OBM Geriatrics

(ISSN 2638-1311)

OBM Geriatrics is an Open Access journal published quarterly online by LIDSEN Publishing Inc. The journal takes the premise that innovative approaches – including gene therapy, cell therapy, and epigenetic modulation – will result in clinical interventions that alter the fundamental pathology and the clinical course of age-related human diseases. We will give strong preference to papers that emphasize an alteration (or a potential alteration) in the fundamental disease course of Alzheimer’s disease, vascular aging diseases, osteoarthritis, osteoporosis, skin aging, immune senescence, and other age-related diseases.

Geriatric medicine is now entering a unique point in history, where the focus will no longer be on palliative, ameliorative, or social aspects of care for age-related disease, but will be capable of stopping, preventing, and reversing major disease constellations that have heretofore been entirely resistant to interventions based on “small molecular” pharmacological approaches. With the changing emphasis from genetic to epigenetic understandings of pathology (including telomere biology), with the use of gene delivery systems (including viral delivery systems), and with the use of cell-based therapies (including stem cell therapies), a fatalistic view of age-related disease is no longer a reasonable clinical default nor an appropriate clinical research paradigm.

Precedence will be given to papers describing fundamental interventions, including interventions that affect cell senescence, patterns of gene expression, telomere biology, stem cell biology, and other innovative, 21st century interventions, especially if the focus is on clinical applications, ongoing clinical trials, or animal trials preparatory to phase 1 human clinical trials.

Papers must be clear and concise, but detailed data is strongly encouraged. The journal publishes research articles, reviews, communications and technical notes. There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.


Archiving: full-text archived in CLOCKSS.

Rapid publication: manuscripts are undertaken in 12 days from acceptance to publication (median values for papers published in this journal in 2021, 1-2 days of FREE language polishing time is also included in this period). 

Current Issue: 2023  Archive: 2022 2021 2020 2019 2018 2017

Special Issue

Do [or Can] Antioxidants Slow the Aging Process?

Submission Deadline: July 01, 2023 (Open) Submit Now

Guest Editor

Karen E. Burke, PhD

Clinical Professor, Department of Dermatology, Icahn School of Medicine, New York, NY, USA

Website | E-Mail

Research Interests: Antioxidants to prevent and reverse photoaging and skin cancer; Environmental aging of the skin

About This Topic

This Special Issue of OBM Geriatrics will explore the most recent scientific research investigating the question “Will antioxidants slow the aging process?”.

There is no doubt that oxidative free-radical damage causes or contributes not only to many diseases of aging including cancer, cardiovascular disease, Alzheimer’s disease, Parkinson’s disease, cataracts, and immune system diseases, but also to “natural” aging processes. Although “oxidative stress” with generation of free radicals is not the only cause of aging, certainly molecular oxidative damage to cellular lipids, proteins, and DNA damages cells and extracellular tissue, contributing to the degenerative symptoms of aging. This damage by reactive oxygen species (ROS) is threefold: (1) peroxidation of membrane lipids by free-radical chain reactions; (2) formation of advanced glycation end products (AGEs); and (3) release of cytokines that stimulate signaling pathways, thereby activating inflammation and genes that modulate aging. With ongoing years, the body is exposed to cumulative external free radical damage from UV-exposure and environmental pollutants including cigarette smoke, industrial and traffic-generated airborne chemicals and particulate matter, ozone, and oxidative trace metal ions such as Fe(II) and Cu(II). All of this extrinsic oxidative stress accelerates aging. To combat this oxidative damage, our body has evolved an exquisite, complex network of interacting enzymes to quench free radicals (glutathione peroxidase and reductase, superoxide dismutase, catalase, thioredoxin reductase, and others). These enzymes interact with endogenous and exogenous low molecular weight nonenzymic antioxidants – some hydrophilic (such as vitamin C and glutathione), some lipohilic (vitamin E, coenzyme Q10, and retinoids) and some trace mineral cofactors (such as selenium and zinc). With aging, enzyme activity diminishes and levels of endogenously synthesized antioxidants decrease. Thus dietary and topical delivery of antioxidants is expected to enhance the body’s natural mechanisms to combat aging and disease.

This Special Issue will present the most recent research about the role, the mechanisms, and the requirements for formulations to assure stability, absorption (topical as well as dietary), activity, and optimal delivery of specific antioxidants. Evidence regarding efficacy of many newly available antioxidants (especially from botanical sources) will be included. This issue details the scientific evidence as to whether and which antioxidants can indeed retard, prevent, and/or reverse aging. Can antioxidants “make the difference between life and death, as well as influence how fast and how well we age,” as proposed by Lester Parker and Carol Coleman in The Antioxidant Manual? This Special Issue investigates this question.


Mechanisms of oxidative aging; Intrinsic oxidative aging; Extrinsic environmental oxidative aging; Antioxidant enzymes; Synergistic antioxidants; Dietary antioxidants; Topical antioxidants