scholarly journals Free Radicals and Cell Signaling in Alzheimer's Disease

2007 ◽  
Vol 11 (2) ◽  
pp. 141-141
Author(s):  
Mingeun Kim ◽  
Juhye Kang ◽  
Misun Lee ◽  
Jiyeon Han ◽  
Geewoo Nam ◽  
...  

We report a minimalistic redox-based design strategy for engineering compact molecules based on the simplest aromatic framework, benzene, with multi-reactivity against free radicals, metal-free amyloid-β, and metal-bound amyloid-β, implicated in the most common form of dementia, Alzheimer’s disease.


2015 ◽  
Vol 51 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Muhammad Yar ◽  
Muhammad Arshad ◽  
Ariba Farooq ◽  
Mazhar Amjad Gilani ◽  
Khurshid Ayub ◽  
...  

Alzheimer's disease (AD) is a fast growing neurodegenerative disorder of the central nervous system and anti-oxidants can be used to help suppress the oxidative stress caused by the free radicals that are responsible for AD. A series of selected synthetic indole derivatives were biologically evaluated to identify potent new antioxidants. Most of the evaluated compounds showed significant to modest antioxidant properties (IC50 value 399.07 140.0±50 µM). Density Functional Theory (DFT) studies were carried out on the compounds and their corresponding free radicals. Differences in the energy of the parent compounds and their corresponding free radicals provided a good justification for the trend found in their IC50 values. In silico, docking of compounds into the proteins acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), which are well known for contributing in AD disease, was also performed to predict anti-AD potential.


2018 ◽  
Vol 1 (1) ◽  
Author(s):  
William G. O'Neal ◽  
Debomoy K. Lahiri, Ph.D ◽  
Mahua Dey, M.D ◽  
Ruizhi Wang

Background: Epidemiological studies suggest an inverse association between cancer and neurodegenerative disorders, including Alzheimer’s disease (AD). AD and cancers, such as glioblastoma multiforme (GBM), are characterized by abnormal but opposing cellular behavior. AD is characterized by accumulation of the processing products of amyloid β (Aβ) and its metabolizing enzymes amyloid precursor protein (APP), β-secretase (or BACE1), and γ-secretase. Our rationale is unraveling cell signaling pathways linking AD and GBM. We hypothesized low-grade gliomas (LGG) and high-grade gliomas (HGG) would have differential expression of neuronal and synaptic markers. Furthermore, protein expression profiles of these markers, APP metabolites, and BACE1 would be different among LGG, HGG, and AD cases.  Experimental Design or project methods: Specific neuronal protein markers (e.g., NSE), presynaptic proteins (e.g., synaptophysin and SNAP25), and post-synaptic proteins (e.g., PSD-95) have been measured in glioma samples. Characterization are done by Western immunoblotting and ELISA. Protein biomarkers will be analyzed in LGG and HGG of biopsy samples, and the results will be compared with brain samples from AD cases.  Results: Using specific primary and secondary antibodies and optimal protein range, we have standardized an immunoblotting procedure to detect our desired proteins in blinded LGG and HGG samples. After unblinding and analyzing results, expression signals will be compared between GBM and AD brain samples.  Conclusion and potential impact: Our results would shed light on diverging and/or shared cell signaling pathways between AD and GBM. In addition, potential impact would be utilizing GBM-derived cultures to test and develop therapeutics for both AD and GBM.


10.5772/64708 ◽  
2016 ◽  
Author(s):  
Martha C. Rosales Hernández ◽  
Maricarmen Hernández Rodríguez ◽  
Jessica E. Mendieta Wejebe ◽  
José Correa Basurto

2015 ◽  
Vol 11 (7S_Part_14) ◽  
pp. P643-P643 ◽  
Author(s):  
Nino Lobjanidze ◽  
Nino Akiashili ◽  
Maia Beridze ◽  
Marina Janelidze

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