Pille Link, Prof. Dr. M. Wink University of Heidelberg

Slides:



Advertisements
Similar presentations
William J. Walsh, Ph.D. Walsh Research Institute Naperville, IL
Advertisements

Effect of Liraglutide Treatment on Inflammation and Oxidative Stress in Young and Old APP/PS1 and WT Mice Supervisors: Dr. Christian Holscher Dr. Kerry.
Alzheimer’s Disease Edwin Onattu P. 3.
The Aging Brain The brain changes with age The frontal cortex & hippocampus are critical to learning, memory, planning and other cognitive activities,
Preventative and Therapeutic Treatment of Resveratrol on Alzheimer’s Disease using CL2006 and CL4176 C. elegan models Bradford Greaves.
Comparing the Toxicity of Zinc Deficient Superoxide Dismutase (SOD) and the Quad SOD mutant: Implications for Amyotrophic Lateral Sclerosis Jesse Fitzpatrick.
Therapeutic Treatment of Resveratrol on Alzheimer’s Disease with CL2006 Bradford Greaves.
Preventative and Therapeutic treatment of resveratrol on Alzheimer’s Disease using CL2006 and CL4176 C. elegan models Bradford Greaves.
Alzheimer’s Disease Nicotine’s relationship and contribution to dementia.
Alzheimer’s Disease Find group of ~4 students ~ 10 minutes Discuss the following personal family connection to AD (if willing only) observations/experiences.
Alzheimer’s Disease By: Ryan Triplett. Alzheimer’s The deterioration of intellectual capabilities, memory, judgment, and personality to the extent that.
AGING AND TRAUMA Key Points Increased longevity results in increased neurological disorders ‘Normal’ age-related changes in brain structure Neurodegenerative.
A view into Neurodegeneration and neurodegenerative diseases Bahareh Eftekharzadeh Laboratory of Dr. Xavier Salvatella SemesterI Crazy about Biomedicine.
Alzheimer's disease Beta amyloid protein and the potential for anti-oxidants drugs.
The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. Susan A. Farr, et al.
ACH: Involvement in diseases Myasthenia gravis Symptoms: loss muscular tonus progression from head to limbs to respiratory muscles.
Roderic G. Eckenhoff, MD Dept. Anesthesiology & Critical Care, University of Pennsylvania Hypothesis: Inhaled anesthetics.
Alzheimer’s Disease Causes, Effects, and Treatments.
Amnesia Syndromes Lesson 22. Wernicke-Korsakoff’s Syndrome n Deficits similar to H.M. l Anterograde l retrograde more severe n Cause: Long-term alcohol.
A carboxylated Zn-phthalocyanine inhibits the fibril formation of Alzheimer’s amyloid β peptide Atsushi Nagai Dept. Laboratory Medicine Shimane University.
COST CM1103 Training School Structure-based drug design for diagnosis and treatment of neurological diseases Istanbul, 9-13 Sept 2013 Mirjana Babić, mag.biol.mol.
1 Department for Neuroscience, Croatian Institute for Brain Research, University of Zagreb Medical School, Zagreb, Croatia 2 Laboratory for Molecular Neuropharmacology,
Introduction Alzheimer’s disease (AD) is a neurodegenerative disease associated with brain shrinkage and the loss of neurons, particularly cholinergic.
PATHOLOGIC AGGREGATION OF THE BRAIN PROTEIN  -SYNUCLEIN CAUSES CELL DEATH IN PARKINSON AND ALZHEIMER DISEASE, Wenbo Zhou, PhD and Curt R. Freed, MD Division.
Alzheimer’s Disease BRAIN, THE FINAL FRONTIER BRAIN, THE FINAL FRONTIER Kiminobu Sugaya, Ph.D.
Protection of rat primary hippocampal cultures from Aβ cytotoxicity by pro-inflammatory molecules is mediated by astrocytes Neurobiology of disease, Vol.
Dr. Sigal fleisher-Berkovich Neuroinflammation is regulated by angiotensin related drugs: possible implications for neurodegenerative diseases.
CLINICAL AND RESEARCH MEMORY CENTER LARIBOISIERE HOSPITAL PARIS FRANCE UNIVERSITY OF PARIS DIDEROT INSERM UNIT 942 INVOLVEMENT OF PKR IN ALZHEIMER’S DISEASE.
Alzheimer’s Disease Gavin Mast, Musa Abdus-Samad, Arash Rezaeian, Sarah Rocha PHM142 Fall 2015 Instructor: Dr. Jeffrey Henderson.
Epidemiology of Alzheimer’s Disease
Bioinformatics: Practical Application of Simulation and Data Mining Protein Aggregation I Prof. Corey O’Hern Department of Mechanical Engineering & Materials.
Under the supervision of miklós jászberényi
Alzheimer’s Disease Today and Tomorrow First case reported in 1906 Reported by Alois Alzheimer Patient Augusta D. first treated at 46 years old Paranoia,
Liquorice Root.
Alzheimer’s Disease Lizzy Butler & Efe Osemeha. Background Info Alzheimer’s Disease is a neurological disease that kill neurons causing the loss of memory.
Neuroprotective Effects of Memantine. Hippocampal slice cultures Brown et al., Soc. Neurosci 2003 Semi-chronic 3-NP toxicity in organotypic hippocampal.
Therapeutic Treatment of Resveratrol on Alzheimer’s Disease with CL2006 Bradford Greaves.
A Correlation Between Alzheimer’s and Parkinson’s: Inflammatory Response to Endogenous Neuro-protective Mechanisms Peter H. Massey.
Fig. 1 Anti-inflammatory drug treatment reduces the number of reactive microglia in the hippocampus of APPV717I mice. APPV717I transgenic mice (10 months.
Syed H. Omar, Christopher J. Scott, Adam S. Hamlin, Hassan K. Obied 
Title: Alzheimer’s disease and the social
Investigating a Fragment of the Leptin C-D loop: Neuroprotective and Behavioural Effects Alison Holiday.
Jiyoung Kim, PhD Seoul National University
Aging.
Research Proposal By Thomas Raymond
Designing drugs for neuroprotection
A potential therapy for ALS
Small section of the neocortex from a patient with Alzheimer disease showing two classical neuropathologic lesions of the disease. A. The modified silver.
Amnesia Syndromes Lecture 21.
Q: How can we prevent or treat Alzheimer’s Disease?
Progress Report on Alzheimer’s Disease
Nat. Rev. Neurol. doi: /nrneurol
Chapter 30 Delirium and Dementia
Methods Objectives Results Conclusions References
GENE EXPRESSION CHANGES TRIGGERED BY AMYLOID BETA TOXICITY
Microglia and the Immune Pathology of Alzheimer Disease
Health & Diseases Health Disease Biological System
Figure 3 VEGF in neurodegenerative disease
Drugs for Degenerative Diseases of the Nervous System
Alzheimer's & Dementia: The Journal of the Alzheimer's Association
Amyloid-beta circulates in blood and brain
Mechanisms Underlying Inflammation in Neurodegeneration
Neuroplasticity Failure in Alzheimer's Disease
Glucose Metabolism: A Sweet Relief of Alzheimer’s Disease
מחלת אלצהיימר: עבר, הווה ועתיד
Targets of thiazolidinedione (TZD) drugs in Alzheimer’s disease.
Chapter 18 Dietary Phytochemicals in Neurodegenerative Disease
Volume 71, Issue 5, Pages (September 2011)
Mouse and Drosophila models of AD
Table 1. Bioactive properties in Coriolus versicolor
Presentation transcript:

Effects of liquorice on beta-amyloid aggregation and toxicity in Caenorhabditis elegans Pille Link, Prof. Dr. M. Wink University of Heidelberg Institute for Pharmacy and Molecular Biotechnology Conflict of interest: nothing to declare

Glycyrrhiza glabra Used to treat ulcers gastritis cough longing for sweets

Alzheimer‘s disease neurofibrillary tangles G. glabra? oxidative stress inflammation neuronal cell death loss of memory neurofibrillary tangles antioxidant anti inflammatory neuroprotective memory-enhancing http://www.alz.org/braintour/images/ plaques_tangles.jpg G. glabra? amyloid-β plaques Aβ plaques Asl MN & Hosseinzadeh H (2008). Review of Pharmacological Effects of Glycyrrhiza sp. and its Bioactive Compounds. Phytotherapy Research 22: 709-724.

Caenorhabditis elegans: a model for Alzheimer’s disease CL2006 Aβ42 expression in muscle cells number of plaques CL4176 temperature inducible Aβ42 expression in muscle cells progressive paralysis Aβ42 toxicity Link CD (2006). C. elegans models of age-associated neurodegenerative diseases: lessons from transgenic worm models of Alzheimer's disease. Exp Gerontol 41: 1007-1013.

Does G. glabra have an effect on Aβ aggregation?

CL2006: thioflavin S staining

Glycyrrhiza glabra isoliquiritigenin (ILG) glycyrrhetinic acid (GRA) G. glabra G. glabra isoliquiritigenin (ILG) glycyrrhetinic acid (GRA) glycyrrhizic acid (GA) * p < 0.01 concentration: 100 µg/ml

Can G. glabra reduce Aβ-induced toxicity?

Paralysis assay in CL4176 temperature inducible Aβ expression paralysis due to Aβ toxicity

Activity against Aβ-toxicity

Conclusions & outlook extract & pure compounds from G. glabra can: decrease the number of Aβ plaques counteract Aβ toxicity most active compound: isoliquiritigenin further work: test more compuonds clarify the mode of action

Thank you for your attention! IPMB University of Heidelberg Thank you for your attention!