Call for Abstract

2nd International Conference on Parkinson’s Disease & Movement Disorders, will be organized around the theme “Leading Innovations and Remedial Insights into the Parkinsons Disease”

Parkinsons 2016 is comprised of 13 tracks and 104 sessions designed to offer comprehensive sessions that address current issues in Parkinsons 2016.

Submit your abstract to any of the mentioned tracks. All related abstracts are accepted.

Register now for the conference by choosing an appropriate package suitable to you.

Improving economy and health in countries like USA, Germany, has increased the life span and changed the emphasis from communicable to non-communicable diseases. It is expected that the prevalence of Parkinson’s disease in the 7MM (US, France, Italy, Spain, Germany, Brazil, and Japan) and UK will increase from 3.2m people in 2012 to 4.3m people in 2022. The global treatment for syndromes of the movement disorders market is anticipated to grow from an estimated $ 12,859.8 million in 2014 to $ 21,154.8 million in 2020 at a CAGR of 8.6% during the forecast period. This increase the prevalence of age-related diseases and movement disorders like Parkinson's disease (PD). We review epidemiological studies to describe: a) Developments in interdisciplinary of Parkinson and movement disorders, b) Aggregation and Protein Misfolding and c) potential of epidemiological research in countries with multiple ethnic races and environmental risks for PD, d) methodological issues, e) Prevalence of movement disorders.

  • Track 1-1Etiology of Parkinsons disease
  • Track 1-2Protein Misfolding & Aggregation
  • Track 1-3Developments in interdisciplinary of Parkinson disease
  • Track 1-4Interdisciplinary care in Parkinsons and other movement disorders

Parkinson's disease, the most common Neuromuscular Disorders, which has a much attention from the clinical and scientific community. The Substantial progress has been made in the understanding of the role of the basal ganglia in the pathophysiology of these hyperkinesia disorders and in muscle tone, cognitive processes, motor control and posture. Although therapies that target pathogenesis are still lacking, the management of hyperkinetic movement disorders demands that physicians are knowledgeable about current and novel pharmacological and surgical approaches. In addition to tetra benzene, a monoamine-depleting drug, new formulations of botulin toxin are being increasingly used in the treatment of these movement disorders. Hyperkinetic movement disorders include dystonia, chorea, tics, myoclonus, stereotypies, tremors, restless legs syndrome, Huntington's disease, Tardive Dystonia/ Tardive Dyskinesia, Wilson's disease, and various other disorders with abnormal involuntary movements.

  • Track 2-1Huntington disease
  • Track 2-2Wilsons disease
  • Track 2-3Tics/Tourettes Syndrome
  • Track 2-4Tardive Dyskinesia / Tardive Dystonia
  • Track 2-5Dystonic tremor
  • Track 2-6Essential tremor
  • Track 2-7Parkinsons disease tremor
  • Track 2-8Chronic traumatic encephalopathy and Movement disorders
  • Track 2-9Spectrum of neuropathological changes
  • Track 2-10Treatment of dystonia
  • Track 2-11The spectrum of isolated and combined dystonia syndromes
  • Track 2-12Movement disorders in neuromuscular diseases
  • Track 2-13Drug-induced movement disorders
  • Track 2-14Alzheimers disease

Neurocognitive are those that affect the muscles and their direct nervous system control. The session describes that Cognitive and neuropsychiatric issues, Genetic syndromes and autoimmune syndromes in the hinterland of movement disorders. The Role of channelopathies in Movement disorders, clinical spectrum of dystonia’s which are responsive to dopamine-related drugs, Novel biomarkers to differentiate neurodegenerative parkinsonian disorders, neurodegenerative spasticity and Aging, Parkinson related dementia, amnesia and Amyotrophic Lateral Sclerosis (ALS).

  • Track 3-1Cognitive dysfunction
  • Track 3-2Vascular disease
  • Track 3-3Aging and Neurodegenerative Spasticity
  • Track 3-4Parkinsons related dementia and Amnesia
  • Track 3-5Amyotrophic Lateral Sclerosis (ALS)
  • Track 3-6Autoimmune movement disorders
  • Track 3-7Clinical spectrum of dystonias that are responsive to dopamine related drugs
  • Track 3-8Novel biomarkers to differentiate neurodegenerative parkinsonian disorders
  • Track 3-9Genetic syndromes in the hinterland of epilepsies and movement disorders
  • Track 3-10Role of channelopathies in movement disorders

A risk factor is something which increases the risk of developing a condition or disease. The risk factors of Parkinson Disease are Age, Gender, Genetics, Toxin exposure, some medications and Area of residence.

Age Where Young adults rarely experience the Parkinson's disease. It begins in middle or late life.  The People usually develop the disease around age 60 or older. Heredity occurs when a close relative (mother, father, brother, sister) with Parkinson's disease which may slightly increases the chances of develop the disease. When compared to others. Men are more likely to develop Parkinson's disease than the women. Even Exposure to toxins such as herbicides and pesticides may slightly increase risk of Parkinson's disease.

  • Track 4-1Heredity
  • Track 4-2Exposure to toxins
  • Track 4-3Declining oestrogen levels
  • Track 4-4Genetic predisposition
  • Track 4-5Head Trauma
  • Track 4-6Comorbid problems associated with Parkinson disease
  • Track 4-7Gene environmental interactions in neurodegenerative diseases, Clinical association and mechanisms
  • Track 4-8Epidemiological evidence linking environmental and lifestyle risk factors in Parkinsons disease
  • Track 4-9Late-breaking clinical trials and clinical science in Parkinsons disease

The Pathophysiology involves the interaction of environmental factors and host susceptibility. A small percentage of cases are genetically linked and genetic factors are being intensely studied. Physiologically, the symptoms associated with Parkinson’s disease are the result of the loss of a number of neurotransmitters, most notably dopamine. Symptoms worsen over time as more and more of the cells affected by the disease are lost. The track Pathophysiology and Neuropharmacology includes Pathophysiology of gastrointestinal dysfunction in Parkinsonism, Management of upper gastrointestinal dysfunction, and dysphagia, Cell death, Bowel dysfunction in Parkinsonism Pathophysiological mechanisms linking Parkinson’s disease and Gaucher’s Disease.

  • Track 5-1Cell death
  • Track 5-2Bowel dysfunction in parkinsonism
  • Track 5-3Pathophysiology of gastrointestinal dysfunction in parkinsonism
  • Track 5-4The use of herbal medicine in Parkinsons disease
  • Track 5-5Management of dysphagia and upper gastrointestinoal dysfunction
  • Track 5-6Pathophysiological mechanisms linking Parkinsons disease and Gaucher’s disease

Making an accurate diagnosis of Parkinson’s particularly in its early stages — is difficult. The use of functional neuroimaging in neurodegenerative diseases has increased in recent years, with applications in research in the underlying pathophysiology, aiding in diagnosis, or evaluating new treatments. In Parkinson's disease (PD), these imaging ways have expanded our understanding of the disease on the far side dopaminergic deficits area unit of diagnostics and Neuroimaging for Parkinson disease are Clinical pathological and genetic overlap in parkinsonism, Detecting prodromal Parkinson’s disease, Nuclear imaging to study Laboratory investigations supporting the diagnosis of MSA, PSP and CBD, Utility of next generation sequencing in the diagnosis of parkinsonian disorders, Clinic-genetic correlations in parkinsonian disorders, Therapeutic strategies in genetic forms of proteinopathies,  pathophysiology to new treatment strategies Insights from the laboratory and Disease-modifying, animal models and Symptomatic treatments, Update on surgical and medical treatment of the dystonia’s, Instrumental analysis of tremor, Instrumental analysis of parkinsonian symptoms, analysis of gait and postural reflexes, Neuroprotective treatments and Complementary Therapy.

  • Track 6-1Disease modifying and symptomatic treatments
  • Track 6-2Huntington’s disease: From natural history studies to experimental therapeutics
  • Track 6-3Pathophysiology to new treatment strategies: Insights from the laboratory and animal models
  • Track 6-4Utility of next generation sequencing in the diagnosis of parkinsonian disorders
  • Track 6-5Laboratory investigations supporting the diagnosis of MSA and PSP/CBD
  • Track 6-6Update on medical and surgical treatment of the dystonias
  • Track 6-7Therapetuic strategies in genetic forms of proteinopathies
  • Track 6-8Clinico-genetic correlations in parkinsonian disorders
  • Track 6-9Myoclonus, Etiology, pathophysiology and treatment
  • Track 6-10Instrumental analysis of tremor
  • Track 6-11Nuclear imaging to study parkinsonian disorders
  • Track 6-12Clinical pathological and genetic overlap in parkinsonism
  • Track 6-13Detecting prodromal Parkinsons disease
  • Track 6-14Analysis of gait and postural reflexes
  • Track 6-15Neuroprotective treatments
  • Track 6-16Complementary Therapy
  • Track 6-17Instrumental analysis of parkinsonian symptoms

Parkinson's disease is not fatal, but it can reduce longevity. The disease progresses more quickly in older patients, and may lead to severe incapacity within 10 - 20 years. Older patients also tend to have freezing and greater declines in mental function and daily functioning than younger people. If PD starts without signs of tremor, it is likely to be more severe than if tremor had been present.

Parkinson's disease will seriously impair the standard of life in many people. The physical and emotional impact on the family shouldn't be underestimated because the patient becomes more and more keen about their support. The potential complications are Swallowing issues, Sleep problems and Sleep disorders, Smell dysfunction, Sexual dysfunction, Bradykinesia, Anxiety and Depression, Obsessive compulsive behavior, Hallucinations and mental illness, Drowsiness and incontinence or retention.

  • Track 7-1Constipation
  • Track 7-2 Smell dysfunction
  • Track 7-3 Sexual dysfunction
  • Track 7-4 Bradykinesia
  • Track 7-5Anxiety and Depression
  • Track 7-6Obsessive compulsive behavior
  • Track 7-7Sleep problems and sleep disorders
  • Track 7-8Hallucinations and psychosis

Parkinson’s disease (PD) is a chronic disease, it is important to develop and maintain a solid PD management plan. Research has shown that those who take an active role in their care see an improvement in their Parkinson’s symptoms. While many medications treat Parkinson's, none actually reverses the effects of the disease or cures it. To managing Parkinson Disease Nutrition, Optimizing the effect of L-dopa in Parkinson Disease, Exercise, Building a health care team, Complementary therapies, Cognitive and psychiatric disturbances in atypical parkinsonian disorders"

  • Track 8-1Nutrition
  • Track 8-2Diet & Fatigue
  • Track 8-3Optimizing the effect of L-Dopa in Parkinsons disease
  • Track 8-4Cognitive and psychiatric disturbances in atypical parkinsonian disorders

Psychotic symptoms are common in Parkinson’s disease (PD), affecting nearly 50% of all patients over the course of the disease. Neurodegenerative  illness in the United States, affecting more than 1 million persons. Disease onset is usually after age 50. In persons older than 70 years, the prevalence is 1.5% to 2.5%.1 while the primary pathology involves degeneration of dopaminergic neurons in the substantia nigra, circuits important in emotion and cognition—such as the serotonergic, adrenergic, cholinergic, frontal dopaminergic pathways, Biological markers, Anxiety disorder, Depression and emotional changes, Lewy Bodies, Antipsychotics, Deep brain Stimulation.

  • Track 9-1Biological markers
  • Track 9-2Anxiety disorder
  • Track 9-3Depression and emotional changes
  • Track 9-4Lewy Bodies
  • Track 9-5Antipsychotics
  • Track 9-6Deep brain stimulation

Parkinson’s disease is that the primary growth driver of the worldwide Parkinson’s disease therapeutics. According to the estimates of the World Health Organization, the worldwide prevalence of Parkinson’s disease was valued at over 10 million in 2012. The share of the world’s population above the age of 65 years can increase from 7-membered in 2000 to 16 PF in 2050. The therapeutics of Parkinson Disease includes designing a Clinical trial for parkinsonian disorders, Outcome of clinical trials in PSP, MSA and CBD, therapeutic options for mood, Cognition and Psychosis, Treatment of Parkinson patient with psychosis,  Rehabilitation therapies for Parkinson Disease, Medical and Surgical treatment, RNAi and antibody-based therapeutic approaches, therapies targeting autophagy in movement disorders, Isogenic human-induced pluripotent stem cells, Human embryonic stem cell-based therapies in Parkinson disease,  Novel proteinopathy based tracers for diagnosis, Therapeutic developments in the treatment of cognitive impairment,  Morphological and molecular basis of levodopa-induced dyskinesia’s, Electrophysiological, and their therapeutic implications.

  • Track 10-1Designing a clinical trial for atypical parkinsonian disorders
  • Track 10-2Outcome of clinical trials in MSA, PSP and CBD
  • Track 10-3Therapeutic options for mood, cognition and psychosis in Parkinson’s disease
  • Track 10-4How to treat anxiety, depression and apathy
  • Track 10-5How to treat the Parkinson’s disease patient with cognitive impairment and psychosis
  • Track 10-6Medical and surgical treatment of Parkinsons disease
  • Track 10-7Rehabilitation therapies for Parkinsons disease
  • Track 10-8RNAi and antibody-based therapeutic approaches
  • Track 10-9Therapies targeting autophagy in movement disorders
  • Track 10-10Isogenic human-induced pluripotent stem cells
  • Track 10-11Human embryonic stem cell-based therapies in Parkinsons disease
  • Track 10-12Novel proteinopathy based tracers for diagnosis
  • Track 10-13Therapeutic developments in the treatment of cognitive impairment
  • Track 10-14Gene therapy for Parkinsons disease and movement disorders
  • Track 10-15Electrophysiological, morphological and molecular basis of levodopa-induced dyskinesias and their therapeutic implications

A movement disorder may be a condition that arises within the brain that causes a baby to move insufficient or too little. Movement disorders will arise from medication, infection, brain injury, autoimmune disease or they'll be inheritable.

This session explains that there is increasing evidence that these disorders are autoimmune and are mediated by antibodies against cell surface or synaptic proteins and cause dysfunction within the central nervous system. Hemiplegia of childhood and rapid onset dystonia-parkinsonism are two separate movement disorders with different dominant mutations in the same gene and Myoclonus shows sudden, brief, shock like movements that may be repetitive or rhythmic.

  • Track 11-1Myoclonus
  • Track 11-2Hemiplegia of childhood and rapid onset dystonia-parkinsonism
  • Track 11-3Movement disorders associated with antibodies against cell surface or synaptic proteins

Non-motor manifestations are integral components of Parkinson disease (PD), and they often have a greater impact on disability and quality of life.

This session will discuss many of the non-motor complications in PD, including Cognitive and neuropsychiatric issues, autonomic, sleep, and sensory difficulties that may occur and the prevalence and tools to assess non-motor features of early and advanced Parkinson’s disease.

  • Track 12-1Cognitive and neuropsychiatric issues
  • Track 12-2Parkinsonian syndromes focus on non-motor issues
  • Track 12-3Prevalence and tools to assess non-motor features of early and advanced Parkinson’s disease
  • Track 13-1Molecular Neuropharmacology
  • Track 13-2Clinical Neuropharmacology
  • Track 13-3Surgical aggression and anesthesia
  • Track 13-4Antipsychotic drugs
  • Track 13-5Molecular neuropharmacology