The Presence Of Rat Model Of Parkinson 's Disease Induced By The Intrastriatal Injection Of Rotenone

Simply because the imaging methods used such as CCT or an MRI are structural neuroimaging methods that cannot provide characteristics that are generally featured in PD, both which are commonly tools used by physicians. However, it is possible for the physician to use functional neuroimaging methods such as PET and SPECT, which are definitive and more accurate in diagnosing patient’s first sign of parkinsonism. This form of early diagnosis does come with a hefty price that many cannot afford along with the fact that it is not broadly available in many clinics or imaging centers. With that said a new method, the TCS is more reliable in effectively diagnosing early symptoms of PD. It was concluded that with the use of the TCS “up to 90%” of patients have shown an enlarged echogenic size (hyperechogenicity) of the substantia nigra (SN). An enlarged echogenic of the SN leads to a diminishment of the nerves in the SN, that is seen in PD. The nerve cells in SN are responsible for control of movements and coordination by sending out signals to tissues on both sides of the brain. A 37-month study led by multiple researchers have determined that an enlarged SN was correlated with a higher risk for PD. TCS has also been known to precisely diagnosis the severity and differentiation of PD patients, distinguishing how sensitive and the specificity of individual patients.

Gamma-Aminobutyric acid commonly referred to as GABA, and glutamate make up around 80 percent of the neurotransmitters found in brain. GABA dampens the activity in the brain while

Parkinson’s disease is a “neurodegenerative disorder of the basal nuclei due to insufficient secretion of the neurotransmitter dopamine” (Marieb & Hoehn, 2013, p. G-17). The cause of Parkinson’s disease is unknown, but many factors play a role in the development of Parkinson’s disease. One factor that has been found in an individual who has Parkinson’s disease causes over activity of targeted dopamine-deprived basal nuclei. This over activity is caused by the breakdown of neurons that release dopamine in the substantia nigra (Marieb & Hoehn, 2013). Another factor that is present in a person who has Parkinson’s disease, is the presence of lewy bodies in the brain stem ("What is lbd?," 2014). Lewy bodies are unusual

Patients will report to physical therapists with a multitude of impairments throughout the progression of the disease. The most prominent impairments will present during cerebellar testing. Patients will show signs of dysmetria, dysphasia, dysdiadochokinesia, and ataxia primarily as a result of the atrophy and damage to the cerebellum. Instability and lack of postural control will be demonstrated during the Romberg's test. Additionally, cranial nerve testing will have positive results for many cranial nerve palsies such as CN III, V, VII, IX, and XII. Patients show weakness in their trunk and extremities during the manual muscle testing. Vestibular testing will result in abnormal VOR, saccades, smooth pursuits and nystagmus. As a result of these impairments, patients experience functional limitations. Primarily, these patients are considered to be “high fall risks,” which ultimately decreases their independence due to weakness, instability and decreased postural control. These patients will feel uncomfortable in many situations and be unable to function independently in the community. This creates an increased risk for further injury. Due to the dysmetria and weakness, patients will also experience difficulty with their daily living skills, such as maintaining proper hygiene; They will have trouble bathing themselves and brushing their teeth without assistive equipment. PT interventions can help minimize and control these limitations. The implementation of balance training and assistive devices will be imperative interventions for an individual to modify and adapt to their gait

The path physiology of Parkinson’s disease is the pathogenesis if Parkinson disease is unknown. Epidemiologic data suggest genetic, viral, and environmental toxins as possible

Parkinson’s disease “is described as a common disorder of the brain caused by a progressive deterioration of the areas that produce the neurotransmitter dopamine” (Fischer, 1999). It affects the nervous system, more specifically it affects the nerve cells in your brain that secrete dopamine. Dopamine is a chemical that is responsible for the movement and coordination of the musculoskeletal system.

Mitochondrial dysfunction and oxidative stress have been consistently observed in brains of PD patients. There is increasing pharmacological and genetic evidence sustain a link between PD and mitochondrial respiratory chain dysfunction, particular a deficit in mitochondrial complex I (Franco-Iborra et al., 2015). Accidental exposure to 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), an mitochondrial complex I inhibitor, has been known to result in acute and irreversible syndrome that was almost indistinguishable from PD (Calne and Langston, 1983; Langston and Ballard, 1983). Later on, mitochondrial complex I inhibition has been identified in the brains of sporadic PD patients (Schapira et al., 1990). In addition, chronic systemic inhibition of mitochondrial complex I by pesticide rotenone has been found to link to sporadic PD (Betarbet et al., 2000). Interestingly, mitochondrial complex I deficiency has been found not only in the postmortem substantia nigra but also in cerebral cortex (Schapira et al., 1990), which is consistent to the cortical glucose hypometabolism observed in PD patients. Indeed, the pathology of PD has been found to involve several brain regions other than the SNc and many neurotransmitters other than dopamine (Lang and Obeso, 2004a, b). PD models using MPTP and rotenone have now been used extensively in PD research (Beal,

where movement is planned or motor behavior is organized. Surely enough, research done on the basal ganglia, namely the striatum and the caudate nucleus, has revealed that dopamine indeed impacts on these areas more prominently in Tourette's patients than in unaffected controls. (5,6) The increased dopamine effect in Tourette's patients may be due to two mechanism. One, the patients may produce more dopamine, hence, their receptors are over-stimulated, leading to excessive neuronal firing, in turn leading to involuntary movements. However, this theory seems to not hold, as presumably neurons would activate compensatory mechanism to deal with the increase in neurotransmitter concentration. If really dopamine was present in excess, one would expect receptor sites to down-regulate. One can assume that dopamine is not present in excess in Tourette's patients. A second mechanism has been proposed. According to this, the dopamine levels in Tourette's patients are equivalent to non-patients, but their receptor sites are supersensitive. This theory seems to hold true and has been successfully confirmed in the laboratory. Research surrounding dopamine binding in implicated structures of the brain yielded, "that binding to D2 dopamine receptors in the caudate nucleus was higher in the sibling

These deficits increase during the course of the disease and are due to loss of dopamine-secreting neurons in the motor circuits in the basal ganglia which are necessary for control and coordination of movements. The symptoms displayed because of this are: bradykinesia, resting tremor, rigidity of muscles and impaired posture (Millage, Vesey, Finkelstein, & Anheluk, 2017). Research indicates that exercise modalities can improve both motor and non-motor aspects of PD (Dashtipour et al., 2015).

Parkinson’s Disease is known as one of the most common progressive and chronic neurodegenerative disorders. It belongs to a group of conditions known as movement disorders. Parkinson disease is a component of hypokinetic disorder because it causes a decreased in bodily movement. It affects people who are usually over the age of 50. It can impair an individual motor as well as non-motor function. Some of the primary symptoms of Parkinson’s disease are characterized by tremors or trembling in hands, legs and arms. In early symptoms the tremor can be unilateral, appearing in one side of body but progression in the disease can cause it to spread to both sides; rigidity or a resistant to movement affects most people with Parkinson’s disease,

Parkinson’s disease is affected by the degeneration of dopaminergic neurons which is responsible to produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta (SNpc) in basal ganglia (O’Sullivan and Schmitz, 2007). Basal ganglia are a collection of interconnected gray matter nuclear masses deep within the brain”. These gray matter masses are caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia receive its input through striatum (O’Sullivan and Schmitz, 2007).

“Stem cells can be used to heal the damage in the brain caused by Parkinson’s disease.” According to scientists in Sweden. They sad that their study on rats helped develop effective treatments for it. There is no known cure for the disease, but medicine and brain stimulation can help relieve symptoms. The disease is caused by the loss of nerve cells in the brain that make dopamine. To stimulate Parkinson’s disease, Lund University researchers killed dopamine producing neurons on one side of the rat’s brain. Then, they converted human embryonic stem cells into neurons that produce dopamine. This was injected into the rat’s brain, and researchers found signs that the damage was reversed. They said “… no human clinical traits of stem-cell-derived

o When dopamine producing cells are reduced by 80%, the physical symptoms of Parkinson’s present themselves

It has been known that PD is a disorder affecting the basal ganglia. The term basal ganglia is generally applied to a collection of nuclei situated deep within the cerebral hemispheres, lying laterally to the thalamus (Gazzeniga, George, and Mangun, 2008). The basal ganglia are important subcortical structures. They are composed of five nuclei: caudate, putamen, globus pallidus, subthalamic nucleus, and substantia nigra. These nuclei are not thought of a single anatomical entity; rather, they form a functional unity whose contribution is greatly to motor control. Interestingly, this system does not influence movement through spinal cord pathways, but rather acts as part of a feedback loop to all areas of the cerebral cortex, with primary input into motor areas (Aird, 2000). A number of excitatory and inhibitory neurotransmitters are what control this whole process, and a balance of both is required to ensure that smooth, purposeful movement takes place. In order to understand the pathways of which the basal ganglia take part in, it is essential to know the input and output connections of the basal ganglia. The input

Rotenone is the most intoxicating member of the rotenoid family and is typically found in tropical plants. It is both an herbicide and insecticide having a half-life of 3-5 days depending on light conditions and degrade quickly in soil and water (Hisata 2002). The toxicity of rotenone comes from its high lipophilia and it can easily cross the blood brain barrier. It is mainly used in rats since, so far, the studies attempting to lesion in mice or monkeys have not been successful (Ferrante et al. 1997; Thiffault et al. 2000). Recently, some studies have tested the toxicity of rotenone when administrated intragastric (Pan-Montojo et al. 2010) or directly in the brain (Alam et al. 2004).