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How Does Parkinson Disease Affect The Nervous System

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How Does Parkinson Disease Affect The Nervous System

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What Are Parkinson Plus Syndromes?

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By Sunisha Aryal Sunisha Aryal Scilit Preprints.org Google Scholar , Taylor Skinner Taylor Skinner Scilit Preprints.org Google Scholar , Bronwyn Bridges Bronwyn Bridges Scilit Preprints.org Google Scholar and John T. Weber John T. Weber Scilit Preprints * Google Scilit Preprints.org

Received: August 25, 2020 / Viewed: September 15, 2020 / Accepted: September 21, 2020 / Published: September 24, 2020

What Brain Areas Are Affected By Parkinson’s?

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons, causing bradykinesia, rigidity, tremor at rest, and postural instability. , lack of sleep, fatigue and behavioral changes. Oxidative stress, mitochondrial dysfunction, α-synuclein protein alterations, and neuroinflammatory processes are thought to be involved in the pathogenesis of PD. There is currently no cure for the disease. Polyphenols are plant secondary metabolites that have been shown to be beneficial in many experimental models of PD. Dietary intake of polyphenols is associated with a lower risk of PD in humans. In this review, we present data supporting PD pathology and the potential neuroprotective potential of dietary polyphenols. Evidence suggests that dietary polyphenols may prevent neurodegeneration and the development of PD. Polyphenols have a positive effect on the gut microbiome, which can reduce disease-causing inflammation. Therefore, a diet rich in polyphenols may reduce symptoms and improve quality of life in PD patients.

More than two centuries ago, in 1817, James Parkinson first described the disease by name in his essay “An Essay on the Palsy of Talisman” [1]. Parkinson’s disease (PD) is a progressive neurodegenerative disease affecting dopaminergic neurons in the substantia nigra pars compacta (SNpc). PD is a debilitating condition that results from a combination of genetic and environmental factors affecting various neuroanatomical domains and begins years before diagnosis [2]. Early disease can be divided into three stages: (i) preclinical PD, the beginning of the neurodegenerative process but without obvious signs or symptoms; (ii) presence of signs and symptoms of prodromal PD, although not sufficient to establish the disease; and (iii) clinical PD with a diagnosis of PD based on the presence of normal motor signs [ 3 ]. Bradykinesia, rigidity, resting tremor, and postural instability are the main symptoms of PD [4]. However, nonmotor symptoms such as olfactory dysfunction, pain, autonomic dysfunction (orthostatic hypotension, GI dysfunction), insomnia, fatigue, and behavioral changes (depression, anxiety, apathy) are also observed [5].

In 2017, the global burden of disease was estimated to be 8.52 (95% CI 7.03–10.18) million with a global prevalence of PD of 1.02 (95% CI 0.85–1, 22) reported that it is million [6]. In 2017, 0.34 (95% UI 0.32–0.35) million people died from PD [7]. The male-to-female mortality ratio for PD was 1.40 (95% CI 1.36–1.43) in 2016 and 1.37 (95% CI 1.34–1.40) in 1990 [ 8 ]. Pooling five separate studies to estimate the prevalence of PD in North America showed an overall prevalence of 572 per 100,000 (95% confidence interval 537–614) among those aged ≥45 years, and this number is expected to increase to approximately 1,238,000. 2030 [9]. In Korea, the incidence is 22.4–27.8 per 100,000, with a female-to-male ratio of 1.6:1 and 1.4:1 in PD [10]. Also, other PD prevalence studies show a steady increase in PD with age and gender [11, 12, 13].

Diagnostic criteria for movement disorder (MDS) describe supportive criteria, absolute exclusion criteria, and red flags. MDS uses a two-step approach to first identify parkinsonism and then to test whether parkinsonism is present in PD. In Parkinsonism, bradykinesia must occur with tremors, rigidity, or both. In PD-induced parkinsonism, both speed and amplitude decrease as movement continues. A clinically established diagnosis of PD requires the absence of absolute exclusion criteria, at least two supporting conditions, and no red flags. Absolute exclusion criteria included nonsignificant cerebellar abnormalities (eg, gait, finger ataxia, or cerebellar oculomotor abnormalities), vertical descending supranuclear palsy, fluctuating frontotemporal dementia, loss of apraxia, or aphasia. It also included parkinsonian features confined to the lower extremities for more than three years, antidopamine therapy, and lack of response to high-dose levodopa. Support measures are motor and non-motor aspects. There should be a clear response to dopaminergic therapy, the presence of levodopa-induced dyskinesia, movement of one limb, and a good outcome of olfactory loss or heart failure. Red flags include early walking deficits, lack of development of motor symptoms, early bulbar deficits, lack of inspiration, absence of severe autonomic dysfunction in the first five years, unknown pyramidal tract signs, and bilateral symmetrical parkinsonism. In addition, recurrent falls due to lack of balance, unbalanced anterocollis, and general non-motor features include: sleep deprivation, autonomic dysfunction, hyposmia, or cognitive dysfunction. This condition does not include postural instability [14].

Vagus Nerve: Function, Stimulation, And Further Research

In PD, the brain is usually macroscopically abnormal, with mild frontal cortex atrophy and ventricular enlargement. Morphological changes characteristic of the PD brain are seen in a transverse section of the brain with the loss of dark areas in the SNpc and locus coeruleus (see Figure 1 for a brain image). This loss is associated with the death of dopamine (DA) neuromelanin-containing neurons in the SNpc and noradrenergic neurons in the locus coeruleus. The ventrolateral level of pars compacta neurons (A9) is characterized by neuronal loss in the substantia nigra (SN), but dorsal and medial neuronal cells are less sensitive [15].

Clinical features of PD are degeneration and death of melanin-containing neurons in SN and Lewy pathology. Lewy pathology includes the formation of intracytoplasmic Lewy bodies (LB) with inclusions containing α-synuclein and ubiquitin and Lewy neurites (LN), which are neuronal projections of the same inclusion [ 16 ].

In 2003, Braak and colleagues performed PD pathology based on a semiquantitative assessment of LB distribution post-mortem, which revealed that LB pathology spreads throughout the brain in a predictable pattern [17]. In Braak stages 1 and 2, LB lesions are found in the dorsal motor nucleus (IX/X), reticular formation, and anterior olfactory nucleus, where the patient is considered asymptomatic/presymptomatic. During these stages, several nonmotor features occur, such as autonomic dysfunction (constipation), impaired olfactory function, and insomnia. Disease progression to stage 3 involves the SNpc with LB pathology and neuronal loss in melanized neurons. Pathology extends to the locus coeruleus and amygdala and reaches the temporal limbic cortex in stage 4. In these two stages, typical clinical motor features begin to appear. All neocortex and regions are involved, including prefrontal cortex and primary sensory and motor areas in stages 5 and 6 [17, 18]. This system has been criticized because it depends only on the prevalence of Lewy pathology and not on neuronal loss [19].

When motor symptoms appear, the loss of nigral DA neurons increases by 60% or more and strongly correlates with motor symptom severity and disease duration. This unique cell loss is a decrease in the nigrostriatal pathway, which leads to a decrease in dopamine in the striatum. Decreased dopaminergic signaling is thought to be responsible for the manifestation of the core symptoms of PD. In addition to the SNpc, diffuse cell loss was observed in several subcortical nuclei, including the locus coeruleus, nucleus basalis of Meynert, dorsal motor nucleus of the vagus nerve, pedunculopontine nucleus, raphe nuclei, hypothalamus, and olfactory bulb. . lights [20]. Many non-dopaminergic neurotransmitter systems are affected, such as cholinergic, glutamatergic, GABAergic, noradrenergic, serotonergic and histaminergic systems [21].

Understanding The Neurological Symptoms Of Gaucher Disease

Many other processes are thought to be involved in the early stages of PD. Nucleus

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