Is Alzheimer's disease a Type 3 Diabetes? A critical appraisal.
TLDR
Significant shared mechanisms between AD and diabetes are discussed and therapeutic avenues for diabetes and AD are provided and the effects of insulin in the pathology of AD through cellular and molecular mechanisms are provided.About:
This article is published in Biochimica et Biophysica Acta.The article was published on 2017-05-01 and is currently open access. It has received 376 citations till now. The article focuses on the topics: Insulin resistance & Insulin.read more
Citations
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Eric Tönnies,Eugenia Trushina +1 more
TL;DR: The role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease are discussed.
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Melatonin and inflammation—Story of a double‐edged blade
TL;DR: A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2.
Journal ArticleDOI
Obesity pandemic: causes, consequences, and solutions—but do we have the will?
TL;DR: The many causes of obesity are described, including key roles that a dysbiotic intestinal microbiome plays in metabolic derangements accompanying obesity, increased calorie absorption, and increased appetite and fat storage.
Journal ArticleDOI
Nutrient regulation of signaling and transcription.
TL;DR: This review will present an overview of the current understanding of O-GlcNAc's regulation, functions, and roles in chronic diseases of aging.
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Comprehensive review of mechanisms of pathogenesis involved in Alzheimer's disease and potential therapeutic strategies.
Piyoosh Sharma,Pavan Srivastava,Ankit Seth,Prabhash Nath Tripathi,Anupam G. Banerjee,Sushant K. Shrivastava +5 more
TL;DR: The present review provides an insight to the different molecular mechanisms involved in the development and progression of the AD and potential therapeutic strategies, enlightening perceptions into structural information of conventional and novel targets along with the successful applications of computational approaches for the design of target-specific inhibitors.
References
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Journal ArticleDOI
Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway
Ganesh M. Shankar,Brenda L. Bloodgood,Matthew Townsend,Dominic M. Walsh,Dennis J. Selkoe,Bernardo L. Sabatini +5 more
TL;DR: It is concluded that soluble, low-n oligomers of human Aβ trigger synapse loss that can be reversed by therapeutic agents and provides a quantitative cellular model for elucidating the molecular basis of Aβ-induced neuronal dysfunction.
Journal ArticleDOI
Immune attack: the role of inflammation in Alzheimer disease
TL;DR: As inflammation in AD primarily concerns the innate immune system — unlike in 'typical' neuroinflammatory diseases such as multiple sclerosis and encephalitides — the concept of neuroinflammation in AD may need refinement.
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Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism
TL;DR: The findings suggest that a CREB family member acts cooperatively with an additional transcription factor(s) to regulate BDNF transcription, and concludes that the BDNF gene is aCREB family target whose protein product functions at synapses to control adaptive neuronal responses.
Journal ArticleDOI
Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline
Konrad Talbot,Hoau-Yan Wang,Hala Kazi,Li-Ying Han,Kalindi Bakshi,Andres Stucky,Robert L. Fuino,Krista R. Kawaguchi,Andrew J. Samoyedny,Robert S. Wilson,Zoe Arvanitakis,Julie A. Schneider,Bryan A. Wolf,David A. Bennett,John Q. Trojanowski,Steven E. Arnold +15 more
TL;DR: Brain insulin resistance appears to be an early and common feature of AD, a phenomenon accompanied by IGF-1 resistance and closely associated with IRS-1 dysfunction potentially triggered by Aβ oligomers and yet promoting cognitive decline independent of classic AD pathology.
Journal ArticleDOI
Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease--is this type 3 diabetes?
Eric J. Steen,Benjamin M. Terry,Enrique J. Rivera,Jennifer L. Cannon,Thomas R. Neely,Rose Tavares,X. Julia Xu,Jack R. Wands,Suzanne M. de la Monte +8 more
TL;DR: The present work demonstrates extensive abnormalities in insulin and insulin-like growth factor type I and II (IGF-I and IGF-II) signaling mechanisms in brains with AD, and shows that while each of the corresponding growth factors is normally made in central nervous system neurons, the expression levels are markedly reduced in AD.
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