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).
Alzheimer's Disease: Current Knowledge and Future Perspectives
Submission Deadline: September 01, 2022 (Open) Submit Now
R. M. Damian Holsinger, PhD
1. Neuroscience, School Wof Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia
2. Laboratory of Molecular Neuroscience and Dementia, The Brain and Mind Centre, The University of Sydney, Camperdown, Australia
Research Interests: Understanding of mechanisms by which complex neurological disorders (with a special interest in Alzheimer's disease) arise and methods of treating these diseases
About This Topic:
Alzheimer’s disease (AD), the leading cause of dementia, is a progressive neurodegenerative disease of the brain that is characterized by memory impairment and cognitive dysfunction. Pathological hallmarks of AD include the extracellular deposition of amyloid beta (Aβ) plaques and the intracellular accumulation of neurofibrillary tangles that is accompanied by neuroinflammation. Age is the most common risk factor for the disease. Recently however, genome wide association studies (GWAS) have identified several AD risk-associated genes. This information is changing the landscape of disease recognition and diagnosis. The literature is repleat with new information and data that is establishing a paradigm shift in the manner in which we investigate and treat individuals with Alzheimer’s.
In this Special Issue, we aim to draw together research from experts in the field that highlight current knowledge of disease entities and therapeutic strategies and interventions and identify future directions that will lead to discoveries and therapies for Alzheimer’s disease.
Aging; Amyloid peptides; Astrocytes; Biomarkers; Cognition; GWAS; Imaging; Memory deficits; Microglia; Neurodegeneration; Neuroinflammation; Oxidative Stress; Plaques; Tangles; Tau protein
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