Chemo Brain (Chemo Fog) as a Potential Side Effect of Doxorubicin Administration: Role of Cytokine-Induced, Oxidative/Nitrosative Stress in Cognitive Dysfunction

Author(s):  
Christopher D. Aluise ◽  
Rukhsana Sultana ◽  
Jitbangjong Tangpong ◽  
Mary Vore ◽  
Daret St. Clair ◽  
...  
2021 ◽  
Author(s):  
Ankit Uniyal ◽  
Akhilesh Kotiyal ◽  
Anagha Gadepalli ◽  
Obulapathi Ummadisetty ◽  
Vinod Tiwari

Abstract Alcohol consumption for a longer period of time is linked with neuronal damage and an increase in inflammatory signaling resulting in cell death and dementia. Natural compounds are the focus of research due to their high efficacy and good safety profile. Here we have investigated the effect of chronic epigallocatechin-3-gallate (EGCG) administration against the alcohol-induced cognitive deficit rats. Male Wistar rats were exposed to the ethanol (10 g/kg; oral gavage) for ten weeks and treated with EGCG (25, 50, and 100 mg/kg) for the same duration. Ethanol exposure led to the impaired spatial memory and learning in rats assessed using the Morris water maze and elevated plus-maze test. Further, we assessed the role of EGCG in mitigating the oxidative stress, neuroinflammatory and cell death signaling associated markers. Co-administration with EGCG significantly prevented all the behavioral, biochemical and molecular alterations in the different brain regions of ethanol-treated rats in a dose-dependent manner. EGCG suppressed the acetylcholinesterase activity, increased oxidative–nitrosative stress, cytokines (TNF-alpha and IL-1beta), NF-kappa β and caspase-3 levels in both the cortex and hippocampus of ethanol-treated rats. Our preliminary study demonstrated that EGCG improves the oxido-nitrosative stress, inflammation, and cell death signaling associated with ethanol-induced cognitive dysfunction. This suggests the potential role of EGCG in mitigating the cognitive deficits associated with chronic alcohol consumption.


2021 ◽  
Author(s):  
Haiyan Wu ◽  
Pengpeng Jia ◽  
Yu Zou ◽  
Jiang Jiang

Photothermal therapy, assisted by local heat generation using photothermal nanoparticles (NPs), is an emerging strategy to treat tumors noninvasively. To improve treatment outcome and to alleviate potential side effect on...


2021 ◽  
pp. 662-666
Author(s):  
Mitra Barahimi ◽  
Scott Lee ◽  
Kindra Clark-Snustad

We report the case of a 51-year-old male with Crohn’s disease (CD) who developed a reproducible pustular rash after ustekinumab (UST) administration. The patient first presented with a pustular rash on his hands, body, extremities, and scalp starting 5 weeks after his initial weight-based UST induction. The rash resolved spontaneously, then recurred 4 weeks after his first subcutaneous maintenance dose of UST 90 mg. Biopsy of the affected area demonstrated subcorneal pustular dermatosis (SPD). UST was discontinued and the rash resolved. Unfortunately, the patient experienced clinical recurrence of CD, and given prior failure of multiple CD medications, UST was restarted with premedication. Two weeks after UST re-induction, the rash recurred, though less severe. Given improvement in CD symptoms, UST was continued and the rash managed with topical corticosteroids. This is the first case of drug-induced SPD associated with UST. One case report has previously described de novo pustular psoriasis associated with UST in a patient with CD and enteropathic arthritis. Notably, SPD and pustular psoriasis can be histologically indistinguishable. The development of a paradoxical psoriasiform rash is thought to be one of the few dose and duration dependent side effects of TNF-antagonist therapy but has not previously been established as a side effect of UST. This case demonstrates a new potential side effect of UST.


2012 ◽  
Vol 71 (5) ◽  
pp. 403-409 ◽  
Author(s):  
Martha Millan Sanchez ◽  
Sietske N. Heyn ◽  
Devsmita Das ◽  
Sarah Moghadam ◽  
Kara J. Martin ◽  
...  

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