Scientific Program

Day 1 :

Keynote Forum

Simon Hooper

CEO RemindMeCare (ReMe)

Keynote: New trends in the use of digital interventions: Digi therapeutics and Digi pharma in care

Time : 10:00 - 10:40 AM

Biography:

A co-founder of RemindMeCare, Simon Hooper has a tech background that is non-medical but which he has brought to bear on the care process, courtesy of his experience with the care needs of his family. Supported by academia and health care professionals, ReMe is the result of extensive work in numerous care settings. The company has worked closely with care facilities, day care centers and hospitals to create systems that are directed at improving care delivery.

 

Abstract:

Technology’s causing treatment paradigms to be reconsidered.. Previously, it was almost impossible to match treatment with cognitive and behavioral changes. Now Digital Therapeutics and Digiceuticals enable more flexible treatment and monitoring alternatives.Digital Therapeutics is defined as immersive programs that act reliably and remotely to change individual’s behaviors to achieve positive clinical outcomes and reduce medical cost growth. They’re often used in conjunction with medication but may replace conventional prescribing.Digi Pharma is consumer focused, such as nutritional supplements. They’re typically not reimbursed, FDA/NHS authorized and low priced, with consumers paying directly after marketing discovery.So where does ReMe fit in? ReMe discovers personal content through interactive response to activities, that positively impacts on behavior and calms agitation, reducing or complimenting the use of medication. ReMe achieves improved wellbeing, shows a propensity to support cognitive retention and recall and can be used in therapy and acute care strategies. So, in terms of definition, ReMe falls into both categories, subject to the deployment used.Current studies in Kingston Hospital, London, aim to establish ReMe’s potential to reduce medication, improve admission processes, enhance person centered care, as well as achieve efficiency and cost savings through digital reporting, reduced staffing, earlier discharge and optimal step down.If it can be shown that ReMe’s digital intervention achieve these outcomes then this dual role of Digi pharma in the community and  Digi therapy in the formal care setting, warrants ReMe being prescribed either as a supplement or alternative to traditional medication.The impact of digital prescribing on cost savings could be substantial and as a result business payment models will be developed that fit the new treatments. Answers will come when the evidence is there. ReMe offers an insight into what one new treatment configuration of the future could look like.

 

Keynote Forum

Markku Kurkinen

Professor Wayne State University School of Medicine USA

Keynote: Alzheimer's drug discovery: targeting synaptic glutamate signaling

Time : 10:40 AM to 11:20 AM

Biography:

Born October 8, 1949, Mikkeli, Finland. 1979 PhD, University of Helsinki, Finland. 1980-1983 postdoctoral work with Brigid Hogan, Imperial Cancer Research Fund (ICRF), Mill Hill London, UK. 1984-1985 Assistant Professor, University of Medicine and Dentistry of New Jersey (UMDNJ), Rutgers Medical School, Piscataway, New Jersey, USA. 1985-1992 Associate Professor, Chief of Connective Tissue Research, UMDNJ, Robert Wood Johnson Medical School (formerly Rutgers Medical School), Piscataway, New Jersey, USA. 1992 - Professor, Wayne State University School of Medicine, Detroit, Michigan, USA. Published work on Matrix Biology,molecular cloning, and gene regulation. Present researchinterests in novel drug discovery methods, targeting astrocyte regulation of synaptic glutamate signaling in developmental and neuropsychiatric brain disorders.

 

Abstract:

Glutamate, a non-essential amino acid, is the signaling molecule of neurons. Glutamate is neurotoxic. As soon as the glutamate signaling starts it is stopped in 0.1-2 ms by astrocytes, which take up and clear glutamate from synapses. This prevents too much glutamate causing impaired synaptic function and loss of neurons. Astrocytes make EAAT2 (excitatory amino acid transporter-2), the major glutamate transporter and 1% of brain protein. In Alzheimer dementia, astrocytes express less EAAT2. In experimental mouse models of Alzheimer, increasing EAAT2 expression slows dementia progression. To discover drugs that can activate EAAT2 in glutamate uptake, I describe a simple assay that targets the EAAT2 protein reconstituted in liposomes and measures glutamate uptake with fluorescent Oxonol VI red light. Importantly, by direct targeting the EAAT2 protein in liposomes, the assay should limit ‘off-targeting’ of drugs and adverse events, which are the main problems in Alzheimer’s drug discovery and clinical development. 

 

Keynote Forum

Joe Sam Robinson

President Georgia Neurosurgical Institute Georgia, USA

Keynote: Cervical Stenosis-Induced Chronic CSF Flow Obstruction as a Contributing Cause of Dementia

Time : 11:20 to 12:00

Biography:

Dr. Robinson is President of Georgia Neurosurgical Institute, Professor and Chief of Neurosurgery at Mercer University, Clinical Professor of Neurosurgery at Medical College of Georgia, and an author of over 100 peer review articles.

 

Abstract:

Statement of the Problem: Obvious CSF flow obstruction is a well-established acute and subacute cause of dementia. Unfortunately, the less-obvious vagaries of CSF production and absorption remain relatively unexplored and, logically, could play a role in neuronal destruction. The Purpose of this Study: The purpose of the study is to demarcate processes (particularly cervical stenosis) by which restricted (often episodic), CSF circulation subtly damages neuronal tissue, and to propose studies and arrangements to track and prevent the onset of such difficulties. Methodology and Theoretical Orientation: To assess the impact of recent new understandings of CSF flow dynamics, and on the possible etiology of dementia, a substantial literature review was conducted, and new suggestions proposed. Findings: A systematic literature review suggests the elevated prevalence of cervical stenosis, concomitant CSF flow obstruction and dementia, in an elderly population. The literature further suggests that cervical stenosis can significantly, often discreetly, compromise CSF circulation, thereby injuring neuronal tissue by direct untoward pressure, by restriction of cerebral CSF bulk flow retarding beta-amyloid clearance, and by ventricular ependymal cell damage allowing trans-ependymal CSF flow neuronal damage. Moreover, such restriction could contribute to the development of sleep apnea, thereby causing concomitant respiratory and circulatory dysfunction, promoting the development of a vicious cycle in which widespread direct neuronal injury as well as further increase in ICP occurs. Conclusion & Significance: We conclude that, among other obstructive possibilities, cervical stenosis could play a role in the development of dementia. Recognition of subtle, chronic CSF alterations (in some ways comparable to chronically abnormal blood pressure) calls for the development of, preferably non-invasive, technology to measure CSF circulation on a 24-hour basis. If the parameters of episodic abnormalities could be better adjudicated, prevention of such events could reasonably be effectuated by cervical decompression, therapeutic drug regimen, and altered sleep position.

 

  • Alzheimer Disease | Causes and Risk Factors | Recent Advances in Dementia Diagnosis |

Session Introduction

Brian H. Tran

Medical Director NeuroActiva, Inc. USA

Title: Lessons learned from the failure of Alzheimer drug development over the past 20 years.
Speaker
Biography:

Brian Tran, MD the Medical Director and Lloyd Tran is the CEO of NeuroActiva, a clinical-stage biopharmaceutical company dedicated to the discovery, development, and commercialization of new drugs to treat Alzheimer’s disease. 

Abstract:

There are more than 5.5 million people in the US and 43 million people worldwide that have Alzheimer’s disease in 2017. Growth in the prevalence of Alzheimer’s disease (AD) over the next few decades is anticipated to result in great pressure on the social and health-care systems of developed and developing economies alike. The current treatment options are considered to be symptomatic.  There is an unmet need for therapies that halt or substantially slow disease progression. There were no new drug approvals for treatment of AD; none have been approved in the USA since 2003. Over the past 20 years a majority of failed AD drugs were based on the guiding principle of the Amyloid hypothesis, which postulates that accumulation of amyloid plaques trigger a cascade that harms neurons and synapses.  Most immunotherapy drugs based on β-secretase, γ-secretase, and  stimulators of α–secretase have been used to target Aβ  pathology include decreasing of Aβ  production, preventing aggregation of, or stimulating clearance of Aβ.  We will highlight a new non-amyloid approach in the development of a new drug in Phase 2 known as NA-831, a novel neuroprotective and neurogenesis agent, for treatment of Alzheimer's disease. The lesson learned from the past AD drug development failure and a new clinical strategy for the development of NA-831 will be presented and discussed.  

Speaker
Biography:

Francesca Pistollato, Ph.D., currently works at the European Union Reference Laboratory for Alternatives to Animal Testing (EURL ECVAM) Joint Research Centre in Ispra (Italy), where she develops and supports the use of alternatives to animal testing in toxicology and regulatory testing and in biomedical research. She previously worked at the Physicians Committee for Responsible Medicine (PCRM), Washington DC, advocating for the use of a holistic, human-based approach for Alzheimer's disease research. Dr. Pistollato holds a master degree in nutrition and dietetics and published several works on the role of nutrition and lifestyle-related factors in the prevention of chronic degenerative diseases, such as Alzheimer's and dementia.  

 

Abstract:

Animal models of Alzheimer's disease (AD) have been extensively utilized in the last few decades in an effort to elucidate the pathophysiological mechanisms of the disease and to test novel therapeutic drugs. However, basic/fundamental and pre-clinical research successes have not translated into effective therapeutic treatments for AD patients. One of the possible reasons behind this translational failure may be the overreliance on animal models for AD, which have been shown useful to recapitulate some AD-associated features, such as amyloidosis and tauopathy, but have failed to deliver effective treatments for AD patients. On the other hand, the use and the implementation of human-based investigational methods, non-invasive neuroimaging technologies, and large scale epidemiological data set repositories, may contribute to the development of new preventive and treatment strategies. Here we present the challenges and opportunities in AD research and propose how we can mitigate this translational barrier by employing human-based methods to elucidate disease processes occurring at multiple levels of complexity (from gene expression to protein, cellular, tissue/organ to individual and population level). Novel human-based cellular and computational models are already being applied in toxicology and regulatory testing, and could be associated with noninvasive neuroimaging tools and epidemiological data to facilitate human-relevant data discovery.A paradigm shift towards human-based research, accounting for a multi-dimensional and multi-disciplinary approach is highly needed to tackle the ever-increasing prevalence of AD in the 21st century.

 

Speaker
Biography:

Smriti Gupta has research focus on glial-neuronal crosstalk to understand the pathophysiology of Alzheimer’s disease using glial-neuronal coculture (cellular) as well as in vivo model system. This study involves the metabolic basis behind the etiology of sporadic Alzheimer’s disease and provides the pathophysiological status of different metabolic pathways such as insulin signaling pathway, glucose uptake and cerebral energy homeostasis. Research findings indicated that under disease condition, glial cells make neuronal cells more vunerable for disease onset and progression. This study provided the clue for several potential molecules which can be considered as potential therapeutic targets.

 

Abstract:

Sporadic Alzheimer’s disease (SAD) is a progressive neurodegenerative disorder with dysfunctional insulin signalling and energy metabolism. Growing evidence supports that impairment in brain insulin responsiveness, glucose utilization and energy metabolism may be a major cause of amyloid precursor protein mishandling. A support for this notion comes from the studies where streptozotocin (STZ) induced brain insulin resistance in murine model, resulting into the SAD like brain pathology with cognitive decline. Intriguingly in vitro models have been used to understand the metabolic basis of SAD. However mechanistic effects of brain insulin resistance on neurons and glia are not well understood. To understand the status of insulin signalling pathway, glucose uptake, glucose metabolism and energy homeostasis, STZ induced glial-neuronal co-culture model of SAD has been established. Present study suggests that glial cells are more compromised for insulin signalling than neurons. The evidence has been supported by glial activation in co-culture SAD model system.  These changes were found to be correlated with amyloid deposition in this cellular model system which indicates that insulin signalling in glia may be a major regulator of amyloidogenesis in SAD brain.

 

Speaker
Biography:

Experienced Psychiatrist with a demonstrated history of working in the medical practice industry. Skilled in Clinical Research, Epidemiology, Medicine, Clinical Trials, and Research. Strong healthcare services professional with a Fellowship focused in Cognitive Neurology and Dementia from EskiÅŸehir Osmangazi University.

Abstract:

Cognitively impaired patients especially with Alzheimer’s disease (AD) can be successfully screened using cognitive screening tools especially in combined versions and best specificity was observed with the combination of the MMSE (Mini-Mental State Examination) and CDT (Clock Drawing Test) in patients with AD. But some disadvantages are observed like as insensitivity to the earliest changes in highly educated individuals or insensitivity to mild AD. Test Your Memory (TYM) introduced as an alternative for common tests in this filed specially in order to meet the criteria of minimal operator time to administrate, test a reasonable range of cognitive functions and to be sensitive to mild AD that makes it unique in this era.100 subjects were recruited for the study from patients referred to our dementia clinic between December 2015 and August 2016. In addition to history taking and general physical examination, specialized neurological examination and structured psychiatric interview was done by specialized neurologist and psychiatrist in the field of dementia. Also laboratory workup, neuroimaging and neuropsychological assessment using MMSE, CDT and TYM-TR was completed in all patients. In this study we compared equivalent cognitive domains in Test Your Memory – Turkish Version (TYM-TR) neuropsychological test with the same domains in the Mini Mental State Examination (MMSE) test in previously clinically diagnosed demented patients according to DSM-5.The analysis of sub-scores of equivalent cognitive domains using paired T-Test demonstrated that there are significant differences in detecting cognitive deficits in registration, recall and visuospatial (only in Letter M drawing item) domains between two tests and the TYM-TR test is more sensitive in detecting cognitive deficit in the mentioned cognitive domains than MMSE test. Also according to Pearson Correlation there are significant relationships between all equivalent cognitive domains.There is emerging need to replace MMSE with some more efficient screening tools for early diagnosis of subtle neurocognitive changes in highly educated patients. TYM-TR is suitable screening tool in detecting subtle cognitive deficits in early stages of neurocognitive disorders. More complex screening tests can eradicate the ceiling effect of more simple tests but they have more floor effect in encountering with sever demented patients. Comparing these two test with more detailed neuropsychological batteries could highlight the limitations of complex and simple tests in various situations.

 

  • Treatment Modalities | Awareness and Care Practices | Case Reports

Session Introduction

Sherin Yohannan

National Institute of Mental Health and Neurosciences,India.

Title: Psychosocial support for families of persons with dementia through home based care program from a developing country
Speaker
Biography:

Ms.Sherin Yohannan, PhD scholar in the department of Psychiatric Social Work, NIMHANS, Bangalore, India. My research area is on Dementia care. I completed my M.Phil. in Psychiatric social work from NIMHANS in 2015 and my dissertation was on stress, burden, social support and desire to institutionalization among caregivers of persons with dementia.I have completed my Masters in Social Work with the specialization in Medical and Psychiatric Social Work from BCM College, India in the year 2012.  
 

Abstract:

Among older people, dementia is the leading chronic disease contributor to disability and need for care. In India, person with dementia continue to live with their families. Dementia care is usually a joint effort by the adult members of the family who stay in the same household (Dementia India report, 2010). In this background, this study proposes to promote a healthy adjustment of the family to the disease, improving quality of life and encouraging the link between family and formal support systems through a multi component home based family care program for the families. The objective of the study is to develop a home based care program for the families of person with dementia and to assess the impact of the programme. The study design is Quasi-experimental design – pre and post assessment without control group. 40 caregivers of dementia patients undergoing treatment from the Geriatric Clinic outpatient department  of National Institute of Mental Health And Neurosciences, Bengaluru were taken through random sampling method.Socio-demographic sheet used to assess background information, The Perceived Stress Scale, Multidimensional Scale of Perceived Social Support, The Zarit Burden Interview and a Self-constructed questionnaire administrated at baseline and post intervention.Intervention modules developed through extensive literature review, opinions and views from field experts, organizations involved in the community and home based care and the family members of patients with dementia. Psychosocial intervention module for home based care programme covers the psychological, social and general health aspects in the broader term based on the family centred participatory and integrated approach. Results showed that home based programme was effective for the caregivers in reducing their unhealthy adjustments, stress and burden by increasing the awareness in caregiving process and meeting their personal and emotional needs. The quality of care for the dementia patients has enhanced through the improvement of physical, social and psychological wellbeing of caregivers. In conclusion, Communitybased care, preferably at home would be ideal, and evidence in support of such care is accumulating.With adequate training, these programs can even be offered by health and welfare sector personnel in the community.