The Role Of VPS35 In Parkinson's Disease

The cause of Parkinson disease, defined by Robert Hauser, who is an author of Medscape, is still unclear. Studies state that there is a combination of environmental and genetic factors for this particular disease. Approximately 10% of cases are currently genetic causes of Parkinson disease. Environmental risk factors such as use of pesticides, living in a rural environment, consumption of well water, exposure to herbicides, and proximity to industrial plants or quarries are commonly associated with the development of Parkinson disease (Hauser, 2016). In addition, according to Hauser, “genetic factors in Parkinson disease appear to be very important when the disease begins at or before age 50 years. In a study of 193 twins, overall concordance for MZ and DZ pairs was similar, but in 16 pairs of twins, in whom Parkinson disease was diagnosed at or before age 50 years, all 4 MZ pairs, but only 2 of 12 DZ pairs, was concordant.The identification of a few families with familial Parkinson disease sparked further interest in the genetics of the disease.

The discovery from the Scripps Research Institute in Florida shows promising results in tackling down the cause of Parkinson’s, and their outcomes led to a funding by the National Institutional Disorders and Stroke Research (NINDS). Research staff within the campus discovers that many diseases that relate in twisting a protein from its original structure will result in a cellular death but it isn’t due to the deformed shape. According to the article “Scripps Florida Scientists' 'Mad Cow' Discovery” (2015), one primal cause that leads to Parkinson’s is the lack of “NAD+” which later prohibits the proper energy function of the mitochondria. Researchers further delved into the study to find out this is preventable, by providing the misshaped protein

Ramig and colleagues (2001) performed a study to examine the long-term effects of using Lee Silverman Voice Treatment (LSVT) to improve vocal function in individuals with Parkinson’s Disease (PD). Ramig and colleagues (2001) compared LSVT to received respiratory therapy (RET) to control for extraneous variables. Subjects were recruited from a variety of sources which helped to reduce recruitment bias (Ramig et al., 2001). Individuals with any laryngeal pathology unrelated to PD were excluded from the study (Ramig et al., 2001). All 33 subjects were stratified based on: age, time post-diagnosis, stage of disease, score on the unified Parkinson’s disease rating scale, and clinical ratings on speech and voice severity (Ramig et al., 2001). Subjects were then randomly divided into 2 groups and received either LSVT or RET provided in four one-hour weekly sessions for four weeks (Ramig et al., 2001).

Parkinson's disease (PD) is an adult-onset neurodegenerative disorder, concomitant with neuronal loss predominantly in the substantia nigra pars compacta (SNpc) and inclusions comprising of the synaptic protein, α-synuclein (α-syn). Recent developments have advanced our understanding on the multitude of inter-mingled deleterious factors contributing to PD neuropathological aetiologies. These encompass “cell autonomous” processes, for instance, autophagy, and mitochondrial dysfunction, and “non-cell autonomous” processes, which embrace trans-synaptic transmission of abnormal proteins and neuro-inflammation (Foltynie and Kahan; 2012). Although the “prion-like” nature of pathological α-syn is a theme of intense research

The PARK7 gene provides instructions for making the DJ-1 protein. This protein is found in many tissues and organs, including the brain. Studies indicate that the DJ-1 protein has several functions, however it is not fully understood how generic changes cause Parkinson’s disease or even understand it’s risks. One of the protein's functions may be to protect cells, particularly brain cells, from oxidative stress. Oxidative stress reflects an imbalance between the generation reactive oxygen species and a biological system’s ability to readily detoxify the reactive species. It occurs when unstable molecules called free radicals accumulate at levels that can damage or kill cells. Many radicals are unstable and highly reactive. They can neither donate or accept an electron. Additionally the DJ-1 protein may assist in delivering selected proteins to proteasomes, which are structures within cells that break down unneeded

Parkinson’s disease is a chronic disorder of the nervous system with a gradual onset that primarily affects the body’s motor system. The symptoms of the disease are mainly caused by the death of dopamine-producing cells in the midbrain. Dopamine is an important neurotransmitter that, among other things, is responsible for playing a role in how the brain controls bodily movements. Therefore, the cardinal symptoms of the disease are movement related, including tremor and rigid, jerky movements. Parkinson’s is a progressive disease, meaning it gets worse over time, until it eventually leads to complete disability. Parkinson’s is a fairly common disease, and several well-known people, such as actor Michael J. Fox and boxer Muhammad Ali have

Parkinson’s disease (PD) is a progressive disorder of unknown etiology that has no cure. It is characterized by bradykinesia, rest tremor, cogwheel rigidity and postural instability, along with a number of non-motor signs. The neurochemical hallmark of PD is dopamine loss in the nigrostriatal dopamine system (Adler, 2011). In the substantia nigra (SN) of people with PD there is a loss of neuronal cells, demonstrated by the degeneration of brainstem nuclei (Brooks, 1998). This typically shows as Lewy bodies – spherical masses of protein that develop inside nerve cells. However the progression of neuronal loss is quite variable in different PD patients and at different phases of the disease. At present there is no treatment that affects the degeneration, for example by slowing the rate of cell death or by protecting neurons.

The brain is the most important part of the body, it controls everything we do. It is one of the most complex organs of the body. It has many parts, including these main bits: The cortex is the outer layer of the brain and it controls thinking and movement. The brain stem/spinal cord is between the spine and the rest of the brain and the controls our sleep and breathing. The cerebellum is in the middle and back of the brain and controls balance and coordination. There are also several lobes which are important to the brain as well. The frontal lobe is responsible for problem solving and judgement and the temporal lobe is responsible for memory and hearing. The parietal lobe is responsible for processing sensory information from

Firstly, genetics is believed to play a role although it only affects a small number of families. Scientists have identified some gene abnormalities and mutations that are linked to Parkinson’s Disease such as the mutation in alpha synuclein gene. The triplication of this gene on a copy of chromosome 4 causes the overproduction of either normal or abnormal alpha synuclein protein, which is toxic to brain cells (Lesage, “Genetics and Parkinson’s Disease: What have we learned?”). Secondly, more and more studies have shown the relation between environmental toxins and Parkinson’s Disease. Exposure to toxins such as certain metals (manganese), pesticides and chemicals (MPTP, an illicit drug) selectively damages neurological cells, causing the disease (“Parkinson’s Disease: Hope through research”). Thirdly, mitochondrial oxidation stress may also contribute to the illness (“What causes Parkinson’s Disease”). By ‘stealing’ electrons from nearby molecules, the unstable free radicals cause damage to cells such as the neurons, and thus interrupt the communication with our

Parkinson’s disease is defined as “a progressive, chronic, neurodegenerative disease” (Medscape, 2014). Parkinson’s disease affects the movement of the body and develops gradually, starting from a slight tremor and can progress into loss of autonomic movements to speech changes and writing changes. In this paper the author will discuss ethical and legal concepts related to Parkinson’s disease and how certain treatments like stem cell transplants can help but also be a major risk factors and have ethical problems. Also the author will discuss the management of care for Parkinson’s disease and how to advocate for your patients, teach them how to deal with their ever changing body and lastly how developing research can help to find a cure or even a better treatment for this progressive neurological disease. Parkinson’s disease has no cure and it is important as a health care professional to understand the state of mind that your patient is in in order to provide the best quality of life so that they can live comfortably and happy as their disease progresses through their bodies.

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).

Parkinson’s Disease is a very common disorder these days. Over 10 million people live daily with Parkinson worldwide. Parkinson’s Disease was named after an English surgeon James Parkinson who wrote a detailed description essay called Shaking Palsy in 1817. The average age for Parkinson’s Disease is between 45 to 70 years old but you can also have juvenile or young onset as well. Most common symptoms of Parkinson are tremors, bradykinesia or akinesia, or rigidity or stiffness, and balance disorder. Parkinson’s Disease doesn’t have a cure and the cause is unknown it could be a number of things genetics, environmental triggers, age, or gender. Parkinson’s Disease happens because the dopaminergic neuron dies and

With the number of cases in the millions, Parkinson’s Disease is one of the most common types of neurological disorders, and continues to be common due to the lack of a cure. However, research has come a long way in determining the exact areas of the brain that affect Parkinson’s Disease, the risk factors associated with this disease, and the exact physiology of the brain that causes a person to have the symptoms specific to

Parkinson’s Disease (PD) is a progressive and neurodegenerating disorder in the central nervous system that affects the motor skills of a patient. It is a long-term disorder that is common to old people ranging ages from the early 60s. Motor symptoms include shaking, rigidity, slowness in movement and difficulty to move limbs; all of these happen due to the result of dead cells coming from the substantia nigra, a region of the midbrain. It is understood that a dopamine deficiency is the root cause of this matter. The disease has no cure but recent studies suggest different kinds of treatments such as the anti-parkinson medication levodopa (L-DOPA).

Parkinson disease (PD) is a common neurodegenerative disease with unknown etiology. PD is commonly referred to as a “motor disease,” reflecting its clinical symptoms, including resting tremors of extremities, muscular rigidity, shuffling gait, stoop posture, and bradykinesia (1). The underlying pathology of PD is progressive neuronal loss, particularly in the substantia nigra pars compacta (SNc), and the presence of abnormal protein- rich aggregates—known as Lewy bodies— in the remaining