Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 5th International Conference on Alzheimer’s Disease & Dementia London, UK.

Day 1 :

Keynote Forum

Claude M Wischik

Claude M Wischik, TauRx Therapeutics, UK

Keynote:

Time : 09:00-09:40

Conference Series Dementia 2016 International Conference Keynote Speaker Claude M Wischik photo
Biography:

Claude M Wischik holds the Chair in Old Age Psychiatry at the University of Aberdeen in Scotland, and is Executive Chairman of TauRx Pharmaceuticals. He studied medicine in Australia, completed his PhD at the Laboratory of Molecular Biology in Cambridge, and also higher psychiatric training in Cambridge. He was the first to identify Tau protein as the main constituent of the Alzheimer tangle and developed the first Tau Aggregation Inhibitors. He has published 121 papers and holds 11 patent groups based on his work with over 40 individual patents.

Abstract:

Keynote Forum

Jerzy Leszek

Jerzy Leszek, Wroclaw Medical University, Poland

Keynote: Dendrimer’s –New hope in the treatment of Alzheimer’s disease

Time : 09:40-10:20

Conference Series Dementia 2016 International Conference Keynote Speaker Jerzy Leszek photo
Biography:

Jerzy Leszek is Professor of Psychiatry, Vice-Head of the Department of Psychiatry and Head of Alzheimer’s Disease Lab at the Medical University in Wroclaw, Poland. He graduated at Medical University of Wroclaw in 1979, was awarded a doctorate in Wroclaw in 1981 and in 1999- examination for the degree of associate professor of psychiatry and since 2007 he is working as full professor of psychiatry at Wroclaw Medical University. He is author and co-author more than 280 papers (especially from old age psychiatry), some chapters to the books published in reputed Polish and international journals and serving as an editorial board member of several journals.

Abstract:

The lack of effective treatment for Alzheimer’s disease(AD) stems mainly from the incomplete understanding of AD causes. Currently there are several hypotheses which try to explain the early molecular mechanisms of AD pathogenesis. Nanomedicine as a biomedical and pharmaceutical application of nanotechnology for making nanocarriers like dendrimers has shown great potential for the treatment of many CNS diseases. Dendrimers are polymeric molecules chemically synthesized with well defined shape size and nanoscopic physicochemical properties reminiscent of proteins. Recently an increasing number of studies have been focused on the potential of dendrimers to prevent aggregation and fibrillation of proteins involved in neurodegenerative disorders such as AD. Some of dendrimers were demonstrated to cross blood-brain barrier, which legitimized research on these compounds as potential drugs for neurological disorders. Recent our studies have revealed that dendrimers possess the intrinsic ability to localize in cells associated with neuroinflammation(activated microglia and astrocytes) and thus can be used as drug carriers in neuroinflammation therapy. Above/mentioned findings may be of high significance in the context of potential application of dendrimers as drug carriers or active compounds per se. According to the opinion the author’s of this presentation ,they are promising macromolecules for further investigations on their applicable in neurodegenerative disorders , for instance AD.

Keynote Forum

Jordan L Holtzman

University of Minnesota, USA

Keynote: Alternative Models for Drug Discovery in Alzheimer’s Disease

Time : 10:20-11:00

Conference Series Dementia 2016 International Conference Keynote Speaker Jordan L Holtzman photo
Biography:

Jordan L. Holtzman, M.D., Ph.D. is Professor, Departments of Pharmacology and Medicine and Division of Environmental Health Sciences, University of Minnesota, Minneapolis, USA. He was graduated from University of Chicago, the Pritzker School of Medicine in 1959. He completed internship from University Ill Rsc/Ed in 1960.

Abstract:

Alzheimer’s disease is described as a progressive dementia associated with the extracellular deposits in the brain of a garbage protein, β-amyloid (Aβ), and the intracellular deposits of tangles. The vast majority of the patients develop the disease in old age while a small portion have an early onset, familial form. Since the 1970’s it has been generally assumed that the dementia seen in the two forms is due to the neurotoxicity of the Aβ. With the purification and sequencing of Aβ in the 1990’s investigators were able to identify the mutations associated with the familial forms. A number of laboratories transfected mice with these mutated genes. Since these animals exhibited many of the pathological and clinical manifestations of the late onset disease, they have been used to screen for new therapeutic agents. Unfortunately, all 244 drugs identified in these models have failed in clinical trials in elderly patients. Work from my laboratory has suggested that plaque deposits of Aβ rather than causing the dementia is merely a biomarker for a decline in the capacity of the endoplasmic reticulum (ER) in the cells to catalyze the posttranslational processing of 40% of cellular proteins, including those synaptic, membrane proteins required for a functioning memory. This paradigm is based on our observation that in the CSF all Aβ is normally N-glycosylated and bound to ER proteins, ERp57 and calreticulin. These data suggest a new direction for drug discovery in which agents are screened for their ability to increase the levels in cell lines of fluorescently labeled components of the ER post-translational pathway. The development of these cell lines would permit rapid screening for potential therapeutic agents in plate readers.

  • Causes and Prevention and Managing Dementia
Location: Hall 4

Chair

Claude M Wischik

TauRx Therapeutics, United Kingdom

Co-Chair

Jerzy Leszek

Wroclaw Medical University, Poland

Session Introduction

Claire Henry

Lourdes Memory Center, USA

Title: Managing behavioral disturbance with the dementia client through Person-centered care model

Time : 11:20-11:40

Biography:

Claire Henry, Lourdes Memory Center Director whose aim is to enhance the quality of life for those individuals with Alzheimer’s and other related behavioral diseases. Responsibilities include managing and coordination of all staff within the memory care unit; evaluating clinical service functions to provide optimum care for each individual resident within the Lourdes Center. Emphasis has been on developing partnerships with families and creating tailored resident care profiles which promotes the highest quality of care for each resident. Functions as an accomplished healthcare educator with demonstrated ability to teach, motivate clinicians, physicians and educators, while maintaining high interest and achievement. Articulate communicator who effectively interacts with diverse  populations of healthcare professionals at a variety of academic levels.

Abstract:

Background: Person-centered care models regarding dementia care has demonstrated positive outcomes for behavioral disturbance.However, leadership, guidance and training on bringing this model into practice is lacking in our health care delivery system. The intent is to increase awareness and understanding about person-centered care for people with dementia. Discusses the complex needs of people with dementia, leading to compromised behavioral symptoms. Discussion includes sleep-wake-cycle disturbance, verbal outbursts and aggression. Further discussion encompasses evidence based outcomes with the use of Person-Centered Care that focuses on preserving the “personhood” of the individual.
 
Objectives:The learner will understand the role of Person Center Care for the dementia client. The learner will identify the difference between Person Centered Care and Task Centered and the significance of moving towards a Person Centered Approach to dementia care. Learners will develop necessary tools to manage challenging behaviors, and how Person Centered Care model can directly impact escalation of behavior symptoms. Learners will recognize that all behavior is a form of communication. The learner will develop necessary skills on communication techniques with the dementia client.

Biography:

Michaela Defrancesco has completed her university education in medicine and PhD in neuroscience in 2013 at the Innsbruck Medical University and finished her psychiatric residency in 2015. She is the head of the memory clinic of the psychiatric department of the University Clinic of Innsbruck. Her scientific work focuses on early signs and predictors of conversion from Mild cognitive impairment to Alzheimer´s disease.

Abstract:

Background: Mild cognitive impairment (MCI) has been suggested to represent a prodromal stage of dementia and confers a high risk for conversion to Alzheimer´s disease (AD). In this study, we examined the predictive value of depressive symptoms and neuropsychological variables on conversion of MCI to AD.
 
Methods: Our sample consisted of 260 MCI patients seen at the Psychiatric Memory Clinic of Innsbruck between 2005 and 2015. Neuropsychological and clincal data of the baseline and at least one follow-up visit were collected retrospectively. Depression was assessed using the Geriatric Depression Scale (GDS). Univariate and logistic regression analyses were performed.
 
Results: Of the 260 patients (mean age 71.5±7.7 years) 83 (32%) converted to AD within a mean follow-up time of 3.2± 2.2 years. The univariate ananlysis showed higher age and GDS score and lower MMSE, verbal memory, Boston naming and Clox I test scores at baseline in converting MCI compared to stable MCI patients. However, logistic regression analysis revealed solely depression, MMSE and verbal memory scores as significant predictors of imminent conversion from MCI to AD.
 
Conclusion: Our results support the previously reported predictive value of deficits in verbal memory and lower MMSE scores in the progression of AD. In addition, we found a strong negative influence of depression on MCI patients before imminent conversion to AD. These results emphasise the importance of depressive symptoms in early stages of AD and their possible impact on conversion from MCI to dementia stage.

 

Biography:

Abstract:

An estimated 90,000 people have dementia in Scotland in 2016 (Alzheimer Scotland, 2016). Two thirds of people with dementia live in the community while one third live in a care homes in UK (Alzheimer Society, 2014). The term stress and distress in dementia refer to the behavioural and psychological symptoms found to be present in people with dementia (Lee et al, 2004). 90% of people with dementia will experience these symptoms at some point (Robert et al, 2005).Psychotropic drugs are often inappropriately used to control these symptoms in spite of documented side effects of these drugs (Banerjee, 2009).The aim of this study is to explore the prescribing dynamics in care homes and assess the reason for prescribing psychotropic drugs in stress and distress; followed by development of an intervention to reduce the use of these drugs. The primary objectives are to explore staff awareness of stress and distress in dementia, their knowledge about the indications and side effects of psychotropic drugs. Secondary objective is to develop a staff training/education package. The research will be mixed methods pre- and post-test study method. Quantitative data will be looking at the prescription rates of psychotropic drugs in care homes and measuring the knowledge and attitude of care staff towards stress and distress. Qualitative data will be collected by semi structured interviews to explore the objectives. An educational intervention to promote the use of alternative non-pharmacological interventions will be developed and tested. The outcome of the intervention will be evaluated by monitoring prescriptions trends. Further, this is a unique study as nurse’s attitude towards psychotropic drugs will be deeply explored. The Theory of planned behavior is followed as the theoretical framework and will be used to change attitude and behavior of care staff to use of psychotropic drugs. Following the themes identified, targeted intervention will be developed to act on the barriers of use of non-pharmacological management of stress and distress.

Biography:

Lawla Law has been graduated from the Hong Kong Polytechnic University as an Occupational Therapist and practiced for about 25 years with extensive experience in acute and community settings in Hong Kong and Australia. She completed her PhD from the James Cook University in Australia and has changed to work in academics since 2014. Presently she has been working as an Assistant Professor at the Tung Wah College in Hong Kong where she has continued her research. Her research interests are in Geriatric rehabilitations with a special emphasis on assessments and innovative interventions for cognitive impairment.

Abstract:

Regular exercise and participation in mentally stimulating and socially engaging activities are commonly recommended to help sustain brain functions particularly for older adults with mild cognitive impairment (MCI). People with MCI have an increased risk of developing dementia. Nevertheless, it is highly possible to delay the onset of dementia through interventions by slowing the rate of cognitive decline or improve the cognitive functions in persons with MCI. Previous studies have demonstrated combined cognitive and physical activities can induce a greater increase in neurogenesis, and may have additional effects in promoting cognitive functions. Daily functional tasks are innately cognitive-demanding and involve components of stretching, strengthening, balance and endurance as seen in a traditional exercise program. Functional task exercise, with an exercise component incorporated into everyday tasks may be more meaningful and practical for individuals with cognitive impairment. This presentation will illustrate this point using the results of a randomized controlled study investigated the potential benefits of a combined cognitive and exercise program, with functional task as intervention, on cognitive functions and functional status in 83 older adults with MCI. Significant differences have shown between the Functional Task Exercise group and the conventional cognitive training group in memory (p<0.01), executive function (p<0.05), and functional status (p<0.05). All improvements were maintained during 3 months follow-up. Furthermore, functional balance was found significantly improved for those in the Functional Task Exercise group (p<0.05). Important contributing factors and future directions of prevention interventions for person with MCI will be discussed.

Biography:

Sangeeta Semwal has completed her Masters in Clinical Psychology at the age of 23 years from Barkatullah University, Bhopal, India in 2008. At present,She is the director of Saathi Care & Nursing Pvt. Ltd. a company dedicated to wellbeing of elderly with and without Dementia. She has been actively working in the field of mental health from last 7 years and dedicated to Elder care from last 2 years and 10 months. Prior to Elder Care, she was involved in Special Education and Counselling for Army personals.

Abstract:

Palliative care is an approach that improves the quality of life of patients and their families facing the problem associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual. Palliative care is an approach which best endorses the aims of person centred Dementia care. Dementia being a progressive irreversible clinical syndrome characterised by widespread impairment of mental function which may include memory loss, language impairment, disorientation, personality change, difficulties with activities of daily living, self-neglect and psychiatric syndromes requires a 360 degree care. Proper and accurate professional care plays a crucial role in dealing with patients with Dementia and their families and for this reason proper training and developing skills of Dementia Care workers is very important. Here, we will discuss the core features of good dementia care training and how they lead to good Dementia care. We will also discuss if the provision of training actually reduces the burden of caring for a family member with dementia by the family care giver as the family care givers play a vital role in the support of people with Dementia.

Biography:

Aman Gupta is involved in caring for patients with cognitive and behavioral problems. Dr. Gupta is running a Memory Clinic for people with problems resulting in decline in memory, confusion, depression etc.Dr. Gupta has completed his Visiting Fellowship –Functional MRI-- Harvard Medical School, Boston ,MA, USA. With a MD , followed up by Masters of Science- Clinical Research,Cranfield University ,School of Health,England, Dr. Gupta has been into Clinical practice over 12 years. Dr Gupta has been affiliated to Premier institutes like Sir GangaramHospital(Department of Neurology)New Delhi, MAX Health Care New Delhi, Banaras Hindu University on various projects. Currently he is conducting research on Dementia & Diabetic association as a PhD-Research Scholar at Amity Institute of Neuropsychology & Neurosciences, Amity University Uttar Pradesh, Noida, India.

Abstract:

Introduction: Diabetes Mellitus is one the major disease burden globally. One of the significant complication of the uncontrolled Diabetics is Cognitive dysfunction & Dementia.In this study we laid focus on the Evaluation of HbA1C as a Biomarker to predict Dementia & Cognitive Dysfunction in Type 2 Diabetic Mellitus.
 
Aim of the study: A pilot study to investigate HbA1C as a Biomarker for prediction of Dementia & Cognitive Dysfunction in Type 2 Diabetic Mellitus in a Hospital Setting.
 
Methods and Results: A prevalence study in which 60 subjects (n=30 Type 2 Diabetics ; n = 30 non -Diabetic)were enrolled. In this study HbA1C values were correlated with that of individual memory & cognition batteries* score.
The mean values of HbA1C in the Diabetic group (n = 30) was found to be 9.19.The corresponding values of Pearson’s Correlation “r” in the diabetic group of the wrt various Cognitive batteries were : General Practitioner Assessment of Cognition (GPCOG)= -0.53; Attendant Informant Tool(AI) = - 0.43;Memory Impairment Screen (MIS) = -0.37 ; MINI COG = -0.29. Negative values of the Pearson’s Correlation “r” indicates that lower the respective battery score , poorer is the cognitive function.Similarly, in the non-Diabetic group (n =30),no significant Dementia &Cognitive Impairment was found when same group of Cognitive Batteries were administered.
 
Conclusion: It is quite evident from the results that HbA1C as biomarker has a great potential to predict Dementia & Cognitivedecline in uncontrolled Diabetes. However, the study needs to be conducted on a larger scale along with comparative analysis with tools like Functional MRI and other standard biomarkers.

Biography:

Abstract:

Alzheimer's disease (AD) is a disease which is being characterized by signs of major oxidative stress, the loss of cholinergic cells, depletion of Acetylcholine enzyme and the excessive activity of acetylcholinesterase enzyme.In this present review we are trying to investigate the role of the total alkaloidal extract and its predomidant carbazole alkaloid Mahanimbine from Murraya koenigii (MKA) leaves on age related oxidative stress, free radical scavenging activity and its effect in cholinergic pathway. The MKA helps to improve the level of protective antioxidants for free radicals scavenging activity such as glutathione peroxidase (GPx), reduced glutathione (GSH), glutathione such as reductase (GRD), superoxide dismutase (SOD) and catalase (CAT) in brain tissues. Interestingly a significant progress can be found with the addition of Murraya koenigii leaf extract,in improving the acetylcholine (ACh) level and reducing the acetylcholinesterase (AChE) activity in Alzheimer’s diseased mouse brain. On the other hand in several studies it was found that a carbazole alkaloid of Murraya koenigii which is known as mahanimbine [3, 5-dimethyl-3-(4- methylpent-3-enyl)-11H-pyrano [5, 6-a] carbazole], can Inhibit AChE activity which was being proved by Ellman's method .A review on AChE inhibitory activity of this carbazole alkaloid has not been reported so far, and this review will help to study this activity of carbazole alkaloid mahanimbine, isolated from Murraya koenigii in preventing Alzheimer’s disease.

Biography:

Abstract:

Overview of Alzheimer’s disease and its Progression: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that leads to memory loss and nerve cell death
throughout the brain. It is a growing public health problem with major socioeconomic burden and often causes complications resulting in death. AD progresses gradually, the progression of the disease is time dependent and just starts spread spontaneously. The rate of progression varies greatly; brain shrinks dramatically over time, plaques and tangles spread affecting nearly all brain functions. There is a lack of data in understanding AD progression. Typically, it progresses slowly in three general stages mild, moderate and severe. In its early stages memory loss is mild, but with late-stage AD individuals lose the ability to carry on a conversation and respond to their environment. Scientists hope to model stages and progression of AD. By identifying the stage of the disease, prediction is possible, symptoms can be expected and the power to find real treatment will be enhanced.
Alzheimer’s disease Risk Factors:
Much attention has been paid to AD risk factors and disease-modifying factors. A number of factors may increase the chances of developing the disease. Some risk factors can be changed or controlled while others cannot. Risk factors mainly include age, genetics, environment and lifestyle. The majority of AD occurs as a result of complex interactions among genes and other risk factors. A connection has been found between a gene called Apolipoprotein E (ApoE) and the development of AD. Modifiable or controlled risk factors include stress, heavy smoking, excessive alcohol drinking, depression, cognitive inactivity or low education, malnutrition and physical inactivity. Exposure to stress represents a risk factor in induction and progression of AD especially in the developed countries, while protein malnutrition (PM) which increases the severity and progression of AD represents socioeconomic problem in the third world and developing countries. On the other hand, researchers believe that depression is a risk factor, whereas others believe it may be an early symptom of the disease. Other medical conditions that can increase chances of developing dementia include diabetes, high blood pressure, obesity, Parkinson's disease, Down syndrome and some other learning disabilities. The risk of developing AD or vascular dementia appears to be increased by conditions that damage the heart or blood vessels. Scientists hope to prevent or delay AD especially in the high-risk individuals.
Protection and Disease-Modifying Factors:
Healthy aging and lifestyle can help reduce the risk of Alzheimer’s disease and other dementias. Cognitive engagement, physical activities, reduce stress, quitting or reducing smoking, avoid excessive alcohol consumption have been associated with decreased risk of AD. Healthy food as well as dietary supplementation of antioxidants, B vitamins, polyphenols, polyunsaturated fatty acids, Zinc and moderate coffee drinking can reduce AD incidence and provide protection. Although the mechanisms of these nutrients on AD are not clear, but reducing oxidative stress, inflammatory mediators and both Aβ & tau pathologies can attenuate cognitive deterioration. On the other hand, some combined treatments showed marked protective effects rather than individual treatments in animal experimental models especially with risk factors. For example, combined therapy of Epigallocatechin-3-gallate (EGCG) and coenzyme Q10 (CoQ10), EGCG and vitamin E & selenium, combined use of vitamin C and vitamin E as well as coadministration of caffeine and nicotine. The deleterious effect of stress on the brain can be also counteracted by using both EGCG and Diazepam. However, further researches are needed to improve the quality of evidence associated with the reduction
of AD prevalence and incidence.

Koorosh Shahpasand

Royan Institute for Stem Cell Biology and Technology, Iran

Title: A Major Early Driver of Tauopathy and Neurodegeneration that is Blocked by Antibody

Time : 14:50-15:10

Biography:

Koorosh Shahpasand has completed his PhD from Tokyo Metropolitan University in 2012, and did his postdoctoral training at Harvard Medical School on the elucitation of cis/trans p-tau conformations during Neurodegeneration; the results of which have been published in Nature. He is now freshly employed assistant professor at Royan Institute and supervising several research projects related to tauopathies. Notably, he has been recently awarded by a prestigous grant from Alzheimer’s Association at Chicago.

Abstract:

Traumatic brain injury (TBI) is the best-known environmental risk factor for Alzheimer’s disease (AD), whose defining pathologic features include tauopathy made of hyperphosphorylated tau (PHF-tau) and is characterized by acute neurological dysfunction. However, tauopathy is undetectable acutely after TBI and how TBI leads to tauopathy which in turn would increase risk of AD is unknown. Here we identify a neurotoxic cis conformation of phosphorylated tau at Thr231 as a major early driver of TBI and neurodegeneration that is effectively blocked by the conformation specific monoclonal antibody. We found robust cis p-tau after sport- and military-related TBI in humans and mice. Acutely after TBI in mice and stress in vitro, neurons prominently produce cis p-tau, which disrupts axonal microtubule network and transport, spreads to other neurons, and leads to apoptosis, a pathogenic process, which we nominated “cistauosis” that appears long before known tauopathy. Treating TBI mice with cis antibody not only blocks early cistauosis, but also prevents tauopathy development and spread, and restores brain histopathological and functional outcomes. These results uncover cistausosis as an early precursor of tauopathy and an early marker of neurodegeneration after sport and military TBI. We anticipate that cis p-tau will be a new early biomarker and that cis p-tau antibody or vaccines may be used to treat or even prevent TBI, chronic traumatic encephalopathy and AD.

  • Special Session
Location: Hall 4

Session Introduction

Lew Lim

Vielight Inc, Canada

Title: Vielight Inc

Time : 15:10-16:00

Biography:

Abstract:

Neurofeedback
Neurofeedback (NFB), also called neurotherapy or neurobiofeedback, is a type of biofeedback that uses real-time displays of brain activity—most commonly electroencephalography (EEG), to teach self-regulation of brain function. Typically, sensors are placed on the scalp to measure activity, with measurements displayed using video displays or sound – to track positive neuroplasticity, the potential that the brain has to reorganize and create new neural pathways. Vielight Inc and Quietmind Foundation are currently in partnership to develop QEEG and brain mapping software that work in sync with the Vielight Neuro.

  • Workshop
Location: Hall 4

Session Introduction

David Truswell

David Truswell, Central and North West London NHS Foundation Trust, UK

Title: Wake up London – Raising awareness of dementia in London’s Black, Asian and Minority ethnic communities

Time : 16:20-17:00

Biography:

David has worked for over thirty years in the UK developing community services for people with complex care needs and enduring mental health problems in a career spanning the voluntary sector, local authority and the NHS. From 2005 to 2008 he led the Delivering Race Equality programme in the CNWL Foundation Trust (one of the largest NHS Trusts in the UK). From 2009 - 2011 was the Dementia Implementation Lead for Commissioning Support for London. More recently he has developed a role as an independent writer and advisor on dementia support and services for Black, Asian and minority ethnic communities.

Abstract:

The UK Prime Minister’s Challenge on Dementia for 2020 drew attention to the implications of living with dementia for black, Asian and minority ethnic communities in London. The Mental Health Foundation and CNWL Trust held an expert seminar in 2015 involving voluntary sector organisations working with raising dementia awareness to explore common experience and share good practice. ‘Wake Up London’ a paper produced based on the seminar looks at the challenges presented to some of the largest older minority-ethnic communities in the UK and some of the recent initiatives across the capital that
are tackling the issues. The seminar group’s discussions and follow-up work produced Race Against Dementia a national Call for Action to create a co-ordinated approach to raising awareness about dementia in Black, Asian and minority communities supported by a comprehensive account of good practice success stories with a variety of community groups.

  • Amyloid Protein in Dementia, Therapeutic Targets and Imaging Techniques
Location: Hall 4

Chair

Jerzy Leszek

Wroclaw Medical University, Poland

Co-Chair

Zhicheng Xiao

Monash University, Australia

Session Introduction

T Y Chang

Geisel School of Medicine at Dartmouth, USA

Title: ACAT1/SOAT1 as a therapeutic target for Alzheimer's disease

Time : 17:00-17:20

Biography:

Chang is internationally known for his research work in the cholesterol metabolism field. His laboratory did ground breaking work on the key cholesterol storage enzyme acyl-CoA:cholesterol acyltransferase 1 (ACAT1/SOAT1). He and his colleagues identified the Acat1/Soat1 gene, performed functional analysis of the enzyme, and demonstrated Acat1/Soat1 as a target for treating several human diseases including Alzheimer’s disease. Dr. Changhas served as an editorial board member of several major scientific journals, and as a review panel member for NIH. He received an NIH Merit Award in 1994, and was elected AAAS Fellow in 2011.

Abstract:

Alzheimer’s disease (AD) is the most common cause of dementia with no cure at present. Cholesterol metabolism is closely associated with AD at several stages. While brain only accounts for 2-3% of the body weight, it occupies 25% of the total body cholesterol.Cholesterol ester (CE) is the storage form of cholesterol. In normal brains, CE levels are less than 1% of free, unesterified cholesterol. However, in the vulnerable regions of brain samples from late-onset AD patients, CE levels were 80% higher; in the brains of three AD mouse models, the CE levels rose to values 3 to 11 fold higher than those in control mice. In addition, when fed with a high-cholesterol diet, the brain CE content in human ApoE4 knock-in mice was 3-fold higher than that in human ApoE3 knock-in mice. These observations suggest a causal relationship between AD and increased CE content in the brain. Acyl-CoA:cholesterol acyltransferase 1 (ACAT1) converts free cholesterol to cholesteryl esters, and plays important roles in cellular cholesterol homeostasisin various tissues including the brain. Recent studies show that in a mouse model, blocking ACAT1 provides multiple beneficial effects on AD. Here I review the current evidence that implicates ACAT1 as a therapeutic target for AD. I also discuss the potential usage of various ACAT inhibitors currently available to treat AD.

Folefac Atem

University of Texas Health Science Center, USA

Title: Imputation and Censored Covariate: Application to Alzheimer Study

Time : 17:20-17:40

Biography:

Folefac Atem, PhD, MS is a Biostatistician. Dr. Atem is an Assistant Professor in the Department of Biostatistics at the University of Texas Health Science Center at Houston. His office is located at UT Southwestern medical school. He completed his PhD from the University of Pittsburgh in 2010 and Postdoc at Harvard in 2014.

Abstract:

The association between maternal age of onset of dementia and beta-amyloid deposition (measured by in vivo PET imaging) in cognitively normal older offspring is of interest. In a regression model for beta-amyloid, special methods are required due to the random right censoring of the covariate of maternal age of onset of dementia. Prior literature has proposed methods to address the problem of censoring due to assay limit of detection, but not random censoring. We propose imputation methods and a survival regression method that do not require parametric assumptions about the distribution of the censored covariate. Existing imputation methods address missing covariates, but not right censored covariates. In simulation studies, we compare these methods to the simple, but inefficient complete case analysis, and to thresholding approaches. We apply the methods to the Alzheimer’s study.

Biography:

Xiao-lin Yu has completed her PhD from Peking University Health Science Center and postdoctoral studies from National Institutes of Health, USA. She is an associate professor of biotechnological drug engineering in Institute of Process Engineering. She has published more than 10 papers in reputed journals.

Abstract:

Overproduction or poor clearance of amyloids lead to amyloid aggregation and even amyloidosis development. Different amyloids may interact synergistically to promote their aggregation and accelerate pathology in amyloidoses. Amyloid oligomers assembled from different amyloids share common structures and epitopes, and are considered the most toxic species in the pathologic processes of amyloidoses, which suggests that an agent targeting the common epitope of toxic oligomers could provide benefit to several amyloidoses. Here we firstly showed that an oligomer-specific single-chain variable fragment antibody, W20 simultaneously attenuated motor and cognitive decline in Parkinson’s disease and Huntington’s disease mouse models, and ameliorated neuropathology by reducing α-synuclein and mutant huntingtin protein aggregate load and preventing synaptic degeneration. Neuroinflammation and oxidative stress in vivo were also markedly attenuated. The proposed strategy targeting the common epitopes of amyloid oligomers presents promising potential for treating Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and other amyloidoses.

Biography:

Krishna prasad pathak has completed PhD at the age of 35 years from Macedoniya university and doing research work on demenita issue in Nepal. He is the lecturer of Amity Global education , kathmandu Nepal. He has published some papers in reputed journals and has been serving as an editorial board member.

Abstract:

Background: Pharmacological treatment for AD and depression are unfortunately few and of limited efficacy to cure the disease.
 
Objectives: To assess the combined effects of rivastigmine and citalopram on Alzheimer's Disease.
 
Methods: Longitudinal clinical prospective study with 1278 AD patients on rivastigmine 9,5mg/patch and citalopram 20-40 mg/day over 48 months was assessed on the basis of DSM-IV, NINCDS-ADRDA, MMSE, FRSSD, GDS, HRS-D and follow up of the patients.
 
Results: Four years after the baseline assessment, there were no significant differences in MMSE, Geriatric depression scale and Hamilton rating scale for depression between patients treated with rivastigmine alone or combined rivastigmine with citalopram with or without depression (p>0.05). Functional Rating Scale for symptoms of dementia, Activities of Daily Living of patients with AD and depression treated with rivastigmine was significantly worse than patients treated with rivastigmine and no depression (p=0.027).
 
Conclusions: The combination of rivastigmine and citalopram had no better results than rivastigmine alone in patients with AD.