Dr. Weeks’ Comment: I have pulled together and presented below the relevant research on curry (tumeric/curcumin) as regards the prevention and treatment of dementia in general and Alzheimer’s disease in particular.

Why hasn’t your neurologist or geriatric doctor or memory specialist told you and your parent(s) about curry? Perhaps because no drug company has (yet) patented the active ingredient of this anti-inflammatory, anti-oxidant and anti-cancer cellular proliferant herb.

Scan below and note the top notch publications who have printed this data which never gets shared with the suffering patients.

Neuroreport. 2010 Nov 30. [Epub ahead of print]

Revisiting dietary antioxidants, neurodegeneration and dementia.

Craggs L, Kalaria RN.

Institute for Ageing and Health, Newcastle University, Newcastle Upon Tyne, UK.

Abstract

Epidemiological studies suggest there is marginal benefit that dietary antioxidants reduce risk of Alzheimer type of dementias. Yet cumulative biological evidence indicates oxidative and nitrosative stresses are precursors of neurodegenerative and neurovascular processes. Different dietary flavonoids and polyphenols found in fruits, vegetables, and spices such as curcumin offer neuroprotection through different mechanisms. A study in this volume shows that tetrahydrocurcumin confers protection against amyloid Î²-induced toxicity by reducing reactive oxygen species and retaining mitochondrial membrane potential. Alzheimer’s disease is a complex disorder. A single target through use of antioxidants may be effective in some but multiple approaches for its control seem to be necessary.

Biomaterials. 2011 Feb;32(6):1635-45. Epub 2010 Dec 4.

Curcumin-decorated nanoliposomes with very high affinity for amyloid-Î²1-42 peptide.

Mourtas S, Canovi M, Zona C, Aurilia D, Niarakis A, La Ferla B, Salmona M, Nicotra F, Gobbi M, Antimisiaris SG.

Laboratory of Pharmaceutical Technology, Department of Pharmacy, University of Patras, Rio 26510, Patras, Greece.

Abstract

Amyloid Î² (AÎ²) aggregates are considered as possible targets for therapy and/or diagnosis of Alzheimer disease (AD). It has been previously shown that curcumin targets AÎ² plaques and interferes with their formation, suggesting a potential role for prevention or treatment of AD. Herein, a click chemistry method was used to generate nanoliposomes decorated with a curcumin derivative, designed to maintain the planar structure required for interaction with AÎ², as directly confirmed by Surface Plasmon Resonance experiments. Another type of liposomes was formed starting from curcumin-phospholipid conjugate, in which the planar structure of curcumin is disrupted. Both types of generated curcumin-decorated vesicles had mean diameters in the nano range (131-207 nm) and slightly negative Î¶-potential values according to their lipid composition, and were stable for periods up to 20 days. They also demonstrated high integrity during incubation in presence of plasma proteins. Surface Plasmon Resonance experiments, measuring the binding of flowing liposomes to immobilized AÎ²1-42, indicated that the liposomes exposing the curcumin derivative (maintaining the planarity) have extremely high affinity for AÎ²1-42 fibrils (1-5 nM), likely because of the occurrence of multivalent interactions, whereas those exposing non-planar curcumin did not bind to AÎ²1-42. In summary, we describe here the preparation and characterization of new nanoparticles with a very high affinity for AÎ²1-42 fibrils, to be exploited as vectors for the targeted delivery of new diagnostic and therapeutic molecules for AD.

Expert Opin Ther Targets. 2010 Nov;14(11):1177-97.

Novel drug targets based on metallobiology of Alzheimer’s disease.

Bandyopadhyay S, Huang X, Lahiri DK, Rogers JT.

Indian Institute of Toxicology Research, Developmental Toxicology, Lucknow, India. sanghmitra@iitr.res.in

Abstract

IMPORTANCE OF THE FIELD: Increased localization of Zn, Fe, Cu and Al within the senile plaques (SP) exacerbates amyloid beta (AÎ²)-mediated oxidative damage, and acts as catalyst for AÎ² aggregation in Alzheimer’s disease (AD). Thus, disruption of aberrant metal-peptide interactions via chelation therapy holds considerable promise as a rational therapeutic strategy against Alzheimer’s amyloid pathogenesis.

AREAS COVERED IN THIS REVIEW: The complexities of metal-induced genesis of SP are reviewed. The recent advances in the molecular mechanism of action of metal chelating agents are discussed with critical assessment of their potential to become drugs.

WHAT THE READER WILL GAIN: Taking into consideration the interaction of metals with the metal-responsive elements on the Alzheimer’s amyloid precursor protein (APP), readers will gain understanding of several points to bear in mind when developing a screening campaign for AD-therapeutics.

TAKE HOME MESSAGE: A functional iron-responsive element (IRE) RNA stem loop in the 5′ untranslated region (UTR) of the APP transcript regulates neural APP translation. Desferrioxamine, clioquinol, tetrathiolmolybdate, dimercaptopropanol, VK-28, and natural antioxidants, such as curcumin and ginko biloba need critical evaluation as AD therapeutics. There is a necessity for novel screens (related to metallobiology) to identify therapeutics effective in AD.

J Biol Chem. 2010 Sep 10;285(37):28472-80. Epub 2010 Jul 9.

Curcumin decreases amyloid-beta peptide levels by attenuating the maturation of amyloid-beta precursor protein.

Zhang C, Browne A, Child D, Tanzi RE.

Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129-2060, USA.

Abstract

Alzheimer disease (AD) is a devastating neurodegenerative disease with no cure. The pathogenesis of AD is believed to be driven primarily by amyloid-beta (Abeta), the principal component of senile plaques. Abeta is an approximately 4-kDa peptide generated via cleavage of the amyloid-beta precursor protein (APP). Curcumin is a compound in the widely used culinary spice, turmeric, which possesses potent and broad biological activities, including anti-inflammatory and antioxidant activities, chemopreventative effects, and effects on protein trafficking. Recent in vivo studies indicate that curcumin is able to reduce Abeta-related pathology in transgenic AD mouse models via unknown molecular mechanisms. Here, we investigated the effects of curcumin on Abeta levels and APP processing in various cell lines and mouse primary cortical neurons. We show for the first time that curcumin potently lowers Abeta levels by attenuating the maturation of APP in the secretory pathway. These data provide a mechanism of action for the ability of curcumin to attenuate amyloid-beta pathology.

Neuroscience. 2010 Sep 1;169(3):1296-306. Epub 2010 Jun 9.

Curcuminoids enhance memory in an amyloid-infused rat model of Alzheimer’s disease.

Ahmed T, Enam SA, Gilani AH.

Natural Products Research Unit, Department of Biological and Biomedical Sciences, The Aga Khan University Medical College, Karachi-74800, Pakistan.

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease. There are a limited number of therapeutic options available for the treatment of AD. Curcuminoids (a mixture of bisdemethoxycurcumin, demethoxycurcumin and curcumin) is the main chemical constituent found in turmeric, a well known curry spice, having potential in the treatment of AD. The objective of this study was to investigate the effects of curcuminoid mixture and individual constituents on spatial learning and memory in an amyloid-beta (Abeta) peptide-infused rat model of AD and on the expression of PSD-95, synaptophysin and camkIV. Curcuminoid mixture showed a memory-enhancing effect in rats displaying AD-like neuronal loss only at 30 mg/kg, whereas individual components were effective at 3-30 mg/kg. A shorter duration treatment with test compounds showed that the curcuminoid mixture and bisdemethoxycurcumin increased PSD-95 expression in the hippocampus at 3-30 mg/kg, with maximum effect at a lower dose (3 mg/kg) with respective values of 470.5 and 587.9%. However, after a longer duration treatment, two other compounds (demethoxycurcumin and curcumin) also increased PSD-95 to 331.7 and 226.2% respectively at 30 mg/kg. When studied for their effect on synaptophysin in the hippocampus after the longer duration treatment, the curcuminoid mixture and all three individual constituents increased synaptophysin expression. Of these, demethoxycurcumin was the most effective showing a 350.1% increase (P<0.01) at 30 mg/kg compared to the neurotoxin group. When studied for their effect on camkIV expression after longer treatment in the hippocampus, only demethoxycurcumin at 30 mg/kg increased levels to 421.2%. These compounds salvaged PSD-95, synaptophysin and camkIV expression levels in the hippocampus in the rat AD model, which suggests multiple target sites with the potential of curcuminoids in spatial memory enhancing and disease modifying in AD.

J Am Osteopath Assoc. 2010 Sep;110(9 Suppl 8):S27-36.

Investigational medications for treatment of patients with Alzheimer disease.

Potter PE.

Department of Pharmacology, Midwestern University/Arizona College of Osteopathic Medicine, Glendale, Arizona 85308-6813, USA. ppotte@midwestern.edu

Abstract

Development of effective treatments for patients with Alzheimer disease has been challenging. Currently approved treatments include acetylcholinesterase inhibitors and the N-methyl-D-aspartate receptor antagonist memantine hydrochloride. To investigate treatments in development for patients with Alzheimer disease, the author conducted a review of the literature. New approaches for treatment or prevention focus on several general areas, including cholinergic receptor agonists, drugs to decrease Î²-amyloid and tau levels, antiinflammatory agents, drugs to increase nitric oxide and cyclic guanosine monophosphate levels, and substances to reduce cell death or promote cellular regeneration. The author focuses on medications currently in clinical trials. Cholinergic agents include orthostatic and allosteric muscarinic M1 agonists and nicotinic receptor agonists. Investigational agents that target Î²-amyloid include vaccines, antibodies, and inhibitors of Î²-amyloid production. Anti-inflammatory agents, including nonsteroidal anti-inflammatory drugs, the natural product curcumin, and the tumor necrosis factor Î± inhibitor etanercept, have also been studied. Some drugs currently approved for other uses may also show promise for treatment of patients with Alzheimer disease. Results of clinical trials with many of these investigational drugs have been disappointing, perhaps because of their use with patients in advanced stages of Alzheimer disease. Effective treatment may need to begin earlier-before neurodegeneration becomes severe enough for symptoms to appear.

Synthesis and biological evaluation of novel N,N’-bis-methylenedioxybenzyl-alkylenediamines as bivalent anti-Alzheimer disease ligands.

Luo W, Li YP, Tan JH, Gu LQ, Huang ZS.

J Enzyme Inhib Med Chem. 2011 Jan 21. [Epub ahead of print]

PMID:: 21250822; [PubMed – as supplied by publisher]

Revisiting dietary antioxidants, neurodegeneration and dementia.

Abstract

Curcumin-decorated nanoliposomes with very high affinity for amyloid-Î²1-42 peptide.

Abstract

Novel drug targets based on metallobiology of Alzheimer’s disease.

Abstract

Curcumin decreases amyloid-beta peptide levels by attenuating the maturation of amyloid-beta precursor protein.

Abstract

Curcuminoids enhance memory in an amyloid-infused rat model of Alzheimer’s disease.

Abstract

Investigational medications for treatment of patients with Alzheimer disease.

Abstract

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