Natural products as a source of Alzheimer's drug leads
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TLDR
This review focuses on recent developments in the use of natural products as therapeutics for Alzheimer's disease and discusses more than 180 compounds and summarizes 400 references.About:
This article is published in Natural Product Reports.The article was published on 2011-01-01 and is currently open access. It has received 327 citations till now.read more
Citations
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Journal ArticleDOI
Development of Multifunctional Molecules as Potential Therapeutic Candidates for Alzheimer’s Disease, Parkinson’s Disease, and Amyotrophic Lateral Sclerosis in the Last Decade
Masha G. Savelieff,Geewoo Nam,Geewoo Nam,Juhye Kang,Juhye Kang,Hyuck Jin Lee,Misun Lee,Misun Lee,Mi Hee Lim +8 more
TL;DR: Possible therapeutic targets in Alzheimer's disease, Parkinson's Disease, and amyotrophic lateral sclerosis are outlined and molecules, previously designed or discovered as potential drug candidates for these disorders with emphasis on multifunctionality are discussed.
Journal ArticleDOI
Neuroprotective Effect of Natural Products Against Alzheimer’s Disease
Musthafa Mohamed Essa,Reshmi K. Vijayan,Gloria Castellano-Gonzalez,M. A. Memon,Nady Braidy,Gilles J. Guillemin,Gilles J. Guillemin +6 more
TL;DR: The neuroprotective effects of various naturally occurring compounds in AD is evaluating in this review.
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Alzheimer's therapeutics: continued clinical failures question the validity of the amyloid hypothesis-but what lies beyond?
TL;DR: Genetic evidence supporting amyloid causality in AD is reviewed in the context of the clinical failures, and progress in tau-based and alternative approaches to AD, where an evolving modus operandi in biomedical research fosters excessive optimism and a preoccupation with unproven and often ephemeral, biomarker/genome-based approaches.
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Inhibition of aggregation of amyloid peptides by beta-sheet breaker peptides and their binding affinity.
TL;DR: By simulations, the relationship between aggregation rates and binding affinity is clarified and it is predicted that LPFFD inhibits/degrades the fibrillogenesis of full-length amyloid peptides better than KLVFF.
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The Role of Phytochemicals in the Treatment and Prevention of Dementia
TL;DR: The potential and actual therapeutic strategies for dementia in relation to the known mechanisms of dementia pathology are presented and plant extracts that have shown relevant mechanistic effects for dementia and promising clinical data, but require more evidence for their clinical efficacy and safety are presented.
References
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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
John Hardy,Dennis J. Selkoe +1 more
TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
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Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families
Elizabeth H. Corder,Ann M. Saunders,Warren J. Strittmatter,Donald E. Schmechel,P. C. Gaskell,Gary W. Small,A. D. Roses,Jonathan L. Haines,Margaret A. Pericak-Vance +8 more
TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.
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Alzheimer's disease: the amyloid cascade hypothesis
John Hardy,Gerald A. Higgins +1 more
TL;DR: An extensive catalog of genes that act in a migrating cell is provided, unique molecular functions involved in nematode cell migration are identified, and similar functions in humans are suggested.
Journal ArticleDOI
Natural Products as Sources of New Drugs over the Last 25 Years
David J. Newman,Gordon M. Cragg +1 more
TL;DR: This review is an updated and expanded version of two prior reviews that were published in this journal in 1997 and 2003 and is able to identify only one de novo combinatorial compound approved as a drug in this 25 plus year time frame.
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Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease.
Alison Goate,Marie-Christine Chartier-Harlin,Michael Mullan,Jeremy P Brown,Fiona Crawford,Liana Fidani,L. Giuffra,Andrew Haynes,N.G. Irving,Louise James,R. Mant,Phillippa Newton,Karen Rooke,P Roques,Christopher Talbot,Margaret A. Pericak-Vance,Alien D. Roses,Robert Williamson,Martin N. Rossor,Michael John Owen,John Hardy +20 more
TL;DR: A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein (APP) gene as discussed by the authors, which suggests that some cases of AD could be caused by mutations in the APP gene.