The presence of insoluble aggregates of amyloid β (Aβ) in the form of neuritic plaques (NPs) is one of the main features that define Alzheimer’s disease. Studies have suggested that the accumulation of these peptides in the brain significantly contributes to extensive neuronal loss. Furthermore, the content and distribution of cholesterol in the membrane have been shown to have an important effect on the production and subsequent accumulation of Aβ peptides in the plasma membrane, contributing to dysfunction and neuronal death. The monomeric forms of these membrane-bound peptides undergo several conformational changes, ranging from oligomeric forms to beta-sheet structures, each presenting different levels of toxicity. Aβ peptides can be internalized by particular receptors and trigger changes from Tau phosphorylation to alterations in cognitive function, through dysfunction of the cholinergic system. The goal of this review is to summarize the current knowledge on the role of lipids in Alzheimer’s disease and their relationship with the basal cholinergic system, as well as potential disease-modifying therapies.

A glioblastoma is an aggressive form of a malignant glial-derived tumor with a poor prognosis despite multimodal therapy approaches. Lactate has a preponderant role in the tumor microenvironment, playing an immunoregulatory role as well as being a carbon source for tumor growth. Lactate homeostasis depends on the proper functioning of intracellular lactate regulation systems, such as transporters and enzymes involved in its synthesis and degradation, with evidence that an intracellular lactate overload generates metabolic stress on tumor cells and tumor cell death. We propose that the delivery of a lactate overload carried in nanoparticles, allowing the intracellular release of lactate, would compromise the survival of tumor cells. We synthesized and characterized silica and titania nanoparticles loaded with lactate to evaluate the cellular uptake, metabolic activity, pH modification, and cytotoxicity on C6 cells under normoxia and chemical hypoxia, and, finally, determined the survival of an orthotopic malignant glioma model after in situ administration. A dose-dependent reduction in metabolic activity of treated cells under normoxia was found, but not under hypoxia, independent of glucose concentration. Lactated-loaded silica nanoparticles were highly cytotoxic (58.1% of dead cells) and generated significant supernatant acidification. In vivo, lactate-loaded silica nanoparticles significantly increased the median survival time of malignant glioma-bearing rats (p = 0.005) when administered in situ. These findings indicate that lactate-loaded silica nanoparticles are cytotoxic on glioma cells in vitro and in vivo.

In the present work, the preparation, characterisation, and efficiency of two different silica nanostructures as release vehicles of Cisplatin are reported. The 1‐hexadeciltrimethyl‐ammonium bromide templating agent was used to obtain mesoporous silica nanoparticles which were later loaded with Cisplatin. While sol–gel silica was very fast prepared using an excess of acetic acid during the hydrolysis–condensation reactions of tetraethylorthosilicate and at the same time the Cisplatin was added. Several physicochemical techniques including spectroscopies, electronic microscopy, X‐ray diffraction, N ₂ adsorption–desorption were used to characterise the silica nanostructures. An in vitro Cisplatin release test was carried out using artificial cerebrospinal fluid. Finally, the toxicity of all silica nanostructures was tested using the C6 cancer cell line. The spectroscopic results showed the suitable stabilisation of Cisplatin into the two different silica nanostructures. A large surface area was obtained for the mesoporous silica nanoparticles, while low areas were obtained in the silica nanoparticles. Cisplatin was released faster from mesoporous silica channels than from inside of aggregates nanoparticles silica. Cisplatin alone, as well as, cisplatin released from both silica nanostructures exerted a toxic effect on cancer cells. In contrast, both silica structures without the drug did not exert any toxic effect.

This study aimed to synthesize a multicationic hydrotalcite and transform it into mixed oxide nanostructures (ZnO/TiO₂/CeO₂/Al₂O₃, referred to as MixO) to serve as a heterogeneous photocatalyst for degrading various pollutants, including methylene blue (MB), methyl orange (MO), paracetamol (PA), and paraquat (PQ). The hydrotalcite was synthesized via an ultrasound-assisted method and calcined at 700 °C to obtain the corresponding mixed metal oxide. A comprehensive characterization of both the multicationic hydrotalcite (MC-LDH) and the mixed metal oxides (MixO) was performed using X-ray diffraction (XRD), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS), X-ray photoelectron spectroscopy (XPS), N₂ adsorption–desorption, Fourier transform infrared spectroscopy (FTIR), Raman spectroscopy, and pH_PZC analysis. The MixO sample exhibited an optical bandgap of 3.19 eV. Photocatalytic performance was evaluated during 240 min of UV irradiation, demonstrating high degradation efficiencies attributable to the synergistic interactions among ZnO, TiO₂, and CeO₂. Degradation efficiencies reached 99.3% for MO and 95.2% for MB, while PA and PQ showed moderate degradation rates of 60% and 15%, respectively. The degradation kinetics of all pollutant compounds followed the Langmuir–Hinshelwood model. Additionally, the MixO catalyst maintained consistent performance over four consecutive degradation cycles, highlighting its reusability and stability. These findings underscore the potential of MixO mixed oxide nanostructures as practical and recyclable photocatalysts for environmental remediation, particularly in wastewater treatment applications.