Alzheimer Mechanisms and Therapeutic Strategies

By Yadong Huang, L. Mucke. Cell, 2012

1,730 citations recorded by the source corpus.

There are still no effective treatments to prevent, halt or reverse Alzheimer’s disease, but research advances over the past three decades could change this gloomy picture. Genetic studies demonstrate that the disease has multiple causes. Interdisciplinary approaches combining biochemistry, molecular and cell biology, and transgenic modeling have revealed some of its molecular mechanisms. Progress in chemistry, radiology, and systems biology is beginning to provide useful biomarkers and the emergence of personalized medicine is poised to transform pharmaceutical development and clinical trials. However, investigative and drug development efforts should be diversified to fully address the multifactoriality of the disease.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/c67b97544af4ba9c6a6197c68935b1a0e4fcf601

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In Cellular and Molecular Neuroscience

1. O. Maier
2. Roman Fischer

In Physiology

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2. Roman Fischer
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Citations in the corpus

• Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, background): “Although more than 90% of AD cases are sporadic, there are also familial forms of this disease, which are caused by mutations in APP or presenilin, the catalytic subunit of γsecretase [15].”
• TREM2 lipid sensing sustains microglia response in an Alzheimer’s disease model (2015, neutral): “…sustains microglia response in an Alzheimer’s disease model Yaming Wang1,5, Marina Cella1, Kaitlin Mallinson2,3,4, Jason D. Ulrich2,3,4, Katherine L. Young2,3,4, Michelle L. Robinette1, Susan Gifillian1, Gokul M. Krishnan1, Shwetha Sudhakar2,3,4, Bernd H. Zinselmeyer1, David M. Holtzman2,3,4, John…”
• APP mouse models for Alzheimer's disease preclinical studies (2017, neutral): “Box 1 summarizes the mutant APP or APP/PS-overexpressing mouse models, including prospective ideas that may be experimentally validated to better consoli-date the APP overexpression paradigm with human AD clinical pathogenesis (Huang & Mucke, 2012; Saito et al , 2014; Palop & Mucke, 2016).”
• The therapeutic potential of resveratrol: a review of clinical trials (2017, background): “For instance, amyloid-β (Aβ) plaque accumulation caused by amyloid beta precursor protein (APP) and apoliporprotein E (APOE) genetic mutations and increased inflammation and oxidative damage have been shown to be associated with AD.(42) Additionally, caloric restriction has been shown to prevent ons”
• Integrated systems approach identifies genetic nodes and networks in late-onset Alzheimer's disease (2013, background): “This is of interest given the strong epidemiological evidence for metabolic- and vascular-based exposure on LOAD (Huang and Mucke, 2012; Murray et al., 2011).”
• Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “More interesting, the promotion of histone acetylation improves learning and memory in a mouse model of AD and increases learning-related gene expression in aged wild-type mice (Kim et al., 2007) suggesting epigenetic regulation of learning and memory in health and disease (Huang and Mucke, 2012).”