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 2 :

OMICS International Dementia 2016 International Conference Keynote Speaker Linda Levine Madori photo

Linda Levine Madori is a two time Fulbright Scholar, Professor, Author, Researcher and Trainer of a non-pharmaceutical approach utilizing all the creative arts for brain stimulation and enhancing socialization found in her first book titled; Therapeutic Thematic Arts Programming, in 2007 (TTAP Her second book; Transcending Dementia through the TTAP Method; A New Psychology of Art, Brain and Cognition, expands on the current significant research demonstrating cost effectiveness utilizing this innovative multimodal approach for the geriatric and Alzheimer’s population.


This paper will establish through a clinical research study of the use of the TTAP Method® on a Dementia and Gero- Psychiatric unit for a one year period (2014). All healthcare staff were taught to engage in “Emotive Conversations” through the use of this replicable multimodel approach with those individuals afflicted with middle to late stages of dementia, and other psychiatric diagnosis. Data collected over a 365 day period from 1800 patients demonstrates increased mood,increased overall time staff spent engaged with patients and decrease in patient falls. This research supports how channeling change through collective impact can significantly effect patients and staff on a gero-psyciatric unit, while successfully impacting healthcare. The TTAP approach is formulated on the basic functional organization of the brain, neuroplasticity, including neurons, neurotransmitters and areas of the brain involved in transforming emotional and perceptual inputs into physiological responses and behaviors (Damasio, 1998, 1999; Golomb, J.,1996, Grober, E., 1999; Kandel, Schwartz & Jessel, 2000; LeDoux, 2000; Levine Madori, 2007-2014). All healthcare staff were given 15 hours of TTAP Certification Training which utilizes person centered themes within the therapeutic process to engaged participants in a twelve step process that incorporates medication & mindfulness, drawing, sculpture, movement, phototherapy and other forms of the creative arts into an ongoing enriching non-pharmaceutical approach. This method substantiates how conversation which is rich in emotions along with the expressive arts is quickly becoming a powerful way in which to break down “silo’s” of responsibility in demanding and complex healthcare units while continually allowing for self-discovery (Cozolino, 2012, Luzebrink, 2013, Hass-Cohen, 2014). Examples of other research studies utilizing this innovative method with the Alzheimer’s population will be presented from the United States and Finland.

Keynote Forum

Zhicheng Xiao,

Monash University, Australia

Keynote: Neurodegeneration research: From molecules, big animal models to human beings

Time : 09:40-10:20

OMICS International Dementia 2016 International Conference Keynote Speaker Zhicheng Xiao, photo

Zhi-cheng Xiao, PhD. He received a Doctor of Natural Science Degree from Swiss Federal Institute of Technology, Zurich. He is current Professor in Monash University. He is the CEO & CFO of iRiccorgPharm, a premier Bio-Tech company. He has published more than 100 papers in reputed journals and serving as editorial board members of more than 10 journals.


Appropriate connections or interactions among different neural cell types are essential for the correct and efficient functioning of the nervous system during development and regeneration after trauma or degeneration. The aim of my research is to understand the molecular events that mediate communication among neural cells in the nervous system during development, myelination, learning and memory, degeneration, and regeneration. These studies have yielded insights into the therapeutic potential of cell signalling molecules to ameliorate or even ablate the detrimental consequences of nervous system injury and neurodegenerative diseases, including stroke, traumatic brain injury, spinal cord injury, Alzheimer Disease (AD), and Multiple Sclerosis (MS). Using genome-wide chromatin immunoprecipitation approaches, we found that AICD is specifically recruited to the regulatory regions of several microRNA genes, and acts as a transcriptional regulator for miR-663, by which suppresses neuronal differentiation in human neural stem cells. We have generated transgenic pigs expressing mutant G93A hSOD1 and showing hind limb motor defects, which are germline transmissible, and motor neuron degeneration in dose- and agedependent manners. Furthermore, in a case report we present the treatment of aggressive MS patient with multiple allogenic human umbilical cord-derived mesenchymal stem cell and autologous bone marrow-derived mesenchymal stem cells over a 4 y period. The treatments were tolerated well with no significant adverse events. Clinical and radiological disease appeared to be suppressed following the treatments and support the expansion of mesenchymal stem cell transplantation into clinical trials as a potential novel therapy for patients with aggressive MS.

Keynote Forum

Xiaoliang Wang

Chinese Academy of Medical Sciences, China

Keynote: Study on Diabetes Induced Dementia and the Mechanisms of Synaptic Plasticity in KK-Ay Mice

Time : 10:20-11:00

OMICS International Dementia 2016 International Conference Keynote Speaker Xiaoliang Wang photo

Wang,Xiaoliang has completed his MD from University of Essen, Germany in 1987. He returned to the Chinese Academy of Medical Sciences, Beijing in 1988 and promoted to full professor in 1993. He served as director of Institute of MateriaMedica, CAMS from 1997 to 2010. His research fields including neurodegenerative diseases, drug discovery and development. He has published 200 papers in reputed journals and has been serving as editorial board membersfor several journals.


Diabetes mellitus (DM) may induce dementia, so-called diabetic encephalopathy. In the present study, the spontaneously obesity-induced Type 2 diabetic model, KK-Ay mice were used to study the relationship between spatial learning and memory deficits and the alteration of hippocampal synaptic plasticity.Our results showed that KK-Ay mice presented typical T2DM syndrome and deterioratedprogressivelyin Morris water maze from early stage (3 month old). Meanwhile, Aßdeposition and Tau phosphorylation increased in hippocampus. LTP (long term potentiation) was also impaired significantly. It is interesting that these deficits in KK-Ay mice could be relieved by diet intervention and anti-AD drugs. Further, we found that the underlying mechanisms of LTP impairment in KK-Ay mice might attribute to abnormal phosphorylation or expression of glutamate receptors subunits rather than alteration of basal synaptic transmission. The expression levels of NR1, NR2A and NR2B subunits of NMDA receptors (NMDARs) were unchanged while the Tyr-dependent phosphorylations of NR2A and NR2B subunits were significantly reduced in KK-Ay mice. The p-Src and CaMKII were also down regulated.In addition, AMPA receptor, GluR1 was decreased, and the GluR2 was significantly increased.In summary, ourresults suggest that deficits in learning and plasticity in KK-Ay mice may mainly arise from the abnormalof NR2 subunits, which were related to the activities of p-Src and CaMKII. It might be recovered by diet interventionand anti-AD treatment.