Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 3rd International Conference on Parkinson’s Disease & Movement Disorders Chicago, USA.

Day 1 :

Keynote Forum

Susan Scanland

Dementia Connection® LLC, USA

Keynote: Management of psychosis in Parkinson’s disease

Time : 10:00-10:45

Conference Series Parkinsons 2017 International Conference Keynote Speaker Susan Scanland photo
Biography:

 

Susan Scanland is a Gerontological Nurse Practitioner and Certified Dementia Practitioner and national Alzheimer’s and Dementia Expert with 34 years of experience. She received her MSN from University of Pittsburgh and BSN from Wilkes University. She has been nationally certified as a Gerontological Nurse Practitioner since 1984 and is also a Certified Dementia Practitioner. She holds a Nursing Faculty Specialist position at the University of Scranton. She taught in geriatric faculty positions at Binghamton University (SUNY) from 1999-2004 and the Wyoming Valley Family Practice Residency in Kingston, Pennsylvania from 1987-1999. She is Founder of Dementia Connection® LLC. She is one of two nurse practitioners in the world to receive the Certified Speaking Professional award (CSP) through the National Speakers Association. She presented to geriatric psychiatrists from 15 countries at the American Association for Geriatric Psychiatry Annual Meeting in Washington DC in March 2016. She is Dementia Consultant to a long-term care facility in northeastern Pennsylvania and also provided rural nursing home consults via telehealth. She co-authored two articles on antipsychotic reduction recently in consultant pharmacist and geriatric nursing. 

Abstract:

Psychosis occurs in over 50% and dementia in approximately 80% of persons with Parkinson’s disease. Treatment with non-selective atypical and typical antipsychotics significantly increases mortality rates in Parkinson’s disease; as well as other dementias. Research on the most commonly used antipsychotic in Parkinson’s, quetiapine, has not revealed significant reduction in Parkinson’s psychotic symptoms. Antipsychotic use, due to dopamine antagonism, is associated with unsteady gait and motor dysfunction; which exacerbates pre-existing Parkinsonian symptoms. Persons with Parkinson’s disease are already at risk for falls with gait asymmetry, short strides and increased stride duration. Parkinson’s patients have an increased hip fracture risk. The newly FDA-approved selective serotonin inverse agonist, pimavanserin, offers targeted treatment at the 5-HT2A receptor site responsible for Parkinson’s psychosis; without affecting dopaminergic receptor binding. Research reveals a decrease in hallucinations and delusions in Parkinson’s psychosis without worsening of motor symptoms. An evidence-based/case study format will present management of Parkinson’s psychosis with or without dementia, using FDA-approved treatment; as opposed to antipsychotics with full black box warnings that are commonly prescribed. Clinical outcomes, cost-effectiveness, quality of life, decreased risk for emergency room visits, hospitalizations and mortality and will be discussed.

Keynote Forum

Srinivasan Avathvadi Venkatesan

DR.M.G.R.Medical University, India

Keynote: The impact of wearing off on quality of life in patients with Parkinson's disease

Time : 11:00-11:45

Conference Series Parkinsons 2017 International Conference Keynote Speaker Srinivasan Avathvadi Venkatesan photo
Biography:

A.V. Srinivasan is the President of Indian Academy of Neurology and also he is the emeritus Professor of The Tamilnadu DR.M.G.R.Medical University. · Dr A V Srinivasan, driven by his quest for excellence and the latest discoveries on human brain related disorders, joined Madras Medical College (MMC) and received MD(General Medicine) in 1978.Later he pursued and received DM in Neurology from his alma mater.He is First Neuro physician of his state Tamil Nadu in India in government service to be conferred, the Fellow of the Royal College of Physicians (FRCP) in London in 2012, fellowship of the Indian Academy of Neurology 2004 and fellowship by the American Academy of Neurology, in 2003.He Is the First Indian to receive American Indian Neurology Award (AINA) in USA in 2001, for the best paper presentation IN STROKE during annual American Academy of Neurology meeting in 2001 in PHILADELPHIA. ByTheTamil Nadu DR. MGR Medical University. Currently serving as a Member –in the ACADEMIC COUNCIL of National institute of Mental health and Neurosciences, Deemed University, Bangalore. 

Abstract:

Introduction: By the year 2040, neuro degenerative disorders are expected to surpass cancer as the second most cause of death in the elderly. One of the most common neuro degenerative disorder is Parkinson’s’ disease with over 4 million victims identified in the world. Motor and non-motor symptoms tend to return during wearing off phenomenon in levodopa treated Parkinson’s patients. The development of wearing off is due to Parkinson’s disease progression and the rapid break down of levodopa in the body resulting in a feeling that levodopa effects are fading out. This results in the disturbances of the quality of life. In this study ten steps approach to improve quality of life and wearing off phenomenon are discussed: Disability and quality of life are assessed; research tools to assess quality of life; early signs and symptoms of wearing off; staging of Parkinson’s disease and the emergence of wearing off ; management of wearing off; impact of non-motor symptoms on HRQOL (Health Related Quality of Life); Parkinson’s disease well-being map and paper version and management of non-motor symptoms improved quality of life in Parkinson’s disease than motor symptoms; living a full life with Parkinson’s disease; helpful hints in daily life, managing stress with exercise, foot teeth care with diet and nutrition; and creative and complementary therapy.


Conclusion: Depression, fatigue, sleep problems and excessive day time sleepiness require special consideration when trying to optimize Parkinson’s management, due to their strong correlation with negative health status and HRQ-ol. Quantifying Parkinson’s symptoms provide an important basis for optimizing treatment and care.

Conference Series Parkinsons 2017 International Conference Keynote Speaker Jayakumar Rajadas photo
Biography:

Jayakumar Rajadas is the Founding Director of Biomaterials and Advanced Drug Delivery Laboratory at Stanford University. He is also an Adjunct Professor at UCSF School of Pharmacy, University of California. He is currently working on the molecular mechanism of neurodegenerative disorders involved in Alzheimer's and Parkinson's diseases. His research has also been involved in transforming nano science ideas into biomaterials and drug delivery technologies. Before moving to Stanford, he served as the Founding Chair Person of the bio-organic and neurochemistry division at one of India’s national laboratories. He is a recipient of several awards including Young Scientist award in Chemistry for the year 1996 from the Government of India. He has also won the Best Scientist award from the Tamil Nadu state Government India in the year 1999. He is co-recipient of nine SPARK transnational awards in Stanford University. He has published over 194 papers with numerous granted/disclosed patents.

 

Abstract:

Parkinson’s disease (PD) is a neurodegenerative disease caused by the death of dopaminergic neurons in the basal ganglia. The golden standard for the treatment of PD is the dopamine (DA) replacement therapy with L-DOPA. DA acts on DA receptors which belong to the superfamily of G Protein coupled receptors (GPCRs). However chronic treatment with L-DOPA results in super sensitivity of DA receptors and unwanted side effects commonly known as L-DOPA induced dyskinesia. Here we screened different formulations of L-DOPA oral route delivery which could result in a slow, sustained and timely delivery of L-DOPA along with repurposed GPCR receptor antagonists that can up regulate two of the G protein coupled receptor kinases GRK3 and 6 in brain that are down regulated in experimental animal models of PD. Our in vitro data in striatal neuronal culture in the presence of DA and GPCR receptor antagonists showed an upregulation of GRK3 and 6 after 24 hours of treatment at lower doses of DA. The behavioral studies in unilateral PD mice with DOPA formulations showed oral delivery of DOPA relieved the akinesia seen in Parkinson’s disease and at the same time had less dyskinetic effects as revealed by mouse cylinder test and AIMS respectively. Together our behavioral and signaling data demonstrate that L-DOPA delivered orally in a sustained release form along with the peripheral DOPA decarboxylase inhibitors carbidopa and benserazide could relieve the dyskinetic effects due to L-DOPA therapy in Parkinson’s disease.

  • Epidemiology of Parkinson Disease | Neurocognitive Disorders
Location: Chicago, USA
Speaker

Chair

Srinivasan Avathvadi Venkatesan

M.G.R.Medical University, India

Speaker
Biography:

Míra Ambrus has her experience in biomechanics, aging muscle strength and muscle in the field of sport science. She started to work early in research fields, during her Bachelor degree in Hungary. Then she decided to do her PhD in Spain under the supervision of Drs. Miguel Fernandezdel Olmo and Jose Andrés Sánchez Molina and started to work with patients who have Parkinson’s disease (PD). Her aim is to improve the PD patients’ movements, abilities, quality of life due to training and also to make the life more comfortable due to sport.

Abstract:

Statement of the Problem: Gait disturbances are one of the principal and most incapacitating symptoms of Parkinson’s disease (PD). Few studies have measured the relationship between stride length and cadence (SLCrel) in PD patient point out to a decreased stride length (SL) with a particular difficulty in its internal regulation. Therefore, improvements of SL should represent the main goal in rehabilitation and exercise interventions in PD patients. However, changes in SL must be analyzed together with changes in cadence in order to elucidate which rehabilitation approach has a specific impact in PD rather than a generalized benefit from exercise. Moreover, it is imperative to know whether the SLCrel is a reliable analysis to be used as an evaluation procedure of gait disturbances in PD patients. The purpose of this study is to explore the reliability of the SLCrel in two different sessions separated by three months in a group of PD patients.

Methodology: 35 PD patients have participated in this study. In each session, patients were asked to walk at self-selected preferred, very slow, slow, fast and very fast speeds. SL and cadence were recorded for each speed and for individual linear regression analysis were conducted over those two parameters to determine the individual slope and interception.

Findings: The slope and interception of the SLCrel showed an excellent reliability in a three months period.

Conclusion: SLC reanalysis should be implemented in order to monitor gait changes in PD patients. 

Speaker
Biography:

Azza A Ali has completed her PhD specialized in Pharmacology and Toxicology from Faculty of Pharmacy, Cairo University, Egypt. Her Postdoctoral studies included different scientific aspects especially on neurodegenerative disorders. She has also developed research line of behavioral pharmacology in Egypt. She is member of many scientific societies as (AAPS) and Alzheimer's Association (ISTAART). She is also the Editorial Board Member of many international Journals such as Brain Disorder & Therapy, Acta Psychopathologica, EC Pharmacology and Toxicology as well as Organizing Committee Member at the 7th International Conference on Dementia and Care Practice. She has published more than 50 papers in reputed journals, supervised and discussed more than 80 PhD and MSc thesis and actively participated by oral and posters presentations at many international conferences especially on Alzheimer's disease and Dementia as Dementia Conferences 2015, 2016 and Alzheimer's Association International Conference (AAIC 2016). She has many appreciation certificates and certificate of best presentation award at 19th International Conference on Environmental Pollution and Pollution Control (ICEPPC 2017). Currently, she is the Head of Pharmacology and Toxicology Department at Al-Azhar University, Egypt. 

Abstract:

Background: Parkinson's disease (PD) represents the most common movement disorder which is characterized by progressive degeneration of dopaminergic neurons as well as dysfunction of the basal ganglia. L-DOPA is still the gold standard effective therapy in PD despite the periodic increase of dosage to achieve stable therapeutic effects along with the long-term treatment side effects. Vinpocetine (Vinp) has been used for treatment of cerebrovascular disorders and may be promising as neuroprotective and PD modifier.

Objective: The objective of this study is to evaluate and compare the efficacy of Vinp and/or L-DOPA against rotenone-induced PD in rats as well as the possibility of L-DOPA dosage reduction without compromising the therapeutic effectiveness.

Methods: Rats were divided to normal group and five rotenone (RT) groups. One of RT (2.5 mg/kg) groups served as control PD model while the others were treated with either L-DOPA (10 or 25 mg/kg), Vinp (6 mg/kg) or both Vinp and L-DOPA (10 mg/kg) all for 19 days. Motor and cognitive performances were assessed using catalepsy, open-field and Y-maze tests. Striatal dopamine, norepinephrine, serotonin and acetylcholinesterase as well as mitochondrial complex I, MDA, SOD, TAC, IL-1β, TNF-α, and caspase-3 expression were measured in addition to histopathological examination of different brain regions.

Results: Concurrent treatment with Vinp and/or L-DOPA significantly ameliorated the impairments in locomotor activities and cognition as well as attenuated the depletions in monoamines and mitochondrial complex1 contents. In addition, the elevations in acetylcholinesterase activity, oxidative stress and inflammatory markers as well as caspase 3 expression induced by RT were also decreased. Combination of Vinp with low dose L-DOPA has an equivalent or almost better effect than the higher dose of L-DOPA alone.

Conclusion: Vinp has beneficial motor, cognitive, neurochemical effects and represents a promising adjuvant to L-DOPA therapy that can be translated into a serious reduction of its therapeutic doses and consequently reduction of the long-term therapy side effects. Consequently, Vinp could be recommended as a disease-modifying therapy of PD especially when given early with L-DOPA. 

  • Special Session by: Srinivasan Avathvadi Venkatesan
Location: Chicago, USA

Session Introduction

Srinivasan Avathvadi Venkatesan

DR.M.G.R.Medical University, India

Title: Motor sensory stimulation (Modulation) in Parkinsonism
Speaker
Biography:

 A.V. Srinivasan is the President of Indian Academy of Neurology and also he is the emeritus Professor of The Tamilnadu DR.M.G.R.Medical University. · Dr A V Srinivasan, driven by his quest for excellence and the latest discoveries on human brain related disorders, joined Madras Medical College (MMC) and received MD(General Medicine) in 1978.Later he pursued and received DM in Neurology from his alma mater.He is First Neuro physician of his state Tamil Nadu in India in government service to be conferred, the Fellow of the Royal College of Physicians (FRCP) in London in 2012, fellowship of the Indian Academy of Neurology 2004 and fellowship by the American Academy of Neurology, in 2003.He Is the First Indian to receive American Indian Neurology Award (AINA) in USA in 2001, for the best paper presentation IN STROKE during annual American Academy of Neurology meeting in 2001 in PHILADELPHIA. ByTheTamil Nadu DR. MGR Medical University. Currently serving as a Member –in the ACADEMIC COUNCIL of National institute of Mental health and Neurosciences, Deemed University, Bangalore. 

Abstract:

Parkinsonism is a neurodegenerative disorder characterized by a progressive loss of midbrain dopaminergic (DA) system. Subsequent reduction in striatal dopamine results in various clinical manifestations with Tremor, Rigidity, Bradikinesia and Postural defect. The term Motor Sensory stimulation (Modulation) encompasses a broad range of treatments, both electrical and chemical, targeting various locations in the Brain and the body to achieve the desired results. Deep brain stimulation (DBS) is a Neurosurgical treatment used in Parkinsonism and other conditions. Electrical stimulation at high frequency in precise locations of the brain results in the restoration of the balance of the circuits that are disrupted in Parkinsonism (Parkinson Disease).  Stimulation in high frequency of the sub thalamic nucleus has now become a standard Neuro Surgical therapy in Parkinson disease. Transplantation of fetal dopaminergic (DA) neurons also produces symptomatic relief. The technical and ethical difficulties in obtaining sufficient and appropriate donor fetal brain tissue are the limitations in the application of this therapy. Neural precursor cells and embryonic stem (ES) cells are going to be the potential donor cells for transplantation.In the mid-1990s, creation of targeted holes in specific areas of the brain or Lesioning were the main approaches.Repalement Cell therapy was tried in some cases..  Transcranial Magnetic Stimulation (TMS) is a non-invasive way of stimulating the brain, have also shown benefit in Posture and gait in some patients of Parkinson Disease. This targeted Stereotactic thalamotomy of the thalamic nucleus ventralis intermedius (VIM) is routinely used for bilateral extrapyramidal movement disorders. This targeted neuromodulator therapies can avoid the side effects. They are easily reversible if and when occurs, they can give an important degree of therapeutic effect in patients

This communication addresses the mainly Deep Brain Stimulation,Transplantaion and Stem Cell therapy  and its Frontiers of the Neurophysiological basis,technical,ethical considerations and its Therapeutic effects in Parkinsonism, Tremor and Dystonia  patients.  

  • Pathophysiology, Pharmacology | Parkinsons Disease Complications | Diagnosis for Parkinson Disease
Location: Chicago, USA
Speaker

Chair

Rajendra D Badgaiyan

University of Richmond, USA

Speaker
Biography:

Aimee J Nelson is an Associate Professor in the Department of Kinesiology at McMaster University. She has completed her PhD at the Institute of Medical Sciences at the University of Toronto. Her first post-doctoral appointment at the McGovern Institute for Brain Research, MIT, and second post-doctoral appointment at Toronto Western Hospital. Her academic appointment began in 2008 at the University of Waterloo and she subsequently joined McMaster University in 2012 as a Canada Research Chair, Tier 2. Her research is in basic neurophysiology and neuroimaging and her research has application in neurological injury and disease wherein hand/arm control is impaired. 

Abstract:

Individuals with Parkinson’s disease (PD) demonstrate abnormalities in somatosensory perception and physiology. Impairments in tactile acuity are well documented for both temporal and spatial perception, and physiological changes are also apparent. Identifying and understanding the origin of somatosensory abnormalities will aid in the treatment of PD. The present research investigates the physiological changes in primary somatosensory cortex that accompany PD, and relates these findings to alterations in brain circuits that mediate sensorimotor integration and tactile perception. Ten individuals with PD were studied on dopaminergic medications and following overnight withdrawal. Data were compared with that obtained from 10 aged-matched healthy controls. Using functional magnetic resonance imagining (fMRI) at 3T, stimulation was delivered to digits 2 and 5 of the most affected hand in PD and left hand in controls. Tactile spatial acuity was assessed using JVP domes. Somatosensory-motor integration was assessed by evoking the short- and long-latency afferent inhibition circuit using transcranial magnetic stimulation. Results indicate that PD exhibit deficient activation of somatosensory cortex, somatosensory-motor integration and impaired tacitile acuity relative to controls. Further, dopaminergic medications yield differential responses in sub-regions of the primary somatosensory cortex. These data provide support for the emerging body of literature demonstrating physiological abnormalities in somatosensory processing in PD that may contribute to the pathology of the disease. Changes in somatosensory processing may provide an explanation for sensory symptoms in PD. Activity in somatosensory cortex is modulated by dopaminergic medications and these changes may contribute to improvements in PD symptoms that occur with dopaminergic treatment.

Speaker
Biography:

John M Baumann inspires and helps real people to live their lives to the fullest, and even embrace their life-changing event, with the goal of uncovering their life’s purpose. He is an internationally-recognized inspiring success speaker. In 2002, working as the top attorney for a public company, he was diagnosed with Parkinson’s disease. From 2005 until 2014, he taught law at the College of Business at the University of Louisville to over 1,000 undergraduates. He was selected the Most Inspiring Professor. He wrote a book entitled, “Decide Success - You Dead Yet”. He earned his Juris Doctorate degree from Cornell Law School after graduating Summa Cum Laude with a Bachelor’s Degree in Business Administration from the University of Massachusetts, School of Management. As an attorney, he has passed the bar and practiced law in Texas, Louisiana and New Jersey before becoming General Counsel of a NASDAQ listed corporation headquartered in Kentucky.

Abstract:

My target audience is all medical personnel. The purpose of this Presentation is to encourage medical personnel who treat those diagnosed with a life-changing condition to go beyond the clinical role and discuss with their patients the importance of: Keeping or, if the disease has caused them to take on a negative attitude, reclaiming a positive perspective, uncover their purpose and staying engaged in whatever they can still do that they love to do using the twelve decide success principles.

Speaker
Biography:

Harish C. Pant received his M.A. and Ph.D. degrees in Physics from Agra University, Agra, India. His postdoctoral studies were conducted on the mechanisms of electron and ion transport in model membrane systems at the Department of Biophysics at Michigan State University. He joined the Laboratory of Neurobiology in the NIMH as a senior staff fellow in 1974 with Dr. Ichiji Tasaki where he studied the function of the axonal cytoskeleton in the squid giant axon. In 1979 he moved to the NIAAA extending his studies on the neuronal cytoskeleton and the effects of alcohol on its regulation. Dr. Pant moved to the NINDS, Laboratory of Neurochemistry in 1987 where he is presently chief of the section on Cytoskeleton Regulation.

Abstract:

Besides the hallmark pathology of aggregated phosphorylated neuronal intermediate filament proteins it has been now well documented that cyclin-dependent kinase 5 (Cdk5), a critical neuronal kinase in nervous system development, function and survival, when deregulated and hyper activated induces AD, PD and ALS like phenotypes in mice. Under physiological conditions, Cdk5 activity is tightly regulated. The deregulation and hyper activation of Cdk5/p25 induces neuropathology. Thus, Cdk5/p25 becomes prime therapeutic target for AD and neurodegenerative diseases associated with the hyper activation of Cdk5. In order to prevent hyper activation of Cdk5/p25, we have designed several small peptides of p25 on the basis of Cdk5/p25 crystal structure and checked for competition with p25 and thus inhibiting selectively the hyperactivity of Cdk5, we discovered a small peptide (p5) comprising of 24 amino acids, inhibited Cdk5 hyper activation. The modification of p5 to TFP5 crosses blood brain barrier (BBB), which was tested in a transgenic AD, PD & ALS models. Post TFP5 injections in AD, PD and ALS model mice displayed significant reduction in Cdk5/p25 hyperactivity, neuroinflammation and hyperphosphorylation of cytoskeletal proteins, along with various behavioral rescues. TFP5 does not inhibit normal Cdk5/p35 activity, and therefore has no toxic side effects. In addition, treated mice rescued synaptic dysfunction and a reduction in phospho-neuronal intermediated neurofilaments and neuronal cell death. These results indicate that TFP5 and TP5 have a potential to be a therapeutic target for AD, PD and ALS neurological diseases.

Speaker
Biography:

Kohji Fukunaga first discovered calcium/calmodulin-dependent protein kinase II (CaMKII) from brain. He received his PhD degrees from Kumamoto University School of Medicine in 1985. During 1988 to 1990, he worked as research fellow in Vanderbilt University (HHMI) under Professor TR Soderling. In 2002, he was appointed a Professor and Chairman in the faculty of graduate school of pharmaceutical sciences. He was Editor-in-Chief of Journal of Pharmacological Sciences (Elsevier) since 2012. He is interested in disease-modifying drug development for neurodegenerative disorders and psychiatry diseases such as autism and mental retardation.

Abstract:

Parkinson's disease (PD) patients frequently reveal deficit in cognitive functions during the early stage in PD. The dopaminergic neurotoxin, MPTP-induced neurodegeneration causes an injury of the basal ganglia and is associated with PD-like behaviors. In this study, we demonstrated that deficits in cognitive functions in MPTP-treated mice were associated with reduced calcium/calmodulin-dependent protein kinase II (CaMKII) autophosphorylation and impaired long-term potentiation (LTP) induction in the hippocampal CA1 region. Mice were injected once a day for 5 days with MPTP (25mg/kg i.p.). The impaired motor coordination was observed one or two week after MPTP treatment as assessed by rota-rod and beam-walking tasks. In immunoblotting analyses, the levels of tyrosine hydroxylase protein and CaMKII autophosphorylation in the striatum were significantly decreased 1week after MPTP treatment. By contrast, deficits of cognitive functions were observed three-four weeks after MPTP treatment as assessed by novel object recognition and passive avoidance tasks but not Y-maze task. Impaired LTP in the hippocampal CA1 region was also observed in MPTP-treated mice. Concomitant with impaired LTP induction, CaMKII autophosphorylation was significantly decreased three weeks after MPTP treatment in the hippocampal CA1 region. Finally, the reduced CaMKII autophosphorylation was closely associated with reduced AMPA-type glutamate receptor subunit 1 (GluR1; Ser-831) phosphorylation in the hippocampal CA1 region of MPTP-treated mice. Taken together, decreased CaMKII activity with concomitant impaired LTP induction in the hippocampus likely account for the learning disability observed in MPTP-treated mice.