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.

Background: The study of phenolic compounds and their potential to contribute to health is a major interest in research. This work was to determine phenolic compound contents as well as antioxidant properties of roasted maize-peanut snack product with and without spices. Methods: HPLC was used to determine the phenolic composition of the maize flours, peanut flour and their composite snacks with and without spices. Total phenolic content (TPC), total flavonoid content (TFC), tannin content (TC) and radical scavenging activity (measured by 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2-azino-bis (3- ethylbenzothiazoline-6-sulphonicacid) (ABTS) and hydrogen peroxide radical scavenging assays was also used. Results: TPC of the extract of roasted maize flour, roasted peanut flour and composite roasted maize-peanut flour ranged from 48.93 to 178.31 mg GAE/100 g, while the TFC was 3.18–25.94 mg CE/100 g and TC (0.22 – 0.73 mg CE/g). The dominant phenolic acid was protocatechuic acid ranged from 13.73 to 1643.54 µg/g. Among the flavonoids, quercetin and catechin were dominant. The extracts of the free soluble fraction exhibited 23.88 – 81.52 %, 49.59 – 85.17 % and 0.58 -5.13 µmol AAE/g of DPPH, hydrogen peroxide and ABTS radical scavenging abilities respectively. Conclusion: Maize–peanut product showed potential ability in contributing to alleviating radical induced oxidative stress.

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.

Nutrition plays a key role in regulating the autonomic nervous system (ANS), which is responsible for controlling involuntary bodily functions such as heart rate, breathing, digestion and body temperature. Some nutrients, such as amino acids, vitamins and minerals, have a specific role in the ANS. For example, amino acids are necessary for the synthesis of neurotransmitters, such as serotonin and dopamine, which regulate mood and anxiety. Vitamins and minerals are important for the proper functioning of the ANS, such as vitamin B12, magnesium and zinc. A balanced diet can help reduce oxidative stress and inflammation, which can negatively affect ANS functioning. On the other hand, a nutrient-poor diet can lead to dysfunctions in the ANS, such as hypertension, changes in heart rate and digestive disorders. Digestive problems such as constipation, diarrhea, irritable bowel syndrome (IBS) and functional dyspepsia can occur when the ANS is not working properly. It is important to maintain a healthy and balanced diet to ensure the proper functioning of the autonomic nervous system.