scholarly journals Involvement of Free Radicals in the Development and Progression of Alzheimer’s Disease

10.5772/64708 ◽  
2016 ◽  
Author(s):  
Martha C. Rosales Hernández ◽  
Maricarmen Hernández Rodríguez ◽  
Jessica E. Mendieta Wejebe ◽  
José Correa Basurto
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radicals

Minimalistic Design Approach for Multi-Reactivity against Free Radicals and Metal-Free and Metal-Bound Amyloid-β Peptides: Redox-Based Substitutions of Benzene

2019 ◽  
Author(s):  
Mingeun Kim ◽  
Juhye Kang ◽  
Misun Lee ◽  
Jiyeon Han ◽  
Geewoo Nam ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radicals ◽  
Amyloid Β ◽  
Design Strategy ◽  
Design Approach ◽  
Metal Free

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.

scholarly journals Synthesis and DPPH scavenging assay of reserpine analogues, computational studies and in silico docking studies in AChE and BChE responsible for Alzheimer's disease

2015 ◽  
Vol 51 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Muhammad Yar ◽  
Muhammad Arshad ◽  
Ariba Farooq ◽  
Mazhar Amjad Gilani ◽  
Khurshid Ayub ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radicals ◽  
In Silico ◽  
Density Functional ◽  
Neurodegenerative Disorder ◽  
Antioxidant Properties ◽  
Docking Studies ◽  
In Silico Docking ◽  
Ic50 Values

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.

P3-068: The role of inflammation and free radicals in Alzheimer's disease type dementia

2015 ◽  
Vol 11 (7S_Part_14) ◽  
pp. P643-P643 ◽  
Author(s):  
Nino Lobjanidze ◽  
Nino Akiashili ◽  
Maia Beridze ◽  
Marina Janelidze
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Free Radicals ◽  
Disease Type

scholarly journals Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 146
Author(s):  
Ryszard Pluta ◽  
Jacek Kiś ◽  
Sławomir Januszewski ◽  
Mirosław Jabłoński ◽  
Stanisław J. Czuczwar
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dna Damage ◽  
Free Radicals ◽  
Brain Ischemia ◽  
Tau Protein ◽  
Dna Damage And Repair ◽  
Ischemic Brain ◽  
Remarkable Progress

Recent years have seen remarkable progress in research into free radicals oxidative stress, particularly in the context of post-ischemic recirculation brain injury. Oxidative stress in post-ischemic tissues violates the integrity of the genome, causing DNA damage, death of neuronal, glial and vascular cells, and impaired neurological outcome after brain ischemia. Indeed, it is now known that DNA damage and repair play a key role in post-stroke white and gray matter remodeling, and restoring the integrity of the blood-brain barrier. This review will present one of the newly characterized mechanisms that emerged with genomic and proteomic development that led to brain ischemia to a new level of post-ischemic neuropathological mechanisms, such as the presence of amyloid plaques and the development of neurofibrillary tangles, which further exacerbate oxidative stress. Finally, we hypothesize that modified amyloid and the tau protein, along with the oxidative stress generated, are new key elements in the vicious circle important in the development of post-ischemic neurodegeneration in a type of Alzheimer’s disease proteinopathy.

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