The application of ginkgolides as a herbal remedy reaches ancient China. Over time many studies confirmed the neuroprotective effect of standard Ginkgo biloba tree extract—the only available ginkgolide source. Ginkgolides present a wide variety of neuroregulatory properties, commonly used in the therapy process of common diseases, such as Alzheimer’s, Parkinson’s, and many other CNS-related diseases and disorders. The neuroregulative properties of ginkgolides include the conditioning of neurotransmitters action, e.g., glutamate or dopamine. Besides, natural compounds induce the inhibition of platelet-activating factors (PAF). Furthermore, ginkgolides influence the inflammatory process. This review focuses on the role of ginkgolides as neurotransmitters or neuromodulators and overviews their impact on the organism at the molecular, cellular, and physiological levels. The clinical application of ginkgolides is discussed as well.

Understanding morphological, biochemical, and functional aspects of cell death is essential for targeting new cancer therapies. Even though many different mechanisms of cell death are identified, it is crucial to highlight the role of new and lesser-known pathways, including methuosis, alkaliptosis, and oxeiptosis. The aim of this review was to summarize the data about cell death mechanisms—methuosis, alkaliptosis, and oxeiptosis—and their role in cancer treatment. Unique molecular mechanisms and cellular outcomes characterize each of these forms of cell death. This research on methuosis, alkaliptosis, and oxeiptosis provides a better understating of cell death biology and creates novel opportunities for neoplasm management.

Nuclear pore complexes (NPCs) play a critical role in regulating transport-dependent gene expression, influencing various stages of cancer development and progression. Dysregulation of nucleocytoplasmic transport has profound implications, particularly in the context of cancer-associated protein mislocalization. This review provides specific information about the relationship between nuclear pore complexes, key regulatory proteins, and their impact on cancer biology. Highlighting the influence of tumor-suppressor proteins as well as the potential of gold nanoparticles and intelligent nanosystems in cancer treatment, their role in inhibiting cell invasion is examined. This article concludes with the clinical implications of nuclear export inhibitors, particularly XPO1, as a therapeutic target in various cancers, with selective inhibitors of nuclear export compounds demonstrating efficacy in both hematological and solid malignancies. The review aims to explore the role of NPCs in cancer biology, focusing on their influence on gene expression, cancer progression, protein mislocalization, and the potential of targeted therapies such as nuclear export inhibitors and intelligent nanosystems in cancer treatment. Despite their significance and the number of research studies, the direct role of NPCs in carcinogenesis remains incompletely understood.

Xenoestrogens (XEs) are a group of exogenous substances that may interfere with the functioning of the endocrine system. They may mimic the function of estrogens, and their sources are plants, water or dust, plastic, chemical agents, and some drugs. Thus, people are highly exposed to their actions. Together with the development of industry, the number of XEs in our environment increases. They interact directly with estrogen receptors, disrupting the transmission of cellular signals. It is proven that XEs exhibit clinical application in e.g., menopause hormone therapy, but some studies observed that intense exposure to XEs leads to the progression of various cancers. Moreover, these substances exhibit the ability to cross the placental barrier, therefore, prenatal exposure may disturb fetus development. Due to the wide range of effects resulting from the biological activity of these substances, there is a need for this knowledge to be systematized. This review aims to comprehensively assess the environmental sources of XEs and their role in increasing cancer risk, focusing on current evidence of their biological and pathological impacts.

Alzheimer’s disease (AD) is the most common cause of dementia worldwide. Pathological deposits of neurotoxin proteins within the brain, such as amyloid-β and hyperphosphorylated tau tangles, are prominent features in AD. The prion protein (PrP) is involved in neurodegeneration via its conversion from the normal cellular form (PrPC) to the infection prion protein scrapie (PrPSc) form. Some studies indicated that post-translationally modified PrPC isoforms play a fundamental role in AD pathological progression. Several studies have shown that the interaction of Aβ oligomers (Aβos) with the N-terminal residues of the PrPC protein region appears critical for neuronal toxicity. PrPC-Aβ binding always occurs in AD brains and is never detected in non-demented controls, and the binding of Aβ aggregates to PrPC is restricted to the N-terminus of PrPC. In this study, we aimed to gather all of the recent information about the connections between PrPC and AD, with potential clinical implications.

Endometriosis is a widely spread disease that affects about 8% of the world’s female population. This condition may be described as a spread of endometrial tissue apart from the uterine cavity, but this process’s pathomechanism is still unsure. Apart from classic endometriosis symptoms, which are pelvic pain, infertility, and bleeding problems, there are neuropsychiatric comorbidities that are usually difficult to diagnose. In our review, we attempted to summarize some of them. Conditions like migraine, anxiety, and depression occur more often in women with endometriosis and have a significant impact on life quality and pain perception. Interestingly, 77% of endometriosis patients with depression also have anxiety. Neuroimaging gives an image of the so-called endometriosis brain, which means alternations in pain processing and cognition, self-regulation, and reward. Genetic factors, including mutations in KRAS, PTEN, and ARID1A, influence cellular proliferation, differentiation, and chromatin remodeling, potentially exacerbating lesion severity and complicating treatment. In this review, we focused on the aspects of sciatic and obturator nerve endometriosis, the emotional well-being of endometriosis-affected patients, and the potential influence of endometriosis on dementia, also focusing on prolonged diagnosis. Addressing endometriosis requires a multidisciplinary approach, encompassing molecular insights, innovative therapies, and attention to its psychological and systemic effects.