Day 2 :
Keynote Forum
Jacqueline A Hinds
Society of Emotional Intelligence, UK
Keynote: Promoting excellence within dementia care: Maintaining emotional intelligence and wellbeing of staff working within dementia care management
Time : 09:45-10:30
Biography:
Jacqueline A Hinds is a Certified Emotional Intelligence Coach (CEIC), Leadership Consultant and, has worked within the national healthcare service for over 10 years in two of the largest merged healthcare organizations in UK and Europe. With 30 years of experience working within the human resource development arena has been paramount whilst working with management and staff during organizational changes; establishing and enabling them to be emotionally intelligent during mergers and organizational changes. From 2006–2010, she was the Leadership Development Consultant pre and post merge of Imperial College Healthcare NHS Trust (circa 10,000 staff) and, from 2010–2015 she was Education Academy Training Manager pre and post merge of Barts Health NHS Trust (circa 15,000 staff). She is now Chair of the Society of Emotional Intelligence, UK Chapter and an independent consultant working on various coaching assignments, and with Culture Dementia UK on training projects within the healthcare and community.
Abstract:
Promoting excellence in service and care for patients with dementia has had a significant impact on the staff working within the dementia care management arena. Stress levels and burnout of caregivers without adequate support has resulted in the essential need of respite by way of development and coaching to support and promote their health and wellbeing whilst they administer and provide essential and effective care to their patients. In the current healthcare climate, the effect of severe cuts in service provisions and staff shortages, whilst maintaining optimum levels of output, has left care givers somewhat jaded over a period of time. Some have gone to the extent of seeking other opportunities due to lack of job satisfaction and challenges around demanding work commitments; consistently taking them beyond their core working hours. The use of the Emotional Intelligence Skills Assessment Profile (EISAP) model as a mode for developing dementia care management staff at all levels, although not referred to or identified as an integral part of their core clinical and non-clinical training or personal development plans, is none-the-less a skill that is interwoven throughout their practices and procedures delivering effective dementia care management. Caring for someone living with dementia is unlike any other form of caring because of the emotional challenges and levels of complexity; EISAP allows the dissemination of complex situations in a relatively accessible way. With the rapid changes with health provisions and more cases of dementia patients being identified, the need for emotionally intelligent care givers is crucial in this day and age. By enabling caregivers to understand their emotions, emotional meanings and to, reflectively regulate these emotions whilst undertaking their roles in effectively. The four quadrants on the EISAP model, enables healthcare and management professionals to tap into their emotional and social skills, enabling them to utilize these skills effectively within their respective working environments.
Keynote Forum
Sandra Gilbert
Noosa Care Inc. Queensland, Australia
Keynote: Family carers are the experts, we are not the experts
Time : 10:30-11:15
Biography:
Sandra Gilbert has over 25 years of experience as a Registered Nurse and is the Group Care Manager of Noosa Care Australia where she manages over 300 care staff. She is also a Dementia Coach and provides education and consultation to businesses and communities on becoming dementia friendly. She is a Dementia Blogger, Podcaster, Keynote Speaker and has led many projects designed to provide enabling environments for people living with dementia. She has won numerous awards for her work in the dementia care space.
Abstract:
In the past, a person living with dementia was handed over to the expert staff when they entered residential aged care. The family carer was told to go home and the expert staff would now handle everything. Transition into care has effects on both the person living with dementia and their family. This presentation will share the journey of Noosa Care, when designing their Memory Support Unit and how as part of that design process, the decision was made to make the family carer the focus of the unit. The resident’s family carer is considered the expert and has since the introduction of this new model, has taught and mentored staff on how to care for their loved one living with dementia. The physical design of the unit was also an important aspect of the model. The design of the unit promotes self-esteem and autonomy for the person living with dementia. This environment allows resident to walk from one room to another, through the gardens and living areas 24 hours per day. The University of The Sunshine Coast Queensland Australia conducted research on the new model, “To understand the perspectives of older people, their families or carers and staff of the effect of a purpose-built Memory Support Unit on the transition into care”. In the findings, family, staff and most importantly the residents living with dementia, expressed an overwhelming positive impact of the built environment and the new model of care.
Keynote Forum
George Paxinos
The University of New South Wales, Australia
Keynote: Brain & Mind: Who is the puppet and who the puppeteer?
Time : 11:30-12:15
Biography:
George Paxinos was borne on Ithaca Greece and studied at the University of California at Berkeley, McGill and Yale. He is currently an NHMRC Senior Principal Research Fellow at Neuroscience Research Australia. He published 51 scientific books and 1 novel. His Rat Brain in Stereotaxic Coordinates is the third most cited book in science. He served as president of the Australian Neuroscience Society and of the IBRO World Congress of Neuroscience.
Abstract:
The question in the title has social, legal and religious implications.
If the mind controls the brain, then there is FREE WILL and its corollaries, dignity and responsibility. You are king in your skull-sized kingdom. You are the architect of your destiny.
If, on the other hand, the brain controls the mind, an incendiary conclusion follows: There can be no FREE WILL, no praise, no punishment and no purgatory.
Our brain is the riverbed that holds and channels our stream of consciousness (Koch, 2012). It is molded by the family and the culture we were raised in. Dementia will pay an unwelcome visit to many of us at the end of life. It will disrupt the internal structure of our neurons or their nourishing blood vessels and we will be living evidence the mind is the product of the brain and has no influence on it.
Keynote Forum
Fan Fan
University of Mississippi Medical Center, USA
Keynote: Disruption of actin cytoskeleton contributes to cerebral vascular dysfunction on alzheimer-like cognitive deficits in diabetic T2DN rats
Time : 12:15-13:00
Biography:
Fan Fan is an Assistant Professor at University of Mississippi Medical Center, USA. Her research focuses on the genetic basis of impaired myogenic response and auto-regulation of cerebral and renal blood flow and end organ damage in aging, hypertension and diabetes. She has published more than 40 papers in peer reviewed journals, and is currently serving as an Editorial Board Member and reviewer for several journals. She is a member of study sections in the Alzheimer’s Association and American Heart Association. She is funded by the National Institute of Health and American Heart Association to study roles of Adducin gamma, CYP4A1 and 20-HETE on aging and hypertension related renal and cerebral vascular and dementia.
Abstract:
Diabetes mellitus is a leading risk factor for cerebrovascular disease and vascular cognitive impairment. However, the underlying mechanisms remain to be elucidated. The present study examines whether disruption of the actin cytoskeleton promotes cerebrovascular dysfunction in diabetic T2DN rat, and if this induces neurodegeneration and Alzheimer-like cognitive deficits. We found that F-Actin area distribution was significantly reduced in the vascular smooth muscle cells (VSMCs) freshly isolated from the middle cerebral arteries (MCAs) of T2DN rats compared with normal Sprague Dawley (SD) rats. The actin cytoskeleton was disrupted similarly in VSMCs treated with H2O2. Both young (4-month) and older (18-month) T2DN diabetic rats exhibit impaired pressure-induced myogenic response in isolated MCA. Forced dilatation occurred at pressures above 140 mmHg in MCAs isolated from elderly T2DN rats with mild hypertension but not controls. Cortical blood flow measured by laser Doppler flowmetry rose by 137±15% and 36±5%, respectively, in T2DN and SD rats when MAP was increased from 100 to 180 mmHg. Cerebral blood flow (CBF) auto-regulation was shifted to lower pressures in elderly hypertensive T2DN rats and they exhibited breakthrough at pressures above 140 mmHg. Levels of IL-1 β and IL-2, and the expression of amyloid β 42 (Aβâ‚„â‚‚) and p-tau (S416) was significantly higher in the brains of T2DN vs. SD rats. T2DN rats exhibited neurodegeneration in the hippocampus and cortex. Elderly T2DN rats showed learning and short and long-term memory disabilities. Latency of escape were longer in an eight-arm water maze test in T2DN rats (2-hour: T2DN 96±12 vs. SD 13±3 seconds; 24-hour: T2DN 105±15 vs. SD 8±2 seconds), and they spent less time in the target arm 48 hours after removal of target platform (T2DN 3.4±2.6 vs. SD 45.0±1.7%). These results indicate that actin cytoskeleton is disrupted in cerebral VSMCs of diabetic T2DN rats, possibly due to elevated oxidative stress, and this contributes to impair of cerebral vascular function, neurodegeneration and Alzheimer-like cognitive deficits.
- Poster Presentations 14:00-14:20 @ Le Foyer
Location: Le Foyer
Session Introduction
Zukhra Gadzhieva
Research Center of Neurology, Russia
Title: fMRI of healthy elderly during Stroop test and the serial count: comparative analysis
Biography:
Zuhra Gadzhieva is a student in the Department of Angioneurology and early rehabilitation after stroke in the Research Center of Neurology (Moscow, Russian Federation). The main goal of her PhD work is to investigate the mechanisms of cognitive decline in patients with cerebral small vessel disease (multimodal neuroimaging and neuropsychological study).
Abstract:
Introduction & Aim: The term executive function (EF) refers to a number of cognitive abilities that enable and control adaptive, goal-oriented behavior. EF is vulnerable to white matter injury and to perturbations in neurotransmitter systems. As a result, EF is impaired in plenty of neurologic and psychiatric conditions. The aim of the current study was to perform a comparative analysis of t cerebral cortex activation in healthy subjects during task-fMRI with a color-word Stroop test modification and a new suggested counting paradigm.
Materials & Methods: 12 healthy control subjects aged 45–63 (2 men) underwent blocked design fMRI on 3T scanner with Stroop test and serial count task. Pre- and post-processing of fMRI data were performed using SPM8.
Results: FMRI analysis showed presence of common activation areas across both tasks including bilateral dorsolateral prefrontal cortex (BA 46, 9), premotor cortex (BA 6), supplementary motor area (BA 6), bilateral parietal cortex (BA 39, 40), right anterior cingulate cortex (BA 32), anterior part of insular cortex (BA13), bilateral cerebellar hemisphere, integrated in executive networks. However, serial count task showed no activation in the lenticular nuclei and occipital cortex, unlike the Stroop test.
Conclusion: According to our results, serial count could be used as alternative paradigm for EF mapping, especially in patients with vision problems.
Yoon Ju Kim
Kyung Hee University, Republic of Korea
Title: Obesity impairs memory and hippocampal post-synaptic structure in chronic cerebral hypoperfusion in rats: Failure of compensatory mechanism
Biography:
Yoon Ju Kim is a registered nurse(RN) in South Korea. She has completed her Master of nursing and now is a PhD student with a major in biological nursing science at the Kyung Hee University. Youn-Jung Kim is a professor at Kyung Hee University. After receiving her Bachelor’s degree in nursing, she completed both master’s degree and PhD in physiology at Kyung Hee University School of Medicine. With interest in neuroscience, she has reported the effect of health-related behaviors on cognitive function in various neurological disease animal models and these findings has been reported in reputed journals.
Abstract:
Obesity is continuously increasing worldwide, and this trend is considered as obesity pandemic. The reason for focusing on obesity as a major health problem is that it causes various diseases such as metabolic diseases and cardiovascular diseases. As one of them, vascular dementia, was reported to be high prevalence in obese population, which was associated with obesity-related insulin resistance or oxidative stress. Thus, previous studies focused on the obesity as a risk factor, however, there were few researches the effect of obesity on disease progression. To confirm the pathological changes in obese vascular dementia, obesity was induced by high-fat diet(HFD) feeding and then, vascular dementia model was proceeded with biliateral common carotid artery occlusion(BCCAO) procedure in rats. After 6 weeks of the procedure, HFD+BCCAO exhibited worse memory performances in Morris water maze test(p<.05) and radial arm maze test(p<.05) than BCCAO. In addition, post-synpatic density-95 in hippocampus were significantly decreased in HFD+BCCAO than BCCAO(p<.05). We confirmed that obesity aggravated memory impairment with disruption of post-synaptic proteins. On the other hand, brain-derived neurotrophin factor, phospho-extracellular signal-regulated kinase(p-ERK) and phospho-cAMP response element binding protein(p-CREB) was respectively increased in BCCAO(all p<.05) more than Sham, but HFD+BCCAO(all p<.05) showed lowest expression level. As a result, the decrease of BDNF, ERK and CREB in HFD+BCCAO, which are related to promote protein synthesis in neuronal dendrites, suggests interruption of a compensatory mechanism in BCCAO procedure. It is first finding that obesity exacerbates memory with damaged post-synaptic structure via disrupting BDNF-ERK-CREB compensatory mechansm. It is suggested that obesity should consider as an aggaravating factor in vascular dementia and we should keep focusing on weight control in patient.
Sally Gilmour
The Meadows Hospital-Stockport Pennine Care NHS Trust, UK
Title: The 2018 Stockport vascular neuro cognitive disorder investigation, treatment and annual review guidelines (Including the spectrum from mild vascular cognitive impairment to vascular dementia) supporting primary and secondary care physicians
Biography:
Sally Gilmour MRCGP worked in Primary care for 18 years, in 2011 worked in Old Age Psychiatry with Dr Katherine Hayden developing an interest in Vascular Dementia. She produced a Dementia Podcast and a Dementia Review Template; integrated into the Stockport Primary Care computer system and has lectured to the National Driving Assessors course regarding Dementia.She works solely in Stockport Old Age Psychiatry since 2015. Dr Peter Ngoma, Stepping Hill Hospital Stroke Clinic lead, Rachel Price, Pennine Care and Professor Alistair Burns have advised also referencing the RCPhysician Stroke Guidelines 2016.
Abstract:
Vascular NeuroCognitive Disorder patients may already be receiving adequate treatment for other cardiovascular disease, but we should reassess ensuring optimum Secondary Cardiovascular Risk Prevention with New Location Target End Organ Damage. A minority are not receiving secondary cardiovascular prevention as Vascular NeuroCognitive Disorder is their first diagnosis of cardiovascular system disease. Many of these newly diagnosed patients may not subsequently receive secondary cardiovascular risk prevention perhaps especially with sub cortical gradual reduction in activities of daily living and change to personality .There is no research evidence to treat Cerebrovascular disease which is proportional to that expected for the patient age on MRI or CT brain. The MRI Fazekas score should reflect the clinical indication of Brain Target Organ Vascular Disease more so than expected age related change. Gradient Echo assesses micro haemorrhage which may mean anti platelets or anticoagulants are contra-indicated, prevalent in Cerebral Amyloid Angiopathy and mixed Vascular and Alzheimer’s pathology. Patient Treatment advice leaflets assist informed shared decisions; although there is no consensus from research evidence that treating blood pressure, cholesterol and using anti platelets or anti coagulation will reduce cognitive decline in vascular NeuroCognitive disorder, there is evidence for secondary cardiovascular prevention once there is diagnosis of target organ damage to the brain with vascular pathological Brain Target Damage. Risk consideration assesses patients and carers, SIGNPOST to healthy lifestyle advocated by Lancet 2017 Dementia Commission. Vascular NeuroCognitive disorder support and healthy lifestyle published leaflets examples include ‘4ME’.
- Workshop
Location: Londres
Session Introduction
P. Giannakopoulos
University of Geneva Switzerland, Swaziland
Title: Multimodal prediction of subtle cognitive decline in elderly controls: an update
Time : 14:20-15:10
Biography:
P. Giannakopoulos was Born in 1965 in Greece and obtained his MD degree in the University of Athens in 1989 before completing a full training on psychiatry and psychotherapy in London (Maudsley Hospital and Geneva) as well as postdoc training in Paris (La Pitié-Sâlpetrière Hospital, Federation of Neurology). In 1998, aged 33 years, he has been appointed as associate professor and medical head of the Division of Geriatric Psychiatry of the University Hospitals of Geneva. Later on (2004) he obtained the position of full tenured professor of Psychiatry in the University of Geneva. From 2003 to 2011, he also assumed a parallel position of full professor of Old Age Psychiatry in the University of Lausanne in order to promote the academic careers of junior staff locally. He has been Chairman of the Department of Mental Health and Psychiatry in Geneva for ten years (2005-2015) and vice dean of the Faculty of Medicine in the University of Geneva in charge of postgraduate and continuous education (2003-2011). From December 1st 2015, he is the medical head of the forensic psychiatry development in Geneva county. Specialist of Alzheimer disase research, he published more than 220 peer reviewed articles in the field of neurobiology of aging with particular focus on predictive biomarkers of cognitive decline.
Abstract:
The presence of apolipoprotein E4 (APOE*E4) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. Our objective was to assess the effect of APOE*E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline.
MATERIALS AND METHODS: This prospective study included 382 community dwelling elderly controls.At baseline,participants under- went MR imaging at 3T, extensive neuropsychological testing, and genotyping. After neuropsychological follow-up at 18 months, participants were classified into cognitively stable controls and cognitively deteriorating controls. Data analysis included whole-brain voxel- based morphometry and ROI analysis of GM.
RESULTS: APOE*E4 related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. There was no APOE*E4-related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. Controls in the cognitively deteriorating group had slightly lower GM concentration in the hippocampus at baseline. Higher GM densities in the hippocampus, middle temporal lobe, and amygdala were associated with a decreased risk for cognitively deteriorating group status at follow-up.
CONCLUSIONS: APOE*E4 related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. This finding might explain the partially conflicting results of previous studies that typically did not include detailed neuropsychological assessment and follow-up. Most important, APOE*E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe.
- Dementia Care Management | Dementia Nursing | Neurodegenerative Disorders | Treating Dementia | Novel Therapeutics
Location: Londres
Chair
George Paxinos
George Paxinos, The University of New South Wales, Australia
Session Introduction
Marwa Ahmed Mohamed Saad
Alexandria University, Egypt
Title: Serum levels of high molecular weight adiponectin and leptin in elderly patients with dementia
Time : 15:15-15:40
Biography:
Marwa Ahmed Mohamed Saad completed her Master degree of Internal Medicine and Doctorate Degree in Internal and Geriatric Medicine at Alexandria University, Egypt. She is currently working assistant professor of Geriatric Medicine, Consultant of Internal and Geriatric medicine and Fellow of Egyptian Society of Geriatrics and gerontology.
Abstract:
Dementia is a progressive impairment of cognitive function sufficient to cause functional decline. It may affect up to 28 million individuals world-wide; 30% of those older than 85 years. Adiponectin is a cytokine released by the adipose tissue, and presents in the cerebrospinal fluid of human. It has important functions in the central nervous system. Leptin is another cytokine was implicated in cognitive decline and dementia processes. We aimed in the present study to determine the serum levels of adiponectin and leptin in elderly patient with dementia. 60 subjects aged 65 years and older were involved, divided into two groups; group (I): 40 demented patients, and group (II): 20 age and sex matched healthy subjects as a control group. Participants with dyslipidemia, hypertension, diabetes mellitus, chronic liver diseases, chronic kidney diseases, thyroid disorders, or morbid obesity were excluded from the study. All participants were subjected to MMSE and MOCA tests, serum adiponectin and leptin were measured. Serum adiponectin was higher, while leptin levels were lower in demented patients. A significant negative correlation between serum levels of adiponectin and both MMSE and MOCA scores, while a high positive correlation was noted between serum levels of leptin and both MMSE and MOCA scores. We concluded that serum adiponectin and leptin were strongly associated with dementia in elderly patients, which may help in understanding of its pathogenesis and emergence of new drugs for better outcome of this devastated disease.
Aanchal Sareen
Uzhhorod National University, Ukraine
Title: Type III Diabetes: A misnomer for Dementia?
Time : 15:40-16:05
Biography:
Aanchal Sareen has completed her higher education from India in 2014 and now is pursuing MD 3rd course in General Medicine from Ukraine. My research was published in International Medical Student’s Conference 2017 Krakow, Poland (Pharmacy and Internal Medicine fields) I have also been an active member at Uzhhorod medical Students Conference, Ukraine 2017.
Abstract:
Diabetes mellitus (DM) is a disease of the peripheral organs while Diabetes inspidus (DI) is a disease of the brain. Both forms of diabetes are characterized by excess levels of blood sugar or glucose. Whereas the former is due to insulin resistance or insufficiency the latter is due to insufficiency of hypophyseal anti-diuretic hormone (ADH). But the causes underlying the accumulation of glucose in circulation are different for DM and DI.
Diabetes mellitus-2types.While type1 diabetes (T1D) is due to autoimmune destruction of insulin-producing pancreatic islets of Langerhans (IL), type 2 diabetes (T2D) is a lifestyle disease due to exhaustion of IL to produce insulin in response to hyperglycemia. Whereas glucose fuel unavailability in the mitochondria leads to deficit of energy production in the form of ATP, its accumulation in blood leads to complications due to inflammatory damage to blood vessels.“The brain uses glucose as a primary source of energy. Cognitive function becomes impaired when blood glucose drops to low levels, and severe hypoglycemia may cause neuronal damage. Recently, Alzheimer's disease (AD) has been hypothesized to be type3 Diabetes (T3D), presumably caused by insulin resistance in the brain, an organ absolutely dependent upon glucose as fuel for ATP biosynthesis.This can create a dangerous spiral, in which a hypoglycemic event caused by T2D can lead to mental deterioration and vice versa.If the brain is starved of energy, it’s possible that neurological problems like dementia and Alzheimer’s disease are more likely to develop.It is found that clinically significant hypoglycemia is associated with a two-fold increased risk for developing dementia and likewise patients with dementia were more likely to experience a severe hypoglycemic event with brain damage in the cerebral cortex and hippocampus.
Babak Zamani
Iran University of medical sciences, Iran
Title: Characteristics of different type of dementia in neurosonology: What we know?
Time : 16:20-16:45
Biography:
Babak zamani, he was born in 1957. He was also working in Iranian board of neurology in 1993. He was also works as a President of Iranian stroke society and Vice President of Iranian neurological society.
Abstract:
Neurosonology of brain parenchyma is a new growing field in different type of brain disorders. There is some data about usefulness of this noninvasive technique in some degenerative disorders like parkinson disease and dystopia .during last few years in our department we studied different neurosonological land marks in different types of Dementias including substantia nigra echogenicity, raphe N echogenicity, midbrain width, 3th ventricular diameter and lenticular nucleus echogenicity. Some of these studies have been published and many of them are under publishing
- Video Presentations
Location: Londres
Session Introduction
James D. Weinstein
Marshall University, USA
Title: A New Direction for Alzheimer’s Research
Time : 16:45-16:55
Biography:
Dr. James Weinstein completed his MD in 1964 from the University of Pennsylvania and his internship from New England Center Hospital in Boston 1965. He worked as a neurosurgeon for more than 40 years in New Jersey and West Virginia. He has published more than 25 papers in reputed journals, his latest relating to this presentation for the conference in Medical Hypothesis, November 2017.
Abstract:
Although billions of dollars have been spent for research on Alzheimer’s disease (AD), little progress has been made in finding a therapy which stops the progressive dementia characteristic of the disease. Numerous drugs, having failed over years of research, suggest the need for a reevaluation of how the research is now being done. To that end, three changes in current AD research methodology are offered and these changes are absolutely necessary to provide the means to find an effective treatment for the disease. First, AD is a disease of four etiologies rather than from a single primary cause. These four should be treated simultaneously for an effective therapy. Second, AD drug testing is wasting much time effort and money by aiming for a statistical verification of the slowing of dementia. The end point should be the complete cessation of progressive dementia, and testing should begin with small cohorts. Third, combination therapies with drugs currently available, used off label, ought to be tried. One example of such a combination is reviewed.