Welcome to Our Parkinson's Place
I copy news articles pertaining to research, news and information for Parkinson's disease, Dementia, the Brain, Depression and Parkinson's with Dystonia. I also post about Fundraising for Parkinson's disease and events. I try to be up-to-date as possible. I have Parkinson's diseases as well and thought it would be nice to have a place where updated news is in one place. That is why I began this blog.
I am not responsible for it's contents, I am just a copier of information searched on the computer. Please understand the copies are just that, copies and at times, I am unable to enlarge the wording or keep it uniformed as I wish. This is for you to read and to always keep an open mind.
Please discuss this with your doctor, should you have any questions, or concerns. Never do anything without talking to your doctor. I do not make any money from this website. I volunteer my time to help all of us to be informed. Please No advertisers, and No Information about Herbal treatments. Please no advertisements.
This is a free site for all.
Friday, August 22, 2014
Thursday, August 21, 2014
Satbir Grover, B.D.S., M.S., and Nelson L. Rhodus, D.M.D., M.P.H.:
At the turn of the new century, while the world — and media around the globe — were worrying about the “Y2K” threat to its computers, a more significant phenomenon crept into the background with hardly a headline: the dawn of “the age of the aged”. This fastest growing segment of our society, also referred to as the “Aging Tsunami”, is over the age of 65 and consists of 14% of the U.S. population today. As shown by the latest estimates, people over 65 years of age will make up to 23% of the U.S. population, or approximately 68 million people, by the year 2050, and people aged 85 years or more will also increase three-fold, thus making this the fastest growing segment of U.S. society.1 This wave of retirees, known as the Baby Boomers, will also be associated with an increasing number of medical conditions having a major impact on the health care system of the nation. One of the most common chronic diseases associated with old age is Parkinson’s disease (PD), which demands a customized interdisciplinary approach, with medical and dental specialties working together for the optimal treatment of the patient.
Parkinson’s disease, or Paralysis agitans, is a progressive, neurodegenerative disorder that affects movement, muscle control, and balance, as well as numerous other non- motor functions. It is part of a group of conditions known as Motor Systems disorders. Also known as the “shaking palsy”, the disease was named for James Parkinson, a general practitioner in London during the 19th century who first described the symptoms of the disease. Symptoms describing Parkinson’s disease are mentioned in writings on medicine in India dating back to 5,000 B.C., as well as in Chinese writings dating back approximately 2,500 years. Parkinson’s disease is the most common movement disorder and the second most common neurodegenerative disorder, the most common being Alzheimer’s disease.
According to the National Institute of Neurological Disorders and Stroke (NINDS) (http://www.ninds.nih.gov), there are approximately 1.5 million people in the U.S. who suffer from Parkinson’s disease — approximately 1-2% of people over the age of 60, and 3-5% of the population over age 85. Various studies have reported the incidence of PD from 8.6-19 per 100,000 people. Approximately 50,000 new cases are diagnosed in the U.S. annually. This number is expected to rise as the general population in the U.S. ages. A typical dental practice could expect approximately four to five patients with PD every day.
Onset of Parkinson’s disease before the age of 40 is still rare. However, all races and ethnic groups are susceptible and can be affected. Some of the studies suggest an equal distribution of PD among males and females before the age of 60, but higher in males past 60 years of age. More information can be collected from the American Parkinson’s Disease Association (http://www.apdaparkinson.org).
Parkinson’s disease occurs when there is a disruption of the neurotransmitters or dopamine production which leads to impaired communication between brain cells in the basal ganglia. The reduced level of dopamine causes the nerve cells to fire out of control and causes a loss of smooth, controlled muscle activity. Also, death of dopamine-producing cells in the substantia nigra eventually results in a reduced level of dopamine in the corpus striatum, which is considered to be the primary pathology in Parkinson’s disease.
By the time symptoms develop, there is at least 60% loss of dopamine-producing cells in the substantia nigra and an 80-90% loss of dopamine in the corpus striatum.
Increasing evidence suggests that Parkinson’s disease is a multisystem brain disease in which various neurotransmitter systems are affected, and related deficits become more prominent over the course of the disease. In addition, it is known that the disease process of PD begins long before motor symptoms are clinically visible. Many patients report that they have already experienced non-motor symptoms associated with PD such as fatigue, constipation, and olfactory changes several years before clinical onset.
Parkinson’s disease is also characterized by the presence of Lewy bodies, structures that are found in the cells of the substantia nigra as well as in other secondary locations. Lewy bodies are strongly correlated with neurodegeneration and are considered a diagnostic hallmark of Parkinson’s disease.2
There is convincing evidence that the Parkinson’s disease neurodegenerative process begins many years before the onset of motor manifestations. Initial estimates based on nigral neuropathological findings or striatal dopamine imaging suggested a five-to six-year preclinical period. However, more recent evidence of Lewy body pathology in other neuronal populations preceding nigral involvement suggests that the preclinical phase may be much longer.3
According to the Parkinson’s Disease Foundation, two major factors are considered the cause for Parkinson’s disease: genetics and environment.
Based upon the current research, the vast majority of Parkinson’s cases are not directly inherited, as about 15 to 25 percent of people with Parkinson’s report having a relative with the disease. In large population studies, researchers have found that, as compared to the general population, people with first degree relatives such as parents or siblings suffering from PD have a four to nine percent greater chance of developing PD. Scientists have discovered mutations in genes that play a role in dopamine cell functions. These genes include alphasynuclein, leucine rich repeat kinase 2 (LRRK-2), and glucocerebrosidase (GBA).4 While it is possible these mutations may be the cause for the disease directly, they seem to affect only a small number of families.
Some studies have demonstrated that prolonged occupational exposure to certain chemicals is associated with an elevated risk of PD. Epidemiological research has identified several factors that may be linked to Parkinson’s, including rural living, well water, manganese, and pesticides. In 2009, the U.S. Department of Veterans Affairs added Parkinson’s to a list of diseases possibly associated with exposure to Agent Orange.
A synthetic neurotoxin agent discovered in the 1980s called MPTP can also cause immediate and permanent Parkinsonism. The compound was found mainly in individuals who injected themselves with a synthetic form of heroin contaminated with MPTP. However, cases of MPTP-induced Parkinson’s in the general population are exceedingly rare.
Recent evidence indicates some other contributing factors which when integrated with the major cause may lead to a high PD rate. They are:
• Oxidative damage: Some researchers consider free radicals or even endogenous toxins circulating in the body to be a contributing factor in PD.5
• Toxins: Chronic exposure to toxins such as pesticides, considering the geologic location and living conditions of the patient, can lead to considerable loss or degeneration of the dopamine-producing cells.
• Occupational hazards: A high prevalence of PD is thought to be present in patients related to occupational fields such as welding, cleaning, or farming. Even drinking water from wells with high concentrations of heavy metals like mercury, iron, zinc, manganese, and so on for an extended period of time may increase the incidence for PD.6
• Aging: The latest evidence indicates the normal aging process is a natural cause in reduced or even accelerated death of dopamine-producing cells in PD patients.7
Scientists have proposed that clinical, neuroimaging, and pathologic examination of the patients having a variety of non-motor symptoms known as the “premotor phase” can precede the classic motor features of Parkinson’s disease by years and, perhaps, even decades.8
Signs and Symptoms
The four primary motor symptoms considered the hallmark of PD are also known by the acronym T.R.A.P: tremor (resting tremor); rigidity (muscle rigidity); akinesia and bradykinesia; and postural instability.9
Tremors in patients with PD can be unilateral or bilateral, most commonly noticed as a “pill-rolling” movement of the thumb and the opposing fingers. Resting tremors which disappear with the motion of the hand are present in approximately 70-80% of the diagnosed cases. This symptom worsens with climatic changes, especially winters, and with anxiety, excitement, or even apprehension.
Rigidity consists of increased tone or stiffness of muscles. It may be not reported in initial cases of PD. However, it may be noticeable upon physical manipulation by the physician. One can also appreciate smooth muscle movements replaced with a broken-up ratchet type of action commonly known as “cogwheel rigidity”, manifesting as reduced swinging of arms with foot dragging while walking.
Akinesia and Bradykinesia
Akinesia refers to significant reduction or absence of spontaneous movement, whereas bradykinesia refers to slowness of movement. PD patients commonly report akinesia to be most distressing, as it makes small tasks time consuming, such as the delay in initiation of the movement required for walking. Bradykinesia can also be frustrating, as it interferes with basic activities such as dressing, household chores, or even sitting down and getting up from a dental chair. It may also manifest as reduced facial expression, commonly known as “mask face”.
Gait changes include asymmetric slowness, reduced arm-swinging, and stooped posture, shuffling, and often leaning forward or backward, leading to a high number of cases of falls in patients with PD.
Other medical symptoms associated with PD can vary from “festination” or “freezing” to sudden inability to initiate movement through a spectrum of non-motor complications10 such as cognitive impairment, dementia/other psychotic symptoms, depression/mood fluctuations, fatigue/pain, shortness of breath, visual disturbances, or sexual dysfunction.
Numerous medical conditions can mimic the symptoms of Parkinson’s disease. They can be divided into three major categories: medicationinduced Parkinsonism, Parkinson-plus syndrome, and essential tremors. Parkinson’s-disease-like symptoms can be secondary to some other underlying conditions or medications such as antipsychotics, antiemetics, antihypertensives, antianginals, or antineoplastics. Because no diagnostic tests can clearly detect PD, the diagnosis requires extensive details regarding the history of the symptoms, clinical examination of the patient, and specific tests or images to rule out the other mimicking diseases such as multi-infarct disease or multiple small strokes (vascular Parkinsonism), Huntington’s disease, Lewy body dementia, progressive supranuclear palsy (PSP), or Wilson’s disease.11
In the famous words of Louis Pasteur, “In the fields of observation, the favorites do prefer the prepared minds.”
Systemic health is often related to oral health. Many systemic diseases are manifested in the oral cavity. In addition, some of the therapies used to treat them have effects on the teeth and mouth. Patients with Parkinson’s disease display a number of oro-facial manifestations. As discussed earlier, these manifestations are secondary to motor and sensory deficits. They can display in a range of symptoms such as the following.
Dysphagia. With PD, even normal swallowing of food or water can be a challenge. This affects up to 75% of PD patients, and even the normal swallowing of saliva is affected. With the progression of disease, the greatest risk, that of “silent aspiration”, also increases. It leads to aspiration of small amounts of food or saliva without normal protective reflexive mechanisms, and thus a high prevalence of pneumonia is reported in patients with PD.12 As well, the tongue does not depress sufficiently to allow food to proceed to the throat.
Salivary dysfunction. In PD patients, the normal salivary function is disrupted and can result in either varying degrees of reduced saliva production or xerostomia. It can also swing in the opposing direction of excess saliva production, or sialorrhea. As a consequence, the normal salivary functions such as lubrication, solubilizing foods, assisting chewing and swallowing, and providing stability to the normal buffer system to protect teeth is disrupted. Parkinson’s disease is often associated with excess saliva, drooling, and difficult swallowing.13 Up to 78% of PD patients report sialorrhea, which manifests as drooling with a high incidence of fungal infection (angular cheilitis) at the corners of mouth. On the other hand, reduced salivary secretion leading to xerostomia, or dry mouth, is a significant factor aggravating the rate of dental decay, especially roots caries.14 Xerostomia may result from the disease process, or from a complex of factors such as treatment of PD, drug therapy side effects, and generalized decrease in saliva associated with aging. In Parkinson’s disease, dry mouth is frequently the side effect of taking anticholinergic medications. It has been found that patients with dry mouth are not only more prone to cavities, but may have tooth sensitivity. Additionally, the tissues in the mouth may become dry and at times painful.
Burning mouth is fairly common in PD patients, compounded by xerostomia, medications, nutritional deficiencies, and even poor oral hygiene resulting from reduced muscle co-ordination required to grip a normal toothbrush.
Changes in taste and smell.
Patients with PD are more vulnerable to changes in their taste and olfactory functions. Altered salivary functions and medications are considered to play a major role for the same. Muscles in the GI tract can be also be affected by PD, resulting in a feeling of food chunks “sticking” either in the throat or stomach and leading to heartburn or gastroesophageal reflux disease (GERD). Thus PD patients may complain of reduced flavor from food or, often, a bad taste in the mouth.
Other symptoms commonly associated with PD are: Speech impairment. Soft voice, slurred words, fast speech, or hesitation before speaking are often and commonly encountered. Difficulty in understanding the patient may result in reduced appreciation and reporting of pain or discomfort by the dental provider. It may be the first non- motor symptom that can indicate possible PD.
Bowel dysfunction — i.e., reduced control over bowel and bladder in patients with Parkinson’s disease — can lead to embarrassment, social isolation, and even admission to long-term care.15 The condition will have to be considered by and for the entire dental team while making extensive treatment plans such as multiple crowns or implants which require extended chair time, as the procedure may need to be stopped to allow frequent restroom trips by the patient.
Orthostatic hypotension is frequently encountered in Parkinson’s disease, and its diagnosis remains manometric (a fall of at least 20 and/or 10 mmHg in standing blood pressure).16 This is of special consideration when planning a dental procedure where the patient will be in a supine position for a long period of time. Orthostatic hypotension can also be a secondary effect of anti-hypertensive drugs.
Physical and mental fatigue is one of the most common complaints of Parkinson’s disease patients, and is often associated with reduced activity and poorer quality of life.17 It ranges from a patient complaining of being tired or feeling uneasy in the middle of treatment to frequent requests to stop the procedure before it has been completed.
Anxiety disorders are common in Parkinson’s disease patients. As the latest research indicates, anxiety disorders decreased with age, and young onset PD patients were more likely to experience anxiety than the late onset subjects. Anxiety adds to the complexity of PD, thus lowering patients’ quality of life.18 Incidences of patients with mood swings are common, and cases of compulsive behaviors are also reported. However, this is of very low degree. It may be of concern when considering the safety not only of the patient but of the dentist and staff.
Parkinson’s disease is a chronic, progressive condition that is associated with increasing disability in areas such as motor function, balance, mood condition, behavior, activities of daily living, and overall quality of life. Patients with varying degrees of dyskinesia of the hands or/and face are often associated with poor oral hygiene and infections of the gums and periodontal tissue. Studies have indicated that patients with a diagnosis of PD may have poorer oral hygiene and a greater incidence of infection as compared to the general public.19
Taking a detailed medical history before the commencement of any dental treatment is the best approach to complete patient care. The dentist should concentrate on the overall medical health of the patient; information regarding the patient’s medical diagnosis; and maintaining a complete list of medications, whether present or discontinued. A history of any surgeries should be collected in the initial visit to the dental clinic.
Conducting medical history reviews and measuring a patient’s vital signs, including blood pressure, heart rate, pulse, and respiratory rate on every visit should be standard practice and performed primarily by the dentist.24 This model always helps guide the dentist in identifying benefits and risks associated with the patient and planning for treatment. Contraindications associated with any concerning medical condition can be determined in these initial stages, and the dentist can refer the patient to his or her primary physician for consultation. Information regarding the medical condition, cognitive status, disease prognosis, drug regimens, and even modifications that need to be done during the dental procedure can be discussed.20 The major challenge for patients with PD is adapting to their progressive disability. The dentist should devise a realistic treatment plan considering the current status of the patient and the degree of dental treatment required. The restorative procedures should be completed in initial stages of the disease, taking into account the reduced ability of the patient to tolerate longer appointments, or even reduced cooperation as the disease progresses. The dentist should be able to discuss an immediate versus long term treatment plan either with the patient or his family/responsible party so as to prevent future complications.
The degree of muscle rigidity can be a challenging factor in the maintenance of oral hygiene. Studies indicate that PD patients had more complaints about their oral health and more problems in oral health behavior than did the general population.19 The dental treatment should always begin with the identification and diagnosis of the disease, its associated risk factors, and discussion between the dentist and the patient or his family members. The dentist plays an integral role in providing complete health care to an individual. The patient should be educated and continuously motivated for the maintenance of good oral hygiene. The role of basic hygiene aids such as toothbrush, tooth paste, and even floss should be explained in detail. The dentist or hygienist can help the patient in modifying the oral hygiene techniques considering the degree and progression of the disease. The importance of good oral hygiene should be reinforced by the fact that it can help reduce complications associated with many systemic conditions such as diabetes. Improvements in oral hygiene may reduce the risk of developing infective endocarditis (IE)21 and also reduce the incidences of aspiration of microorganisms leading to aspiration pneumonia.22 With the progressing tremors and poor muscle coordination, patients may face concerns with their grip and therefore overall dexterity to clean the teeth. This can range from reduced grip over the toothbrush to squeezing toothpaste out of the tube. The toothbrushes with the wider grip can be more handy for patients with PD. The brush can be fixed inside the bike handlebar grips or the tennis balls so as to increase its surface area, thus making it comfortable to grip and use by the patients. The newly available power toothbrushes have proven to be a boon to these patients. They come with a thicker handle, improving the grip substantially. The improved versions have a timer with an On/Off switch, keeping the patient on track for the proper brushing for the suggested length of time. Toothbrushes with soft bristles and smaller heads so as to reach all the corners of mouth should be preferred. The toothbrushes should be replaced after every three months or when the bristles start showing indications of fanning out. Toothpaste pumps are available to dispense a fixed amount of toothpaste as required. The patient should also be motivated for the regular use of dental floss to improve oral tissue condition and reduce plaque build-up. Waxed or non-waxed dental floss is available for the patient’s choice, with floss holders and interproximal brushes to aid in better cleaning. If the patient is partially or fully edentulous, and uses partial, fixed, or complete dentures, emphasis should be placed for the regular cleansing of the dentures.
With the growing demand for dental aids, mouthwashes have developed to suit the individual. Patients with PD can be informed about various mouthwashes available.23 Emphasis should be placed on the use of non-alcoholic, fluoridated mouth rinses to improve overall benefit with other hygiene aids. Based on current studies, a combination of fluoridated toothpaste and anti-microbial mouth rinses such as chlorhexedine is a useful, simple, quick, and non-invasive method for the control and management of existing root caries lesions. Simultaneously, the patient should be informed regarding the proper method for the use of mouthwash, as spitting it out can be a challenge with the progression of the disease. Patients with reduced oral muscle control can be trained to either dip their brushes in the mouthwashes before brushing or to bend down over the sink and rinse, as gravity will allow the mouthwash to flow down the sink, thus reducing the incidence of uncontrolled swallowing by the patient.
Patients having memory issues and difficulty remembering details about brushing or flossing can post sticky notes at the brushing area to remind them to follow the steps every day. Family members or caretakers can remind patients to brush and floss as well. For complete oral hygiene, the tongue should be thoroughly cleaned, as it can be a trap for food particles, particularly with PD-related xerostomia.
Maintenance of the oral health of patients with Parkinson’s disease should be of prime importance in providing complete health care to this fastest growing segment of our society. Dentists who are well informed about the manifestations of PD, with its direct and indirect effects on oral health, will be in a better position to provide complete dental care to patients suffering from this disease.
1. Dr. Robert Kane; Clinical Geriatrics.
2. Pathophysiology of Parkinson’s Disease. Zingmond MJ, Burke RE. Neuropsychopharmacology: 1,782. The Fifth Generation of Progress.
3. Savica R, Rocca WA, Ahlskog JE. When does Parkinson’s disease start? Arch Neurol 68(1);Jan 2011:137-8.
4. Lees AJ, Hardy J, Revesz T. Parkinson’s disease. Lancet 374(9,691);Aug 29,2009:684.
5. Surendran S, Rajasankar S. Parkinson’s disease: oxidative stress and therapeutic approaches. Neurol Sci 31(5);Oct2010:531-40. Epub March 10, 2010.
6. Guilarte TR. (2010) Manganese and Parkinson’s disease: a critical review and new findings. Environ Health Perspect Aug; 118(8);Aug2010:1,071-80. Epub April 19, 2010.
7. Halliday GM, McCann H. The progression of pathology in Parkinson’s disease. Ann NY Acad Sci Jan 2010;1,184:188-95.
8. Tolosa E, Gaig C, Santamaría J, Compta Y. (2009) Diagnosis and the premotor phase of Parkinson’s disease. Neurology 72(7 Suppl);Feb 17,2009:S12-20.
9. Little JW, Falace DA, Miller CS, Rhodus NL. Dental Management of the Medically Compromised Patient, Seventh Edition, 2008.
10. Chaudhuri KR, Schapira AH.(2009) Non-motor symptoms of Parkinson’s disease: dopaminergic pathophysiology and treatment. Lancet Neurol 8(5);May2009:464-74.
11. Gama RL, Távora DF, Bomfim RC, Silva CE, Bruin VM, Bruin PF.(2010) Morphometry MRI in the differential diagnosis of parkinsonian syndromes. Arq Neuropsiquiatr 68(3);Jun2010:333-8.
12. Parkinson’s Disease and Oral health. Michaell A.Huber.
13. Proulx M, de Courval FP, Wiseman MA, Panisset M. Salivary production in Parkinson’s disease. Mov Disord 20(2);Feb 2005:204-7.
14. Friedlander AH. (2009) Sjögren syndrome. J Am Dent Assoc 140(3);Mar2009:279.
15. Kyle G. (2010) The physical, social and emotional effects of bowel dysfunction in Parkinson’s disease. Nurs Times 106(33);Aug24-30 2010:20-2.
16. Senard JM, Pathak A. Neurogenic orthostatic hypotension of Parkinson’s disease: What exploration for what treatment? Rev Neurol (Paris) 166(10);Oct 2010:779-84.
17. Lou JS. Physical and mental fatigue in Parkinson’s disease: epidemiology, pathophysiology and treatment. Drugs Aging 26(3);2009:195-208.
18. Dissanayaka NN, Sellbach A, Matheson S, O’Sullivan JD, Silburn PA, Byrne GJ, Marsh R, Mellick GD. Anxiety disorders in Parkinson’s disease: prevalence and risk factors. Mov Disord 25(7);May 15, 2010:838-45.
19. Nakayama Y, Washio M, Mori M. (2004) Oral health conditions in patients with Parkinson’s disease. J Epidemiol 14(5);Sept2004:143-50.
20. Friedlander AH, Mahler M, Norman KM, Ettinger RL. (2009) Parkinson disease: systemic and oro-facial manifestations, medical and dental management. J Am Dent Assoc 140 (6);Jun2009:658-69.
21. Lockhart PB, Brennan MT, Thornhill M, Michalowicz BS, Noll J, Bahrani-Mougeot FK, Sasser HC. Poor oral hygiene as a risk factor for infective endocarditis-related bacteremia. J Am Dent Assoc 140(10);Oct 2009:1,238-44.
22. Pace CC, McCullough GH. The association between oral microorganisms and aspiration pneumonia in the institutionalized elderly: review and recommendations. Dysphagia 25(4);Dec2010:307-22. Epub Sept. 8, 2010.
23. Brailsford SR, Fiske J, Gilbert S, Clark D, Beighton D. The effects of the combination of chlorhexidine/thymol- and fluoride-containing varnishes on the severity of root caries lesions in frail institutionalized elderly people. J Dent 30(7-8);Sept-Nov2002:319-24.
24. Malamed SF. Knowing your patients. J Am Dent Assoc 141;3S-7S:2010.
*Dr. Grover is a senior dental fellow in the Oral Health Services for Older Adults, Department of Primary Dental Care, University of Minnesota School of Dentistry, Minneapolis, MN 55455.
**Dr. Rhodus is professor and Director, Division of Oral Medicine and adjunct professor, Department of Otolaryngology, School of Medicine, University of Minnesota, Minneapolis, MN 55455.
Wednesday, August 20, 2014
Tuesday, August 19, 2014
A new drosophila model to study the interaction between genetic and environmental factors in Parkinson's disease.
Brain Res. 2014 Aug 14. pii: S0006-8993(14)01085-3. doi: 10.1016/j.brainres.2014.08.021. [Epub ahead of print]
The fruit fly Drosophila melanogaster has long been used as a model organism for human diseases, including Parkinson's disease (PD). Its short lifespan, simple maintenance, and the widespread availability of genetic tools allow researchers to study disease mechanisms as well as potential drug therapies. Many different PD models have already been developed, including ones utilizing mutated α-Syn and chronic exposure to rotenone. However, few animal models have been used to study interaction between the PD causing factors. In this study, we developed a new model of PD for use in the larval stage in order to study interaction between genetic and environmental factors. First, the 3rd instar larvae (90-94 hours after egg laying) expressing a mutated form of human α-Syn (A53T) in dopaminergic (DA) neurons were video-taped and quantified for locomotion (e.g. crawling pattern and speed) using ImageJ software. A53T mutant larvae showed locomotion deficits and also loss of DA neurons in age-dependent manner. Similarly, larvae chronically exposed to rotenone (10μM in food) showed age-dependent decline in locomotion accompanied by loss of DA neurons. We further show that combining the two models, by exposing A53T mutant larvae to rotenone, causes a much more severe PD phenotype (i.e. locomotor deficit). Our finding shows interaction between genetic and environmental factors underlying development of PD symptoms. This model can be used to further study mechanisms underlying the interaction between genes and different environmental PD factors, as well as to explore potential therapies for PD treatment.
Copyright © 2014. Published by Elsevier B.V.