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Aug 2026
E. Bredesen DaleCorresponding author
Background/Objectives The etiology and pathophysiology of neurodegenerative diseases are incompletely understood, and the treatments largely ineffective. A unifying theory that explains otherwise poorly understood observations may help to enhance therapeutic outcomes. Methods Here is proposed a unifying theory of neurodegenerative disease, the Pr2 theory, describing the origin, pathophysiology, optimal evaluation and treatment of patients, explanation of observations not explained by previous theories, and implications for further research and translation. The theory proposes that neurodegenerative diseases represent network insufficiencies, networks jeopardized by antagonistic pleiotropy. Through repeated evolutionary selection for performance over durability, highly functional and finely tuned neural subnetworks subserving key survival features such as lethal force and behavioral modification have evolved at the expense of durability and reserve. The Pr2 theory focuses on the physiology associated with the causes of neurodegeneration rather than the pathology that is largely reactive but has been the focus of the lion’s share of the research and attempted treatment of neurodegenerative diseases. Results Initial translation of the Pr2 theory to a precision medicine approach to cognitive decline has led to superior outcomes compared to other therapeutic approaches, and at least in some cases, sustained improvement for over a decade has been achieved. Conclusions The proposed theory explains key features of neurodegenerative disease pathophysiology and suggests novel therapeutic targets. Initial predictions have been validated in two proof-of-concept trials and one randomized controlled trial for patients with mild cognitive impairment or early-stage dementia.
Nov 2025 DOI 10.14302/issn.2326-0793.jpgr-25-5573
E. Imiruaye OghenetegaCorresponding author
Advancements in proteomic and genomic technologies have transformed molecular biology by enabling comprehensive analysis of biological systems at the molecular level. This literature review explores the evolution, methodologies, and practical applications of key proteomic and genomic techniques. In proteomics, tools such as two-dimensional electrophoresis, mass spectrometry, Western blotting, Edman degradation, and functional protein microarrays have facilitated high-throughput protein identification, post-translational modification analysis, and biomarker discovery. Similarly, genomic methodologies like PCR, recombinant DNA technology, gel electrophoresis, and Southern blotting have revolutionized gene detection, manipulation, and expression profiling. The review also highlights the interdisciplinary impact of these technologies across clinical diagnostics, oncology, autoimmune disorders, infectious disease surveillance, cardiovascular research, and personalized nutrition. Integrative approaches combining proteomics and genomics are enabling the discovery of novel therapeutic targets, improving disease classification, and advancing precision medicine. Despite current limitations, such as the absence of amplification techniques for proteins and challenges in data interpretation, ongoing innovations promise to bridge these gaps. This synthesis underscores the pivotal role of molecular techniques in deepening our understanding of human biology and accelerating biomedical advancements for improved healthcare outcomes.
Jul 2017 DOI 10.14302/issn.2574-4372.jesr-17-1705
Varma VijayalakshmiCorresponding author
Biomarkers and Alternative Models Branch, Division of Systems Biology, National Center for Toxicological Studies, Jefferson, AR
Drug-induced cardiotoxicity is one of the predominant reasons for drug attrition and withdrawals. This is of critical concern when potentially cardiotoxic drugs are administered to individuals with inherited arrhythmogenic cardiac diseases or with metabolic diseases such as obesity and diabetes, which are key risk factors for cardiovascular diseases. Pathophysiological alteration prevalent under such conditions can alter or exacerbate cardiotoxic responses. The growing incidence of obesity, diabetes and metabolic syndrome subject a significant percentage of the population to drug treatments, thereby augmenting their risk for drug-induced cardiovascular toxicity. Hence, screening for drug-induced cardiotoxicity early in the preclinical stages of drug development, by using appropriate human disease models, can be effective in ensuring safety in clinical trials and preventing late stage and post-marketing drug withdrawals owing to cardiotoxicity. The advent of human pluripotent stem cells (hPSC) and induced pluripotent stem cell (iPSC)-derived cardiomyocytes are revolutionizing safety/toxicity screening in human cells by providing relevant human-specific, renewable model systems to explore human drug toxicity. The ability to generate patient-specific iPSCs that can model cardiac diseases, now offers a valuable option that can further improve drug safety assessments and enable a more accurate prediction of toxicity that occurs in the representative population that are prescribed the drugs. Use of appropriate disease models will not only provide cost savings by decreasing potential drug attrition and withdrawals, seen with many drugs, but will also be a promising option to advance precision medicine