Breast cancer is a complex disease for which pharmacological treatment does not guarantee success or cure. In addition, current pharmacological therapies induce unwanted side effects due to their lack of specificity or selectivity. Therefore, it is necessary to develop new therapeutic options to improve these aspects. Currently, phytochemicals with antineoplastic properties have been identified from a wide variety of plant sources, and new therapeutic options have been developed based on the conjugation of drugs with polymeric matrices, resulting in nanoparticles or hydrogels with improved properties. Some antineoplastic drugs have been conjugated with antibodies to improve their selectivity and specificity. One of the most important advances in the treatment of breast cancer has been the development of cyclin inhibitors and gene therapy. This review provides an overview of drugs derived from medicinal plants and polymeric matrices with high potential for use in the treatment of breast cancer. We also highlight the clinical evidence for the use of anti-HER2 monoclonal antibodies and cyclin inhibitors in breast cancer, as well as the advantages of using conjugated antibodies. Finally, we mention some considerations that should be taken into account in the search for new therapeutic agents from phytochemicals, polymers, antibodies, cyclin inhibitors, and gene therapy focused on the treatment of breast cancer.

Background/Objectives: Neuropsychiatric disorders such as Parkinson’s disease, depression, and Alzheimer’s disease are characterized by deficits in catecholaminergic neurotransmission. Conventional pharmacotherapies have several limitations, including poor blood–brain barrier permeability, rapid peripheral metabolism, systemic toxicity, and suboptimal brain bioavailability. This review evaluates nanoparticle-based strategies that can overcome these limitations by enhancing the delivery of catecholaminergic drugs to the central nervous system (CNS). Methods: A narrative synthesis was conducted based on a comprehensive review of research articles published by July 2025. Articles were retrieved from PubMed, Scopus, and Web of Science. The studies examined nanoformulations of catecholaminergic agents with a focus on CNS delivery, BBB penetration, toxicity, and therapeutic outcomes in neuropsychiatric disease models. Results: Evidence shows that nanoparticle platforms can stabilize drugs and extend their release time. They can also enable BBB penetration. These platforms reduce peripheral side effects and improve behavioral and neurochemical outcomes in preclinical models. Conclusions: Nanoparticles are a promising strategy for optimizing pharmacotherapy for CNS disorders associated with catecholamine deficiencies. However, more research is needed on their long-term safety, bioaccumulation, and clinical feasibility before they can be widely adopted.

Type 2 diabetes mellitus (T2DM) has been associated with cognitive impairment and an increased risk of dementia in women. This study examined the effects of subchronic metformin treatment on recognition memory and brain pathology in female diabetic mice. T2DM was induced by streptozotocin and nicotinamide injections. Then, the mice received metformin (50, 150, or 250 mg/kg) orally for 28 days. Recognition memory was assessed using the Novel Object Recognition Test (n = 72). Biochemical analyses of whole-brain homogenates evaluated insulin, tau, and insoluble Aβ₄₂ (n = 4). Histological analyses evaluated neuronal damage and amyloid-like deposits in the hippocampal Cornu Ammonis 1 (CA1) region, cerebral cortex, and cerebellum (n = 4). The diabetic mice exhibited hyperglycemia, hyperinsulinemia, dyslipidemia, impaired recognition memory, and neuronal damage. Metformin reduced blood glucose levels and improved recognition memory. Metformin also normalized serum and brain insulin levels and reduced neuronal damage in the CA1 region, cortex, and cerebellum. Metformin reduced cerebellar Congo red-positive amyloid-like deposits and decreased insoluble Aβ₄₂ levels in whole-brain homogenates. However, at 250 mg/kg, metformin increased total and phosphorylated tau levels. These results suggest that metformin mitigates recognition memory deficits, attenuates neuronal damage, and reduces cerebellar amyloid-like deposits in female mice.