in the substantia nigra brain structure, which leads to decreased dopamine levels of the striatum and dopaminergic innervation reductions. In neural samples for Parkinson’s disease patients, it has been seen that α-synuclein is present in a larger than normal characteristic, where synaptic and neuronal death in the pathological area are caused. Cases of healthy individuals experiencing little-to-no cell death were also seen with this enhancement.
Role of Dopamine and Neurotransmitter Imbalance
Synthesis and release of dopamine, the major neurotransmitter in the nigra, are responsible for the inhibitory effects of the globus pallidus and the striatum on the thalamus, while the excitatory effects of the subthalamic nucleus are mediated by the release of GABA. This equilibrium is altered in Parkinson’s disease and consequently leads to the observed symptoms. On degeneration of the nigro-striatal pathway, dopamine release is reduced in the striatum. Since the indirect pathway medium spiny neurons express mainly D2 dopamine receptors, reduced dopamine causes increased thalamic activity. However, the direct pathway medium spiny neurons, which express mainly D1 dopamine receptors, are affected more since the overall inhibition from the nigra is lost, and thus they cannot inhibit the globus pallidus. Increased activity of the globus pallidus causes increased walking or dystonia. Neurotransmitter imbalance is responsible for diphasic dyskinesias in patients with PD on long-term levodopa treatment. GABA is partially synthesized in patients with advanced Parkinson’s disease in a small group of DOPA-in olders that co-localize with GABA. The former GABA-ir nerve terminals seem to consist of a novel type of short/interneuron. GABA is partially synthesized and released in the striatum, which might contribute to the fine-tuning of the output from the motor control circuits under baseline conditions.
The following changes in the activity of the distal dendrites: Intermittent excitation of the long primary dendritic segments of the direct pathway neurons. Permanent overactivation of the long primary dendritic segments of the direct pathway neurons. Activation of the proximal segments of the dendrites of the indirect pathway neurons. The first of these two alterations supposedly leads to the pulsatile release of GABA in the striatum, which might contribute to the dyskinesias seen in patients on long-term levodopa treatment. The second one is a crucial substrate of the severe motor fluctuations in PD patients, and the third leads to the persistence also. Prompted by the pharmacologically induced dopamine depletion in dopaminergic cells and parkinsonian symptoms observed in monkeys with selective dopamine depletion. The evidence for a role of other neurotransmitters in the pathophysiology of PD is circumstantial and mostly comes from experimental models of parkinsonism. Thus, serotonergic, noradrenergic, cholinergic, and other systems are involved with parkinsonism. However, a very clear consensus for the specificity of the most new models has yet to emerge.
Genetic and Environmental Factors OF Parkinson’s Disease
Individually, both genetic and environmental factors can cause Parkinson’s disease, and it is highly probable that the mechanism through which these factors interact and lead to disease formation is related to individual variability of a large group of factors influencing the vulnerability of an individual to the pathological process. The main evidence pointing to genetic factors in the etiological chains of Parkinson’s disease comes from epidemiological studies performed on twins, which show lower concordance in identical twins, with 10-30% of cases occurring in individuals who share the same genetic inheritance. The genetic influence in the development of PD is the strongest risk factor, age being the most important because the incidence is very low in early life, infrequent between 40-60 years, and rising steeply from 60 years in all geographic areas. In more recent family-based studies, age and dose smaller than the risk observed in early-onset families were described, confirming the view that both genetic and environmental factors act in concert in Parkinson’s disease.
Conclusion
In conclusion, Parkinson’s disease presents a significant challenge due to its progressive nature and impact on motor and non-motor functions. While there is currently no cure, ongoing research and advancements in treatment offer hope for improved management and quality of life for those affected. Early diagnosis, tailored therapies, and supportive care remain crucial in addressing the multifaceted needs of individuals with Parkinson’s. Continued awareness and research are essential to uncover new therapies and ultimately find a cure for this debilitating condition.
INTERNATIONAL HEALTH AND MEDICINE ORGANIZATION IHMO
