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What makes Parkinson's disease a neurodegenerative disease?

Parkinson's disease (PD) is known to be a neurodegenerative disorder that is generally present in later life with Bradykinesia. It is seen that the key symptoms of this disease are associated with the loss of smell, mood disorders, dysfunction of sleep, excess salivation, excessive periodic limb movements during sleeping (REM behaviour disorder) and constipation (Gunduz, 2019). However, as declared by some previous research, due to the disorder of Basal Ganglia composed of other nuclei, the striatum receives the inhibitory and excitatory input from the various parts of the cortex. On that note, in terms of key pathology, dopaminergic neurons loss has occurred that leads to these symptoms. PD is said to be the second and most common neurodegenerative condition across the globe.

Etiology:

Based on the above figure, it can be stated that the concerned condition is caused due to the slow deterioration of the nerve cells present in the brain. These cells create dopamine that is considered a natural substance across the human brain. These play key roles in the bodies and the brains by messaging through which a human is able to communicate across the various systems. According to Gitler, Dhillon& Shorter (2017), the reasons for PD are associated with the use of herbicides, pesticides, and proximity to industrial plants.

On that note, after getting injected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the concerned chemical turned out to be accumulated in the mitochondria (W?odarek, 2019). As discussed in this research, the generation and the oxidation of free radicals leads to damage to the thalamic nuclei. However, genes consisted of the other significant roles of increasing PD if any family members have been found with this disorder. As stated by W?odarek (2019), the different functions of the alpha-synuclein sometimes play a role in the etiology of PD. However, there are some other factors (following factors) that could be considered having key roles in making Parkinson's disease a neurodegenerative disease.

Correlation with age:

The age factor in PD is considered the main factor. As such, according to the research, a prevalence of 0.1% of the total population across the globe is seen to be suffered in PD due to the age factor (Chalazonitis& Rao, 2018). As demonstrated by this research, the influence of age in the clinical progression in PD leads to advanced ageing, which is also correlated with the faster rate of motor progression. Apart from the other factors that are associated with the age factor is the responsiveness of decreased levodopa, postural impairment and severe gait.

Rate of Motor Progression

According to cross-sectional studies, patients with subsequent onset PD get a rapid rate of motor progression than those with previous onset PD due to relatively lower disease duration in the configuration of a comparable type of disability and a significantly more serious motor impairment in the configuration of a similar duration of illness. Many longitudinal studies have shown an association between older age at onset and quicker development of motor signs of illness in patients with PD.

 For example, in a population-based longitudinal study, the start increasing per year in the total Unified Parkinson Disease Rating Scale motor score (range, 0 [normal] – 108 [most severe impairment]) was found to be significantly higher than the increasing trend per year in the total Unified Parkinson Disease Rating Scale motor score (range, 0 [normal] – 108 [most intense was 2.6 points for individuals 50 years old at the time of onset and 3.8 units for individuals 70 years old at the time of commencement) (Gerhardt &Mohajeri, 2018).

Levodopa Responsiveness

Granerus et al. 14 observed shortly after the introduction of levodopa therapy that progress in the context of daily functioning with levodopa was inversely linked with age at the commencement of medication.

Studies comparing the amount of response to levodopa using a standardised levodopa challenge have found that older individuals with PD have a lesser degree of a reaction than younger patients with PD. In the later stages of Parkinson's disease, gait and postural deficits are generally resistant to levodopa therapy, but tremors, stiffness, and Bradykinesia improve to levodopa treatment throughout the disease Gerhardt &Mohajeri, 2018). 18 This suggests that non-dopaminergic lesions have a function in gait and postural dysfunction in Parkinson's disease.

Gait and Postural Impairment

It is plausible that the link between older age and reduced levodopa responsiveness is connected to the link between older age and more significant gait and postural deficits in Parkinson's disease. Several studies have found a link between older age and more serious gait and postural deficits in Parkinson's disease (Ali et al., 2019). The level of gait and postural disability was substantially associated with age at a screening in a peer sample of individuals with PD, however not with the severity of rigidity, stiffness, or BradykinesiaBradykinesia.

The participation of age at review to the severity of sequential gearbox signs in PD, as evaluated by additional variability fully compensated for in regressors, was significantly greater for gait and postural impairment (13.6 per cent) than for tremor, hardness, and Bradykinesia (5.0 per cent) in a service-based survey with a wide number of disease duration and age.

Justification:

 Cross-sectional neuropsychological investigations have found that individuals with PD who are older at the time of start had more severe cognitive problems. According to epidemiologic research, the age-specific frequency of dementia in people with Parkinson's disease ranged from 12.4 per cent in people aged 50 to 59 years to 68.7 per cent in those over 80 years old (Ali et al., 2019).The factors discussed above make Parkinson's disease a neurodegenerative disease.

Discuss whether the Stroke is vascular disease or a neuronal disease

Since 1955, Stroke has been misclassified in the International Classification of Diseases (ICD); however, in the new ICD-11, it is now classified as a neurological illness. The categorisation necessitated a bureaucratic battle among physicians and the World Health Organization, and it will result in significant advantages. According to Puig, Brenna & Magnus (2018), Stroke is one of the main causes of disability globally, but its brain impact has gone unnoticed since it is categorised as a cardiovascular illness by the WHO. Stroke has been categorised as a neurological illness in the most recent edition of the WHO International Classification of Diseases (ICD-11). This move not only recognises that neuroscientists treat stroke patients and that stroke patients must live with life-altering neurological effects; however, it is also expected to increase awareness of the burden of Stroke and enhance financing for stroke study and patient treatment (Puig, Brenna & Magnus, 2018). From mechanistic and clinical research to preventive, acute therapy, rehabilitative, and post-stroke disorders, the collection covers the whole continuum of Stroke.

Considering several previous studies, it can be stated that Stroke is a neuronal disease. In support of this statement, the following discussion has been made.

According to Wu et al. (2019), the most common type of Stroke is ischemic Stroke, which is caused by an obstruction in a brain artery. The region with significant hypoperfusion is termed as the nucleus of the infarct, where neurons are gruesomely damaged after a brief or chronic loss of blood flow and, therefore, of glucose and oxygen delivery to the brain (Wu et al. 2019). This region is bordered by a less hypoperfused area (known as the penumbra), where cells are energy-dense for a short time before dying or surviving, depending on conditions. Stroke-related neuronal cell death is multifaceted and complicated, including a number of factors such as excitotoxicity, oxidative, mitochondrial malfunction, and neuroinflammation. The quest for neuroprotection mechanisms in this domain is a subject of great interest (Puig, Brenna & Magnus, 2018). The only therapeutic alternatives now available are regional recanalisation and universal thrombolysis, both of which have a limited therapeutic period, with just 20% of patients suitable for these procedures.

Importantly, the degree of irreparable harm is related to the length of ischemia; hence, it is critical to restoring blood flow as quickly as feasible. Surprisingly, the required reperfusion also leads to the production of reactive oxygen species (ROS) and nitrosylation, which stimulates the immune system, resulting in neuroinflammation with negative effects (Russo et al., 2018). Microglia cells (the brain's resident immune cells) are the first cells to react to ischemic injury during neuroinflammation, and the immune reaction is accompanied by infiltration of macrophages, lymphocytes, neutrophils, and lymphocytes into the ischemic parenchyma due to blood-brain barrier collapse, which intensifies the deterioration. In addition to brain injury and healing, neuroinflammation is important (Russo et al., 2018). Neurons are the first brain cells to perish in the zone directly impacted by severe blood loss because of their intrinsic high energy consumption. Relying on the cellular features of the region affected, neuron loss might last for hours or even days following resuscitation. Neuronal cell death is a multi-step process that necessitates a coordinated reaction from a variety of brain cells (Kanazawa, Ninomiya, Hatakeyama, Takahashi &Shimohata, 2017). On the one hand, neurons are connected to one another via synaptic transmission, establishing a vast communication network. Disconnectedness and transsynaptic degeneration result from synaptic failure, resulting in neuronal malfunction and induce apoptosis. The NVU, for example, not only controls cerebral blood flow in response to the brain's energy demands. However, it also plays a key role in preserving the blood-brain barrier (Goulay, Romo, Hol&Dijkhuizen, 2020). Communication between cells is essential for the maintenance of these formations.

Loss of Synapses in the Penumbra

The brain consumes a lot of energy; it accounts for only 2% of body mass; however, it consumes 20% of all oxygen required by the body. The synapse is where the majority of energy is expended. Thus, in the visual cortex, the procedure of releasing one glutamate vesicle (which includes delivering the vesicle to the postsynaptic terminal, releasing it, and recycling the vesicle) consists of transporting the neurotransmitter to the presynaptic membrane, releasing it, and recycling the vesicle and glutamate by the astrocyte) uses up around 1.64 × 105 ATP molecules (Puig, Brenna & Magnus, 2018). Nerve impulses and postsynaptic potentials have a higher energy consumption. The consumption is estimated to be three times more in humans with fewer neurons per mm and more synapses. The brain's major source of ATP comes from full oxidative phosphorylation in the mitochondria, a mechanism that also occurs at the synaptic level. Although neurons absorb glucose from the plasma membrane, astrocytes can also supply oxidation precursors to neurons (glutamine, lactate, or ketone bodies). Because synapses require a lot of energy, the shortage of glucose and oxygen caused by temporary ischemia is a major problem for them, and it can contribute to neurodegenerative diseases (Wimmer, Zrzavy&Lassmann, 2018).

As previously indicated, neurons in the penumbra are architecturally preserved and metabolically active; nevertheless, synaptic failure causes them to go into electric quiet owing to low ATP levels. This electric quiet might be a strategy for conserving energy while homeostatic circumstances are reestablished, or it could be the result of synapse changes (Wimmer, Zrzavy&Lassmann, 2018). Thus, presynaptic modifications such as changes in Ca2+-dependent activities or insufficient synapsis phosphorylation might cause synaptic failure, resulting in poor docking to the presynaptic membrane. It might also be related to postsynaptic failure, which is most likely caused by Ca2+ entry (Puig, Brenna & Magnus, 2018). Recent research has found that synaptic quiet in rodent neurons exposed to an in vitro model of hypoxia is caused by a lack of normal vesicle endocytosis and reduced exocytosis, suggesting that synaptic silence is caused by presynaptic compartment changes. Furthermore, excitotoxicity causes cytoskeleton disintegration, translation shutdown, reduced endocytosis, and calpain activation, which results in changes in synaptic protein location (Hachinski et al. 2019). Synaptic dysfunction and neuronal death are the end results.

Justification

Based on the discussion made above, it can be stated that the most common type of Stroke is ischemic Stroke, which is caused by an obstruction in a brain artery (Cai et al., 2017). The region with significant hypo-perfusion is termed as the base of the infarction, where neurons are fatally damaged after transitory or permanent loss of blood circulation and consequently glucose and oxygen delivery to the brains. Therefore, Stroke isa neuronal disease.

References

Ali, L., Zhu, C., Gorillaz, N. A., Javeed, A., Zhou, M., & Liu, Y. (2019). Reliable Parkinson's disease detection by analysing handwritten drawings: construction of an unbiased cascaded learning system based on feature selection and adaptive boosting model. Ieee Access, 7, 116480-116489.

Cai, W., Zhang, K., Li, P., Zhu, L., Xu, J., Yang, B., & Chen, J. (2017). Dysfunction of the neurovascular unit in ischemic Stroke and neurodegenerative diseases: an ageing effect. Ageing research reviews, 34, 77-87.

Chalazonitis, A., & Rao, M. (2018). Enteric nervous system manifestations of neurodegenerative disease. Brain Research, 1693, 207-213.

Gerhardt, S., &Mohajeri, M. H. (2018). Changes of colonic bacterial composition in Parkinson’s disease and other neurodegenerative diseases. Nutrients, 10(6), 708.

Gitler, A. D., Dhillon, P., & Shorter, J. (2017). Neurodegenerative disease: models, mechanisms, and new hope.

Goulay, R., Romo, L. M., Hol, E. M., &Dijkhuizen, R. M. (2020). From Stroke to dementia: a comprehensive review exposing tight interactions between Stroke and Amyloid-β formation. Translational stroke research, 11(4), 601-614.

Gunduz, H. (2019). Deep learning-based Parkinson’s disease classification using vocal feature sets. IEEE Access, 7, 115540-115551.

Hachinski, V., Einhäupl, K., Ganten, D., Alladi, S., Brayne, C., Stephan, B. C., & Khachaturian, Z. S. (2019). Preventing dementia by preventing Stroke: the Berlin Manifesto. Alzheimer's & Dementia, 15(7), 961-984.

Kanazawa, M., Ninomiya, I., Hatakeyama, M., Takahashi, T., &Shimohata, T. (2017). Microglia and monocytes/macrophages polarisation reveal novel therapeutic mechanisms against Stroke. International journal of molecular sciences, 18(10), 2135.

Puig, B., Brenna, S., & Magnus, T. (2018). Molecular communication of a dying neuron in Stroke. International journal of molecular sciences, 19(9), 2834.

Russo, E., Nguyen, H., Lippert, T., Tuazon, J., Borlongan, C. V., & Napoli, E. (2018). Mitochondrial targeting as a novel therapy for Stroke. Brain circulation, 4(3), 84.

Wimmer, I., Zrzavy, T., &Lassmann, H. (2018). Neuroinflammatory responses in experimental and human stroke lesions. Journal of neuroimmunology, 323, 10-18.

W?odarek, D. (2019). Role of ketogenic diets in neurodegenerative diseases (Alzheimer’s disease and Parkinson’s disease). Nutrients, 11(1), 169.

Wu, F., Han, B., Wu, S., Yang, L., Leng, S., Li, M., & Yao, H. (2019). Circular RNA TLK1 aggravates neuronal injury and neurological deficits after ischemic Stroke via miR-335-3p/TIPARP. Journal of Neuroscience, 39(37), 7369-7393.

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