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.

The therapeutic effect of Cyclophosphamide (CPA) is thus attributed to phosphoramide mustard and acrolein leads to the formation of high levels of reactive oxygen species (ROS), which results in decreased antioxidant activity. Excessive production of ROS could also culminate in oxidative stress. Objectives: This study aims to evaluate the effect of sub-lethal dose of the cyclophosphamide, 5-FU, combination of 5-FU, and CPA on testicular antioxidant status, and oxidative stress in male albino rats. Materials and Methods: Twenty-eight male adult rats were grouped randomly into four groups (n=5 each group). Group I (control): Rats were injected with saline intraperitoneally and at a dose of 1.0 ml/kg b.w. for 14 days. Group II cyclophosphamide (CPA): Cyclophosphamide at a dose of 10 mg/kg day by day through i.p. to rats for 14 days. Group III Fluorouracil (5-FU): 5-Fluorouracil at a dose of 10 mg/kg day by day in saline was given through i.p. to rats for 14 days. Group IV (CPA+5-FU): Rats were given CPA followed by 5-FU at a dose of 10 mg/kg per day (day by day) through i.p. to rats for 14 days. At the end of the experimental period, rats were anesthetized using light ether. Blood and testes tissue samples were taken and prepared for biochemical measurements. Biochemical parameters in rat serum and tissues were evaluated. Results: Individual injection of CPA and 5-FU to rats were reduced testes TAC, GSH concentration, GR, and CAT activities compared to control. However, the combination treatment of rats with 5-FU and CPA increased the levels of these non-enzymatic and enzymatic antioxidant compared with those treated with CPA alone. Also, results showed significantly increased TBARS and NO concentration in the testes of CPA treated rats when compared to normal ones, while 5-FU increased NO only compared with the control. Conclusion: It can be concluded that treatment of rats with CPA is associated with the production of free radicals that leads to hazardous alterations in certain non-enzymatic, and enzymatic functions. The increase in lipid peroxidation probably leads to the intracellular accumulation of ROS with the subsequent development of testes tissue injury. However, 5-FU and CPA combination could produce a significant amelioration in most cases for these changes, and it may be considered as a potentially useful candidate in the combination chemotherapy with CPA to combat oxidative stress mediated non target organs injury even if it was not a complete protection. Future work should consider combined chemotherapy regimens, as two or more mechanisms of action of chemotherapeutic drugs could be more powerful than one mechanism.

Background: Cyclophosphamide (CPA) induces acute inflammation of the urinary bladder, renal damage, and liver damage, thereby limiting its therapeutic use. Objectives: The present study aimed to evaluate the hepatorenal toxicity induced by cyclophosphamide and amelioration by 5-fluorouracil in male albino rats. Materials and Methods: Twenty-eight male adult rats were grouped randomly into four groups (n=5 for each group). Group I (control): Rats were injected with saline intraperitoneally and at a dose of 1.0 ml/kg b.w. for 14 days. Group II cyclophosphamide (CPA): Cyclophosphamide at a dose of 10 mg/kg day by day through i.p. to rats for 14 days. Group III Fluorouracil (5-FU): 5-Fluorouracil at a dose of 10 mg/kg day by day in saline was given through i.p. to rats for 14 days. Group IV (CPA+5-FU): Rats were given CPA followed by 5-FU at a dose of 10 mg/kg per day (day by day) through i.p. to rats for 14 days. At the end of the experimental period, rats were anesthetized using light ether. Blood samples were taken and prepared for biochemical measurements. Results: Serum total protein, albumin, and globulin concentration significantly reduced in animal groups that received cyclophosphamide. 5-FU and CPA combination reduced the changes in total protein, albumin, and globulin compared to CPA treated group. A significant increase in LDH serum concentration was found in CPA, 5-FU, and their combination-treated animals. The mean values of the combination of chemotherapy were above that in CPA followed by 5-FU treatment. Administration of CPA, 5-FU resulted in a significant increase in serum AST, ALT, ALP, and bilirubin compared to the control. Co-treatment 5-FU with CPA significantly attenuated the increase in serum AST, ALT, ALP, and bilirubin when compared to CPA – treated rats. Compared to controls, urea and creatinine levels were increased in CPA-treated rats, while uric acid was reduced in CPA, 5-FU, and their combination. The changes in urea and creatinine produced by the chemotherapy were restored when rats received CPA in combination with 5-FU. Conclusion: It could be concluded that the treatment of mammals with chemotherapy is associated with the production of free radicals that lead to hazardous alterations in biochemical parameters. However, 5-FU and CPA combination could produce a significant amelioration in most cases for these changes, and it may be considered as a potentially useful candidate in the combination chemotherapy with CPA to combat oxidative stress-mediated non-target organ injury even if it was not complete protection. Future work should consider combined chemotherapy regimens, as two or more mechanisms of action of chemotherapeutic drugs could be more powerful than one mechanism. Toxicological studies must be performed before using drugs as a combination before application. Further research is required on the toxicological impacts of drugs and pollutants mixtures.