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).
Perspectives on Telomeres and Aging II
Submission Deadline: May 15, 2023 (Open) Submit Now
Michael Fossel, MD, PhD
1. President of Telocyte (http://www.telocyte.com), Grand Rapids, MI 49503, USA
2. Retired Clinical Professor of Medicine, Michigan State University, Ada, MI 49301, USA
Research Interests: human aging; telomeres; telomerase therapy; age-related diseases; Alzheimer's disease
Kurt Whittemore, Post-Doctoral Research Fellow
Harvard Medical School/Boston Children's Hospital
Research Interests: Molecular biology; Aging; Gene therapy; Telomeres; Telomerase
About This Topic
The role of telomeres in the aging process is still not fully defined and can even be controversial. Leonard Hayflick first discovered that mammalian cells divide a limited number of times before reaching a limit and entering senescence. The introduction of telomerase into such cells can overcome this limit. Telomerase is also over-expressed in most cancers, allowing these cells to divide indefinitely. However, the idea that telomere length is a key part of the aging process in mammals has been complicated by the fact that lab mice are born with much longer telomeres than humans, and telomerase knockout mice do not live much shorter lives until subsequent generations. Some researchers argue that telomeres play little role in the aging process and that epigenetic changes measured by tools such as methylation clocks are a more effective means of studying the aging process. On the other hand, over-expression of the telomerase gene in mice has resulted in longer lifespans or improved health in the studies from several independent research groups. Given the evidence accumulated over the decades, what is the role of telomere length, telomere shortening rate, telomerase, and senescent cells on the aging process?
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