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What Does Parkinson's Disease Affect
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Trial Of Deferiprone In Parkinson’s Disease
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By Sunisha Aryal Sunisha Aryal Skillit Preprints.org Google Scholar , Taylor Skinner Taylor Skinner Skillit Preprints.org Google Scholar , Bronwyn Bridges Bronwyn Bridges Skillit Preprints.org Google Scholar and John T. Weber John T. Weber Skillet Google Preprints *.
Received: 25 August 2020 / Revised: 15 September 2020 / Accepted: 21 September 2020 / Published: 24 September 2020
Signs It Could Be More Than Parkinson’s Disease
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons, leading to bradykinesia, rigidity, tremor at rest, and postural instability, as well as non-motor symptoms such as impaired smell, pain, Lack of autonomy. , with difficulty sleeping, fatigue, and behavioral changes. The pathogenesis of PD is believed to include oxidative stress, disruption of mitochondria, changes in α-synuclein protein, and neuroinflammatory processes. Currently there is no cure for this disease. Polyphenols are plant secondary metabolites that have shown benefit in several experimental models of PD. Dietary intake of polyphenols has also been associated with lower PD risk in humans. In this review, we provide an overview of PD pathology and data supporting the potential neuroprotective potential of dietary polyphenols. Evidence suggests that dietary polyphenol intake may prevent neurodegeneration and progression of PD. Polyphenols appear to have a positive effect on the gut microbiome, which can reduce inflammation that contributes to disease. Therefore, a diet rich in polyphenols may reduce symptoms and improve quality of life in PD patients.
More than two hundred years ago, in 1817, James Parkinson first mentioned the disease in his essay, An Essay on the Shaking Palsy [1]. Parkinson’s disease (PD) is a slowly progressive neurodegenerative disorder that primarily affects dopaminergic neurons in the substantia nigra pars compacta (SNpc). PD is a debilitating condition caused by a combination of genetic and environmental factors that affect different neuroanatomical sites and begins many years before diagnosis [ 2 ]. Early disease can be divided into three stages: (i) preclinical PD, the onset of neurodegenerative processes but no obvious signs or symptoms; (ii) prodromal PD, the presence of signs and symptoms, although insufficient to define the disease; and (iii) clinical PD, with the diagnosis of PD based on the presence of classic motor signs [3]. Bradykinesia, rigidity, tremor at rest, and postural instability are the main symptoms of PD [4]. However, non-motor symptoms such as olfactory impairment, pain, lack of autonomic control (orthostatic hypotension, GI dysfunction), disturbed sleep, fatigue, and behavioral changes (depression, anxiety, apathy) are also observed [5].
The 2017 Global Burden of Disease Study reported that the global prevalence of PD was 8.52 (95% uncertainty interval (UI) 7.03–10.18) million and the incidence was 1.02 (95% UI 0.85–1.22) million [ 6 ]. In 2017, 0.34 (95% UI 0.32-0.35) million people died from PD [7]. Male-to-female ratios of PD age-standardized prevalence rates were 1.40 (95% UI 1.36–1.43) in 2016 and 1.37 (95% UI 1.34–1.40) in 1990 [ 8 ]. A combination of five different cohort studies to estimate the prevalence of PD in North America indicates an overall incidence of 572 per 100,000 (95% confidence interval 537–614) in people aged ≥45 years, and this number ranges from approximately 1 expected to increase, to 238,000 in 2030 [9]. In Korea, the annual incidence of PD ranged between 22.4–27.8 cases per 100,000 people, and the female-to-male ratio of PD incidence was 1.6:1 while the incidence of PD was 1.4:1. 1 [10]. Also, other PD prevalence studies consistently show an increase in PD with age and male gender [ 11 , 12 , 13 ].
The Movement Disorder Society (MDS) diagnostic criteria define supportive criteria, absolute exclusion criteria, and red flags. MDS uses a two-step approach, first defining parkinsonism, and then examining whether parkinsonism is due to PD. In parkinsonism, bradykinesia may be accompanied by rest tremor, rigidity, or both. PD-induced parkinsonism is characterized by a decline in movement or amplitude of movements. A clinically established PD diagnosis requires complete exclusion criteria, at least two supporting criteria, and no red flags. Absolute exclusion criteria included vague cerebellar abnormalities (eg, gait, limb ataxia, or cerebellar oculomotor abnormalities), vertical descending supranuclear palsy, frontotemporal variable depression, loss of consciousness unique cortical, apraxia, or a. It also includes parkinsonian features limited to the lower limbs for more than three years, lack of response to anti-dopamine therapy, and high-dose levodopa. Complementary criteria have both motor and non-motor aspects. Dopaminergic therapy should have a positive outcome in the presence of levodopa-induced dyskinesia, resting limb tremors, and olfactory loss or cardiac dysfunction. Red flags include early motor impairment, lack of improvement in motor symptoms, early bulbar dysregulation, lack of attention, severe autonomic failure in the first five years, vague pyramidal tract signs, and parkinsonian bilateral symmetry. In addition, these include defective balance, unbalanced enterocollis, and recurrent falls due to common nonmotor features: insomnia, lack of autonomic control, hyposmia, or psychotic dysfunction. This criterion does not include postural instability [14].
Modulation Of Mir 181 Influences Dopaminergic Neuronal Degeneration In A Mouse Model Of Parkinson’s Disease: Molecular Therapy
The brain in PD is often macroscopically unremarkable with mild atrophy of the frontal cortex and ventricular dilatation. The typical morphological change in the PD brain is seen in transverse section of the brainstem with loss of darkly colored areas in the SNpc and locus coeruleus (see Fig. 1 for 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 layer of neurons of the pars compacta (A9) is mainly expressed in neuronal loss in the substantia nigra (SN), while dorsal and medial neuronal cells are less sensitive [ 15 ].
The main pathological features of PD include degeneration and death of melanin-containing neurons of the SN and Lewy pathology. Lewy pathology mainly involves the formation of intracytoplasmic Lewy bodies (LB) with α-synuclein and ubiquitin and Lewy neurites (LN), which are neuronal projections of similar inclusions [ 16 ].
Brack and colleagues established PD pathology in 2003 based on a semiquantitative assessment of LB distribution at autopsy, which revealed that LB pathology spreads rostrocaudally in the brain in a chronologically predictable sequence [17]. is At brake levels 1 and 2, LB lesions can be seen in the dorsal motor nucleus (IX/X), reticular formation, and anterior olfactory nucleus where patients are considered symptomatic/presymptomatic. Some non-motor features such as autonomic disorders (constipation), olfactory dysfunction, and sleep-related dysfunction appear at these stages. Disease progression to stage 3 involves SNpc with LB pathology, and neuronal loss of melanized neurons is observed. Pathology extends to the locus coeruleus and amygdala, eventually reaching the temporal limbic cortex at stage 4. During these two stages, specific clinical motor features begin to emerge. Stages 5 and 6 [17, 18] involve the entire neocortex and regions including the prefrontal cortex and primary sensory and motor areas. This system has been criticized for being based only on the classification of Lewy pathology but not on neuronal damage [ 19 ].
After motor symptoms appear, nigral DA neuron loss increases to 60% or more and is strongly associated with severity of motor characteristics and disease duration. This dramatic cell loss is caused by the nigrostriatal pathway, which lowers dopamine levels in the striatum. Decreased dopaminergic signaling is thought to be responsible for the appearance of major motor symptoms in PD. In addition to the SNpc, extensive cell loss is found in many subcortical nuclei, including the locus coeruleus, nucleus basalis Meynert, dorsal motor nucleus of the vagus nerve, pedunculopontine nucleus, raphe nucleus, hypothalophalamus, and hypothalamus. Multiple non-dopaminergic neurotransmitter systems are affected in the bulb [20], such as cholinergic, glutamatergic, GABAergic, noradrenergic, serotonergic, and histaminergic systems [21].
Parkinson’s Disease Outside The Brain: Targeting The Autonomic Nervous System
At the onset of PD, several other processes are thought to be involved. nuclear
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