^{14th World Summit on} Alzheimer’s Disease, Dementia Care Research and Awareness August 30-31, 2018 Boston, Massachusetts, USA

Biography:

Dr.Keerthi Paramasivam completed her MBBS degree in DR NTR University of Health Sciences, Andhra Pradesh and went on to graduate with Masters in Clinical Neuroscience from King’s College, London. She has currently completed her PhD in Neuroscience from Harvard Medical School. She is a fully registered medical practitioner recognized by the General Medical Council, The Medical Council of India and the Malaysian Medical Council. She currently works at the National Neuroscience Institute of Singapore and has assisted and worked in several clinical research and trials. She has conducted several Neuroscience seminars and workshops in Malaysia and is a Member of the Malaysian Society of Neurosciences.
 

Abstract:

This study was done to demonstrate the effects of Ephedrine HCL ,Turmerone & Curcumin in Neurogenesis and Inhibition of Beta Amyloids in Transgenic Mice. The transgenic mice models used contain mutations associated with familial Alzheimer's disease (APP Swedish,MAPT P301L,and PSEN1 M146V). These mice develop age-related, progressive neuropathology including plaques and tangles. Ten-month-old male and female APPSw Tg+ and Tg− mice from 12 litters were randomly split between treatment groups. Tg+ mice were fed either chow containing a low dose of curcumin (160 ppm;n=9; a high dose of curcumin (5000ppm;n=6), or no drug (n=8) for 6 months. Mice with low and high dose of curcumin were given specific doses of 0.02% Ephedrine HCL injection every 72 hours and underwent a single intracerebroventricular injection of 3mg ar-turmerone. To evaluate whether curcumin treatment affected plaque pathology, cryostat hemibrain sections from Tg+ control and Tg+ low-dose curcumin-treated mice were immunostained with an antibody against Aβ1–13(DAE). Two-factor ANOVA revealed a significant reduction in plaque burden in curcumin, Ephedrine HCL and turmerone treated animals (F (1,60) = 4.74; p=0.03), in which amyloid burden was decreased by 43.6% in treated animals compared with untreated animals. Soluble Aβ in Tg+ untreated and Tg+ low-dose curcumin mice were measured by sandwich ELISA. Two-way ANOVA showed significant treatment effects in decreasing the levels of soluble Aβ (*p < 0.05). Underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via exon array analysis of cortical and hippocampal mRNA transcription showed a positive result.

Biography:

Sarah Jung is an experienced researcher on the subject of neurodegenerative diseases and public health. She has done field research about public health in the Peruvian Amazonian communities to have a better comprehension about the type of medical aid natives in the Amazon rainforest have. Sarah has also written a scientific report on using brain maps for better understanding Parkinson’s disease. She focused on utilizing brain maps in hopes of encouraging more scientists Sarah Jung is an experienced researcher on the subject of neurodegenerative diseases and public health. She has done field research about public health in the Peruvian Amazonian communities to have a better comprehension about the type of medical aid natives in the Amazon rainforest have. Sarah has also written a scientific report on using brain maps for better understanding Parkinson’s disease. She focused on utilizing brain maps in hopes of encouraging more scientists to examine data on the brain for expedited drug development process.

Abstract:

 There have been many endeavors to find an effective drug for Parkinson’s disease. However, when the drug development process comes across humans in clinical trials, it frequently encounters serious side effects or no curative effects. Failures are often attributed to the widespread use of animals such as mice for drug discovery. Using mice has been the conventional way to embark on developing a new drug. However, the fact that mice are not accurate models must be taken into deep consideration to reduce the risk of undesired medicinal results in humans. To better understand the extent to which humans and mice differ, a careful comparison in a comprehensive level is critical. Here, we investigated the expression pattern of 5 drug target genes for Parkinson’s disease (SNCA, LRRK2, GBA, PINK1, NR4A2) using brain maps of normal humans and mice. This comparative analysis revealed gene expression patterns similar or different between humans and mice, and across a hundred different brain regions. Notably, we observed variations in a key brain structures related to the motor or non-motor symptoms of Parkinson’s disease, including the cerebellar cortex, basal ganglia, claustrum, and hippocampus. By analyzing brain maps, this research could help the drug development process be more effective and safer for common PD drug target genes. Existing medications can also be improved by reducing possible side effects through predicting human consequences more accurately with the knowledge we obtained from such gene expression study.

Biography:

Dr. Jun Tan received his Bachelors of Medicine in China in 1983. He earned his Masters of Science in human genetics at Fudan University in 1989. He completed his Doctoral degree in biological medicine in China and postdoctoral studies in 1996 at the University of Michigan, Ann Arbor. In 1998 he became Assistant Professor of Psychiatry & Behavioral Medicine at USF and was promoted to Associate Professor in 2004 and Professor in 2007. Over the past 20 years, Dr. Tan has authored more than 150 original scientific papers in prestigious international journals such as Science, Nature Neuroscience and Nature Commutations. Dr. Tan’s philosophy is that everyone on his team has a strength and that the best way to lead is to find a way to utilize those strengths together in building a concerted effort toward success. “You can achieve great things in the USF Silver Child Development Center if you believe”.

Abstract:

Lithium has been marketed in the United States of America since the 1970s as a treatment for bipolar disorder. More recently, studies have shown that lithium can improve cognitive decline associated with Alzheimer’s disease (AD). However, current the United States Food and Drug Administration-approved lithium pharmaceutics (carbonate and citrate chemical forms) have a narrow therapeutic window and unstable pharmacokinetics that, without careful monitoring, can cause serious adverse effects. Here, we investigated the safety profile, pharmacokinetics, and therapeutic efficacy of LISPRO (ionic co-crystal of lithium salicylate and l-proline), lithium salicylate, and lithium carbonate (Li2CO3). We found that LISPRO (8-week oral treatment) reduces β-amyloid plaques and phosphorylation of tau by reducing neuroinflammation and inactivating glycogen synthase kinase 3β in transgenic Tg2576 mice. Specifically, cytokine profiles from the brain, plasma, and splenocytes suggested that 8-week oral treatment with LISPRO down-regulates pro-inflammatory cytokines, up-regulates anti-inflammatory cytokines, and suppresses renal cyclooxygenase 2 expression in transgenic Tg2576 mice. Pharmacokinetic studies indicated that LISPRO provides significantly higher brain lithium levels and more steady plasma lithium levels in both B6129F2/J (2-week oral treatment) and transgenic Tg2576 (8-week oral treatment) mice compared to Li2CO3. Oral administration of LISPRO for 28 weeks significantly reduced β-amyloid plaques and tau-phosphorylation. In addition, LISPRO significantly elevated pre-synaptic (synaptophysin) and post-synaptic protein (postsynaptic density protein 95) expression in brains from transgenic 3XTg-AD mice. Taken together, our data suggest that LISPRO may be a superior form of lithium with improved safety and efficacy as a potential new disease modifying drug for AD.

Biography:

Prof Sunita Tiwari is working as Head of the Department of Physiology, King George’s Medical University, Lucknow, UP, India since January 2004. My core interest lies in teaching and training of undergraduate and postgraduate students and pursuing research. My field of interest is Obesity, Metabolic Syndrome-related risk factors and cognitive impairment in senile dementia. Several research projects funded by ICMR, DRDO, CCRYN, AYUSH & UPCST was undertaken in Neurophysiology lab for BAER, ANS & NCV testing, Spirometry lab, Molecular Lab, Sleep research lab and Exercise Physiology lab under my guidance as principal investigator. Several postgraduate (MD and PhD) thesis has been undertaken under my supervision. I have also organized many national and international conferences. Presently I am chairing the IMA-AMS (UP chapter) and have successfully organized superspecialty CME’s & workshop in collaboration with Apollo hospital New Delhi, Max Hospital New Delhi and others.

Abstract:

Introduction: Alzheimer’s disease is the most common form of age related cognitive impairment. Aim of the present study was to see the effect of vitamin D and calorie supplementation on cognitive function in elderly.

Material and methods: A total of 80 subjects were enrolled based on Mini Mental State Examination (MMSE) score < 24 and vitamin D deficiency. They were divided into two groups as Group A (case) and Group B (control), each group having 40 subjects. Both groups are on same medical treatment. Intervention (Vitamin D and calorie supplementation) was given to only Group A. The assessment of dementia was done by Mini Mental State Examination (MMSE) score. Nutritional assessment was done by Food frequency questionnaire (Designed by Indian Council of Medical Research). Oral nutritional supplementation was given twice daily for six month in addition to their usual diet. Two serving provide 600 Kcal. per day.120000 IU of cholecalciferol was given every month in the form of Calcirol granules.

Results: Gender, weight, height, BMI, residence and education were similar between two groups. A significant change in MMSE score was observed in both Group A and Group B from baseline to 3 & 6 months and from 3 to 6 months, however, mean change was higher in Group A than Group B.

Conclusion: In conclusion, vitamin D and calorie supplementation causes significant improvement in the cognitive performance in subjects with senile dementia.

Biography:

Kendall Shirey is a physician assistant student at The University of Texas Medical Branch at Galveston. Prior to attending the physician assistant program, she graduated from The University of Texas at Austin with a B.S. degree in Nutrition and The University of North Texas Health Science Center in Fort Worth with a M.S. degree in Medical Science. In addition to her clinical experience during her physician assistant program, Kendall is interested in pursuing a career in family medicine and desires to continue being a lifelong learner.

Abstract:

Donepezil, an acetylcholinesterase inhibitor, is a commonly prescribed drug in Alzheimer’s dementia patients used to slow disease progression.⁸ Memantine, a N-methyl-Daspartate antagonist, can be used as an adjunct with Donepezil to improve symptoms.⁸ The purpose of this analysis is to determine the efficacy of combined Donepezil and Memantine in comparison to Donepezil monotherapy at slowing the progression of cognitive impairment in Alzheimer’s disease as measured by serial mini mental status exams.

Methods: An electronic search was conducted using PubMed and Google Scholar databases. Articles chosen evaluated the efficacy of combined treatment of Donepezil and Memantine versus Donepezil monotherapy on slowing the progression of cognitive impairment in AD. Studies used mini mental status exams (MMSEs) to assess cognitive decline.

Results: Eleven studies were analyzed to assess the effect of Donepezil alone versus Donepezil and Memantine combination therapy for the treatment of Alzheimer’s dementia. An aggregate of 4,720 patients were included in our analysis. A large majority of the studies revealed that there was no significant statistical benefit of combination therapy compared to Donepezil monotherapy based on MMSE scores and clinical outcome. However, combination therapy was indeed found to help improve cognitive function and reduce neuropsychiatric symptoms, particularly in patients with moderate to severe Alzheimer’s dementia.

Conclusion: In conclusion, combination therapy is superior to monotherapy in patients with moderate to severe AD as assessed by MMSEs despite a lack of strong statistical significance between the two drug regimens. In a patient with mild AD, the addition of Memantine to the acetylcholinesterase inhibitor therapeutic framework does not appear to be of any clinical benefit, but further research needs to be performed to make this determination.