Abstract
In a previous in vitro study, the standardized turmeric extract, HSS-888, showed strong inhibition of Aβ aggregation and secretion in vitro, indicating that HSS-888 might be therapeutically important. Therefore, in the present study, HSS-888 was evaluated in vivo using transgenic ‘Alzheimer’ mice (Tg2576) over-expressing Aβ protein. Following a six-month prevention period where mice received extract HSS-888 (5mg/mouse/day), tetrahydrocurcumin (THC) or a control through ingestion of customized animal feed pellets (0.1% w/w treatment), HSS-888 significantly reduced brain levels of soluble (∼40%) and insoluble (∼20%) Aβ as well as phosphorylated Tau protein (∼80%). In addition, primary cultures of microglia from these mice showed increased expression of the cytokines IL-4 and IL-2. In contrast, THC treatment only weakly reduced phosphorylated Tau protein and failed to significantly alter plaque burden and cytokine expression. The findings reveal that the optimized turmeric extract HSS-888 represents an important step in botanical based therapies for Alzheimer’s disease by inhibiting or improving plaque burden, Tau phosphorylation, and microglial inflammation leading to neuronal toxicity.
Keywords: Alzheimer’s disease, Tau phosphorylation, turmeric, curcuminoids, Aß cascade hypothesis, chronic inflammation
Current Alzheimer Research
Title:Optimized Turmeric Extract Reduces β-Amyloid and Phosphorylated Tau Protein Burden in Alzheimer’s Transgenic Mice
Volume: 9 Issue: 4
Author(s): R. Douglas Shytle, Jun Tan, Paula C. Bickford, Kavon Rezai-zadeh, L Hou, Jin Zeng, Paul R. Sanberg and Cyndy D. Sanberg, Randall S. Alberte, Ryan C. Fink, Bill Roschek Jr
Affiliation:
Keywords: Alzheimer’s disease, Tau phosphorylation, turmeric, curcuminoids, Aß cascade hypothesis, chronic inflammation
Abstract: In a previous in vitro study, the standardized turmeric extract, HSS-888, showed strong inhibition of Aβ aggregation and secretion in vitro, indicating that HSS-888 might be therapeutically important. Therefore, in the present study, HSS-888 was evaluated in vivo using transgenic ‘Alzheimer’ mice (Tg2576) over-expressing Aβ protein. Following a six-month prevention period where mice received extract HSS-888 (5mg/mouse/day), tetrahydrocurcumin (THC) or a control through ingestion of customized animal feed pellets (0.1% w/w treatment), HSS-888 significantly reduced brain levels of soluble (∼40%) and insoluble (∼20%) Aβ as well as phosphorylated Tau protein (∼80%). In addition, primary cultures of microglia from these mice showed increased expression of the cytokines IL-4 and IL-2. In contrast, THC treatment only weakly reduced phosphorylated Tau protein and failed to significantly alter plaque burden and cytokine expression. The findings reveal that the optimized turmeric extract HSS-888 represents an important step in botanical based therapies for Alzheimer’s disease by inhibiting or improving plaque burden, Tau phosphorylation, and microglial inflammation leading to neuronal toxicity.
Export Options
About this article
Cite this article as:
R. Douglas Shytle, Jun Tan, Paula C. Bickford, Kavon Rezai-zadeh, L Hou, Jin Zeng, Paul R. Sanberg and Cyndy D. Sanberg, Randall S. Alberte, Ryan C. Fink, Bill Roschek Jr , Optimized Turmeric Extract Reduces β-Amyloid and Phosphorylated Tau Protein Burden in Alzheimer’s Transgenic Mice, Current Alzheimer Research 2012; 9 (4) . https://dx.doi.org/10.2174/156720512800492459
DOI https://dx.doi.org/10.2174/156720512800492459 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Reduced Mitochondrial Activity is Early and Steady in the Entorhinal Cortex but it is Mainly Unmodified in the Frontal Cortex in Alzheimer's Disease
Current Alzheimer Research Models for Non-Alcoholic Fatty Liver Disease: A Link with Vascular Risk
Current Pharmaceutical Design Inappropriate Drug Use in People with Cognitive Impairment and Dementia: A Systematic Review
Current Clinical Pharmacology Functional Neuroimaging of Sleep Disorders
Current Pharmaceutical Design Ginkgo Biloba Extract in an Animal Model of Parkinson’s Disease: A Systematic Review
Current Neuropharmacology Subject Index to Volume 3
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents Peripheral Blood Adipokines and Insulin Levels in Patients with Alzheimer's Disease: A Replication Study and Meta-Analysis
Current Alzheimer Research Editorial (Thematic Issue: Current Update on Association Between Alzheimer’s Disease and Type 2 Diabetes: Volume I)
CNS & Neurological Disorders - Drug Targets Protection Mechanisms Against Aβ42 Aggregation
Current Alzheimer Research Interleukin-4-Induced Oxidative Stress Via Microglial NADPH Oxidase Contributes to the Death of Hippocampal Neurons In Vivo
Current Aging Science Genetics of Alzheimer's Disease and Frontotemporal Dementia
Current Molecular Medicine Induced Pluripotent Stem Cell-Based Studies of Parkinson's Disease: Challenges and Promises
CNS & Neurological Disorders - Drug Targets Tools in the Design of Therapeutic Drugs for CNS Disorders: An up-to-date Review
Current Molecular Pharmacology Epigenetic Drugs in Cognitive Disorders
Current Pharmaceutical Design Calpain Inhibition: A Therapeutic Strategy Targeting Multiple Disease States
Current Pharmaceutical Design Blood Pressure and Vascular Alterations with Growth in Childhood
Current Pharmaceutical Design Dry Age-Related Macular Degeneration: Recent Progress of Therapeutic approaches
Current Molecular Pharmacology Therapeutic Use of Agonists of the Nuclear Receptor PPARγ in Alzheimers Disease
Current Alzheimer Research Diuretic-Associated Electrolyte Disorders in the Elderly: Risk Factors, Impact, Management and Prevention
Current Drug Safety Mitochondrial Triglyceride Transfer Protein Inhibition: New Achievements in the Treatment of Dyslipidemias
Current Pharmaceutical Design