Background: Type 2 Diabetes Mellitus (T2DM) and Alzheimer’s Disease (AD) are increasingly linked through shared pathophysiological mechanisms, giving rise to the concept of Type 3 Diabetes Mellitus (T3DM). Brain insulin resistance, oxidative stress, and neuroinflammation are central to both conditions, contributing to cognitive decline and AD progression. Aim: This review aims to explore this emerging relationship and its implications for prevention and management. Methods: Using an integrative review, 21 studies were systematically analyzed. The review focused on identifying demographic, genetic, and lifestyle factors contributing to T2DM and AD and examined shared molecular pathways such as insulin dysregulation and amyloid-beta accumulation. Results: The findings reveal that T3DM shares key features with T2DM and AD, including insulin resistance and chronic inflammation. Lifestyle interventions, such as diet and exercise, alongside routine cognitive and metabolic screenings, are critical in mitigating progression. Conclusions: Further research into diagnostic biomarkers and targeted therapies is essential to manage T3DM and its impact on AD. The role of nursing professionals in early detection, education, and holistic management is emphasized as vital in addressing this dual disease burden. This review offers actionable insights into integrated strategies for addressing these interconnected conditions.

Early-onset neurodegenerative diseases (EO-NDs), such as early-onset Alzheimer’s disease (EOAD), Parkinson’s disease (EOPD), and familial amyotrophic lateral sclerosis (fALS), often stem from monogenic causes and manifest before typical age thresholds. These disorders frequently feature disrupted mitochondrial function and heightened oxidative stress, which together accelerate neuronal damage and degeneration. In this work, the author performs a comprehensive analysis of the literature and data related to mitochondrial dysfunction and redox imbalance in EO-NDs. Bibliometric trends were assessed using R-based tools on PubMed datasets, highlighting keyword networks and publication surges in recent years. Publicly available RNA-seq datasets from GEO and SRA were examined, with example DESeq2 analysis illustrating altered mitochondrial gene expression in EO-ND patient-derived samples. Network modeling of redox pathways using Python’s networkx demonstrates how oxidative stress can propagate through metabolic networks. Together, these computational approaches reinforce that mitochondrial DNA mutations, impaired electron transport chain (ETC) function, and reactive oxygen species (ROS) accumulation play central roles in EO-ND pathogenesis. The discussion further evaluates why antioxidant clinical trials have largely failed and how emerging therapies such as gene replacement, antisense oligonucleotides, and mitochondrial biogenesis modulators may provide more effective interventions.

The effects on the elderly are disproportionately Alzheimer’s disease (AD) is one of the most prevalent and chronic types of dementia. Alzheimer's disease (AD), a fatal illness that can harm brain structures and cells long before symptoms appear, is currently incurable and incurable. Using brain MRI pictures from a publicly accessible Kaggle dataset, this study suggests a prediction model based on Convolutional Neural Networks (CNNs) to help with the early detection of Alzheimer's disease. Four levels of dementia have been applied to the 6,400 photos in the collection: not demented, slightly demented, moderately demented, and considerably mildly demented. Pixel normalization, class balancing utilizing data augmentation techniques, and picture scaling to 128×128 pixels were all part of a thorough workflow for data preparation. To improve the gathering of spatial dependence in volumetric MRI data, a 3D convolutional neural network (CNN) architecture was used. We used important performance measures including F1-score, recall, accuracy, precision, and log loss to gauge the model's effectiveness. A review of the available data indicates that the total F1-score, accuracy, recall, and precision were 99.0%, 99.0%, and 99.38%, respectively. The findings demonstrate the model's potential for practical use in early AD diagnosis and establish its robustness with the help of confusion matrix analysis and performance curves.