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Role of Oxidative Stress in the Onset of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Tasnuva Sarowar, Md. Hafiz Uddin
Several antioxidants have been tested in clinical trials with some initial success. For example, idebenone, an analog of ubiquinone, a known antioxidant, has been shown to improve memory and attention in AD patients (Senin et al. 1992). However, it failed in a later stage study (Thal et al. 2003). Some of the other tested antioxidants are mitoquinone mesylate (mitoQ), dimebon, curcumin, acetyl-L-carnitine (ALCAR), vitamin C and E, and pramiprexol. MitoQ is also a ubiquinone derivative and has been applied to reduce oxidative stress (Smith and Murphy 2010). Dimebon, an antihistamine, showed promising results initially, but in phase III trials the patients did not show any improvement (Bezprozvanny 2010). Other antioxidants also could not show any favorable result. The major problem with such drugs is their penetration through the blood–brain barrier. In this regard, delivering the drugs encapsulated in nanoparticles could be an option. Such an approach has already shown some success in animal models (Vilella et al. 2018).
Pharmacological Management of Alzheimer’s Disease
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rakesh Kumar, Rajan Kumar, Abhinav Anand, Neha Sharma, Navneet Khurana
Dimebon is a trade name of latrepirdine which is also known as dimebolin. In 1983 it was used as antihistamine drug in Russia. But as per clinical research, latrepirdine improved cognitive function in AD patients while destroying the psychopathic symptoms. Dimebon is administered orally to show cholinesterase inhibition and NMDA-antagonist activities. It has been predicted the brain cell death inhibition in the animal model of the AD. Due to a non-reactive result in a human trial, it couldn’t show the positive response in AD patients. That is why dimebon was unlicensed for neurodegenerative conditions (Doody et al., 2008; Jones, 2010).
Misconnecting the dots: altered mitochondrial protein-protein interactions and their role in neurodegenerative disorders
Published in Expert Review of Proteomics, 2020
Mara Zilocchi, Mohamed Taha Moutaoufik, Matthew Jessulat, Sadhna Phanse, Khaled A. Aly, Mohan Babu
At the center of most obstacles comes the lack of a comprehensive and complete characterization of the mt interactome in various NDs, and of a reference database that includes both strictly mt proteins and mt-associated proteins. These still represent a pitfall in the study of mt diseases. In particular, the creation of web-based tools that collect information regarding alterations of mt protein complexes in every cellular model (cell lines, primary skin fibroblasts, iPSC-derived neurons and brain organoids) could advance the characterization of the pathological pathways that signify each ND, and provide insights into the impact of different cellular environments on PPIs. Data collection on altered mtPPI restorations using specific mt targeting medicines can expand on current therapeutic strategies against these debilitating disorders. Indeed, drugs with different mechanisms of action have been tried in several endeavors to restore mt impairment [200]. For example, it has been reported that mt respiratory activity is restored using metformin, a drug that activates CREB-binding protein upon increased phosphorylation of AMPK [201]. Notably, CREB-binding protein increases the expression of several other mt genes, thereby mediating neuronal protection [202]. Starting in 2015 onward, there have been hundreds of clinical trials that can be searched at https://clinicaltrials.gov which contain mt as a keyword. Drug development attempts are exemplified by CoQ10 for PD treatment through ROS scavenging, Dimebon for AD treatment and others [203]. Yet, the impact of these medicines on the global mt interactome is still understudied.
Have there been improvements in Alzheimer’s disease drug discovery over the past 5 years?
Published in Expert Opinion on Drug Discovery, 2018
Several histaminergic drugs have been recently incorporated into the AD pipeline, especially histamine H3 receptor antagonists (S 38093, GSK239512, E159, SAR110894, Ciproxifan, Clobenpropit, Benzo[h][1,6]naphthyridine derivatives, 3-substituted-indole derivatives, UW-MD-71, benzazepine class of histamine H3 receptor antagonists) and atypical non-selective antihistaminics, such as Latrepirdine (Dimebon) [16].