Association of Inflammatory Consequences with Oxidative Stress and the Impact of Antioxidants Supplementation in Alzheimer’s Disease | Chapter 8 | Current Topics on Chemistry and Biochemistry Vol. 9

 Alzheimer's disease [AD] is an age-connected progressive neurodegenerative ailment characterized by severe neurodegeneration in concerned individuals' hippocampus and neocortical domains of the brain. Inflammation and oxidative stress can contribute to the growth and progression AD. Here, we determined the association of oxidative stress accompanying inflammation in the pathophysiological consequences in cases with AD. For this, we driven Malondialdehyde [MDA], Nitric oxide [NO] metabolites, Erythrocyte-GSH (RBC-GSH), total antioxidant capacity [TAC] and the venture of Adenosine deaminase [ADA] as inflammatory stone levels and compared accompanying controls. We also aimed to estimate the influence of antioxidant supplementation in AD. The equating between ADA accompanying parameters of oxidative stress was more evaluated. Significant increase in the levels of oxidative and inflammatory limits was observed in inmates. Significant decreased levels of antioxidants were observed in inmates with AD. The meaningful positive equivalence was found between ADA and MDA levels and negative equivalence between ADA venture and the levels RBC-GSH and TAC. We conclude from the observation that the raised serum ADA project indicates instigative consequences and increased MDA accompanying decreased antioxidant ability indicates oxidative stress in AD patients. Increased angering and oxidative stress biomarkers, as well as their equivalence, are strongly connected to neuronal loss and other pathophysiological processes in Alzheimer's disease sufferers. The data accompanied that antioxidant supplementation reduced MDA and ADA levels while growing TAC. These findings are more significant than those got by the normal treatment group alone. Thus, antioxidant tests would be advantageous in preventing or restricting disease progression by underrating oxidative damage and, to a certain extent, modulating instigative consequences that prevent further neuronal misfortune in AD.

Author(s) Details:

Santoshi R. Ghodake,
Department of Biochemistry, SMBT Dental College and Hospital, Sangamner, Maharashtra, India.

A. N. Suryakar,
Dr. D. Y. Patil Vidyapeeth, India.

Please see the link here: https://stm.bookpi.org/CTCB-V9/article/view/9978