Drug Designing: Open Access is a peer-reviewed and open access journal with an aim to provide rapid and reliable source of information in the mode of original articles, review articles, case reports, short communications, etc. in all areas of the field and making them freely available through online without any restrictions or any other subscriptions to researchers worldwide.

The Journal, Drug Designing: Open Access publishes the highest quality scientific articles amalgamating broad range of fields including molecular modeling, clinical research and drug discovery and delivery.

Neurodegeneration and cancer are fast becoming the leading causes of age-associated disability, dementia and ultimately death worldwide. Although oxidative stress has been intensely studied, little analysis has been done in chronic oxidative stress-induced mitochondrial models. In this regard, DNA-overproliferation and/or deletion initiate mitochondrial deregulation causing energy failure, which has been implicated in the pathogenesis of Alzheimer disease (AD), tumor growth, and metastasis. In this regard, decline in mitochondrial normal homeostasis during the development and maturation of the neurodegeneration, tumor growth, and/or metastases is characterized by tissue and cellular oxygen deficiency, which leads to subcellular energy defects. In addition, the overexpression of the cascades initiates the formation and release of large amounts of reactive free radicals [mainly nitric oxide (NO) via the overexpression of NO synthases (NOS)], which cause the oxidative stress, cellular alterations, and concomitant mitochondrial lesions and decline in normal organ function. The present study explores the intimate, i.e. direct relationship between chronic oxidative stress and mitochondrial damage as a vital life-supporter for cells and/ or the microcirculatory systems whose damage occurs before the development of human AD. Our study highlights the effects of chronic oxidative stress-induced mitochondrial DNA overproliferation and/or deletion and mitochondrial enzyme activities during the development of human AD. Mitochondrial DNA damage also leads to other pathologies, including colorectal cancer in liver metastasis, and malignant brain cancers. We hypothesize that mitochondrial lesions, especially mitochondrial DNA abnormalities, are detrimental to cell viability and thus mitochondrial DNA damage could be used as a new diagnostic tool and/or criterion for the early detection of AD and other diseases. Further extension of this approach will enable us not only for the better understanding of the blood brain barrier (BBB) homeostasis, which most likely plays a key role in the development of AD and some of forms of the cancer, but also for the development of new and more specific treatment strategies.

We publish the article related to the effects of dual diagnosis, Treatment, outcomes of the treatment. We invite different types of science communications including original research article, systematic reviews, short note communications, case reports, Editorials, letters to the Editors and expert opinions & commentaries from different regions for publication.

Manuscripts can be published through the online link. Or to the given below Email Id.

With Regards,
Sherry Peterson 
Drug Designing: Open Access
Editorial Manager
Email: drugdesign@longdom.org
Whats App:+1-947-333-4405