OBM Geriatrics is an international peer-reviewed 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 a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.
Publication Speed (median values for papers published in 2024): Submission to First Decision: 6.3 weeks; Submission to Acceptance: 11.4 weeks; Acceptance to Publication: 7 days (1-2 days of FREE language polishing included)
Special Issue
Senescent Cells as Therapeutic Targets
Submission Deadline:
January 15, 2026 (Open)
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Guest Editors
Urs Nydegger,
MD
Labormedizinisches Zentrum Dr. Risch, Bern-Liebefeld, CH 3097, Switzerland
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Research Interests: Senescence; red blood cell; complement system; autoimmunity; hematology; immunology
Lorenz Risch,
MD
Labormedizinisches Zentrum Dr. Risch, Bern-Liebefeld, CH 3097, Switzerland
Website | E-Mail
Research Interests: Hematologic diseases; insulin resistance; hypertension; atherosclerosis; diabetes; public health; pharmacology; blood pressure
Benjamin Sakem,
PhD
Labormedizinisches Zentrum Dr. Risch, Bern-Liebefeld, CH 3097, Switzerland
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Research Interests: DNA; cell culture; PCR; serum and urine electrophoresis; monoclonal gammopathy; diabetes; vitamin D; geriatrics and senescence
About This Topic
Currently, both scientific and lay press are filled with text releases on work that would explain to the reader biological reasons for the ever-prolonging healthy life expectancy of us humans. The field of cell biology with its major chapters of cell receptors/ligands, intracellular information transfer, mitochondrial energy procurement, and chromosomal biology involving recent insights into genetics, has allowed us to focus our interest on the senescence of single cell types all by comparing those located at various anatomical locations of the human body. Distinction of cell types refines at a fast pace thanks to evolving lab tests, e.g. cytofluorometry (go to: https://cytometryschool.ch). Identification of the activation status using FACS (fluorescence-activating cell sorting) has allowed ascribing senescent cells a whole list of markers the most important being p16 and p21; new terminology on cell-based therapies is slowly but surely becoming established; such designations as checkpoint inhibitors, CAR T cells to engineer patients’ immune cells or else in the cancer fields have become common language among medics and they conquer the pharmaceutical industries field. Senescent is a cell clone that becomes unable to divide, eventually dying off. The cell then releases interleukins and other metabolites leaving traces in the microenvironment – a multitude of effects favourable or moldy now explored by many research labs.
Medics get attentive when the pharmaceutical industry does and vice versa; thus, senescence is not merely "dying off" but bears pharmaceutical significance in the network of innate and acquired immunity.
Luckily today, a large amount of knowledge on cell-aging in plants, animals and primates has accrued, and modern laboratory techniques now allow to monitor aging sequence biochemistry using CRISPR, PCR, kinetically confined single cell analysis, gene expression profiling and DNA methylation quantification. Another impetus looking into senescence comes from Francis S. Collins MD who saw a woman afflicted with progeria, i.e. accelerated aging, now known to express the T letter instead of C in the middle of the gene coding lamin A, this nuclear structural protein. Indeed, genome-wide disease association (GWDA) has revealed 16 different loci associated with old age; the most prominent: TP53, TNF, APOE and IL6. Such advances have made insights into senescence to become a precious field of interest for geriatrics. Are different cellular functions undergoing different senescence pathways - typical for any given function? Certainly, an insulin producing beta islet cell features a different senescing biology in T2 diabetes mellitus as compared with Langerhans’ islet cells in healthy individuals but while this is plausible, nature keeps the way this is governed secret. May this special issue of OBM Geriatrics stimulate colleagues’ and scientists’ imagination. At least, senescent cells of the senescent immune system make place for immunocompetent acquired immunity.
Acknowledgments: The linguistic support by Levi Jaun, cand math, is kindly acknowledged.
Keywords
Telomer biomarker; protein glycation helicase; mitochondria CpG sites; inflammasome CAR T; target of rapamycine (TOR); CRISPR
Manuscript Submission Information
Manuscripts should be submitted through the LIDSEN Submission System. Detailed information on manuscript preparation and submission is available in the Instructions for Authors. All submitted articles will be thoroughly refereed through a single-blind peer-review process and will be processed following the Editorial Process and Quality Control policy. Upon acceptance, the article will be immediately published in a regular issue of the journal and will be listed together on the special issue website, with a label that the article belongs to the Special Issue. LIDSEN distributes articles under the Creative Commons Attribution (CC BY 4.0) License in an open-access model. The authors own the copyright to the article, and the article can be free to access, distribute, and reuse provided that the original work is correctly cited.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). Research articles and review articles are highly invited. Authors are encouraged to send the tentative title and abstract of the planned paper to the Editorial Office (geriatrics@lidsen.com) for record. If you have any questions, please do not hesitate to contact the Editorial Office.
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Publication
Abstract
In addition to their hemostatic functions, platelets play an essential role in immunologic interactions, which is confirmed by the observation of an increase in platelet counts in patients with immune-related thrombocytopenia and other autoimmune diseases after immunomodulatory treatment with intravenous human immunoglobulin concentrate. The [...]
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Urs Nydegger
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