Stem cells are undifferentiated cells with the ability to proliferate and convert to different types of differentiated cells that make up the various tissues and organs in the body. They exist both in embryos as pluripotent stem cells that can differentiate into the three germ layers and as multipotent or unipotent stem cells in adult tissues to aid in repair and homeostasis. Perturbations in these cells’ normal functions can give rise to a wide variety of diseases. In this review, we discuss the origin of different stem cell types, their properties and characteristics, their role in tissue homeostasis, current research, and their potential applications in various life-threatening diseases. We focus on neural stem cells, their role in neurogenesis and how they can be exploited to treat diseases of the brain including neurodegenerative diseases and cancer. Next, we explore current research in Induced Pluripotent Stem Cells (iPSC) techniques and their clinical applications in regenerative and personalized medicine. Lastly, we tackle a special type of stem cells called Cancer Stem Cells (CSCs) and how they can be responsible for therapy resistance and tumor recurrence and explore ways to target them.

Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis. Adult male Sprague Dawley rats received an intra-urethral injection of an Escherichia coli (E. coli) clinical isolate (10⁸ CFU/mL). We found that rats with a UTI (CFU/mL ≥ 10⁵) had reduced proliferation of neural stem cells (NSCs) at an early time point post infection (day 4) and neurogenesis at a later time point (day 34). This was associated with the decreased expression in mRNA of BDNF, NGF, and FGF2, and elevated expression of IL-1β in the hippocampus at 6 h post infection, but with no changes in optical intensity of the microglia and astrocytes. In addition, infected rats spent less time exploring a novel arm in the Y-maze test. Treatment with an anti-inflammatory drug did not revert the effect on NSCs, while treatment with antibiotics further decreased the basal level of their proliferation. This study presents novel findings on the impact of urinary tract infections on hippocampal neurogenesis that could be correlated with cognitive impairment.

Adult hippocampal neurogenesis is prone to modulation by several intrinsic and extrinsic factors. The anterior nucleus (AN) of the thalamus has extensive connections with the hippocampus, and stimulation of this region may play a role in altering neurogenesis. We have previously shown that electrical stimulation of the AN can substantially boost hippocampal neurogenesis in adult rats. Here, we performed selective unilateral chemical excitation of the cell bodies of the AN as it offers a more specific and sustained stimulation when compared to electrical stimulation. Our aim is to investigate the long-term effects of KA stimulation of the AN on baseline hippocampal proliferation of neural stem cells and neurogenesis. Continuous micro-perfusion of very low doses of kainic acid (KA) was administered into the right AN for seven days. Afterwards, adult male rats received 5′-bromo-2′-deoxyuridine (BrdU) injections (200 mg/kg, i.p) and were euthanized at either one week or four weeks post micro-perfusion. Open field and Y-maze tests were performed before euthanasia. The KA stimulation of the AN evoked sustained hippocampal neurogenesis that was associated with improved spatial memory in the Y-maze test. Administering dexamethasone prior to and simultaneously with the KA stimulation decreased both the hippocampal neurogenesis and the improved spatial recognition memory previously seen in the Y-maze test. These results suggest that hippocampal neurogenesis may be a downstream effect of stimulation in general, and of excitation of the cell bodies of the AN in particular, and that stimulation of that area improves spatial memory in rats.

Urinary tract infections (UTIs) remain among the most common bacterial infections worldwide, affecting millions every year. While Escherichia coli ( E . coli ) is the predominant pathogen, a broad range of Gram‐negative and Gram‐positive organisms can be implicated. Treating UTIs, particularly complicated or severe infections, frequently relies on broad‐spectrum antibiotics, often started empirically before identifying the causative pathogen. However, despite their ability to cover a wide spectrum of pathogens, they have become a growing threat to public health, mainly due to the rise of antimicrobial resistance, but also due to the many other adverse effects they can potentially cause. Neurotoxicity represents one of the most consequential yet underrecognized complications of antibiotic therapy. Broad‐spectrum agents commonly used for UTIs, including fosfomycin, fluoroquinolones, carbapenems, and cephalosporins, have been associated with a wide range of neurologic manifestations such as epileptic seizures, encephalopathy, movement disorders, delirium, and psychosis, varying in onset, duration, severity, and reversibility. To induce such reactions, antibiotics interact with the central nervous system (CNS) in several ways that can threaten its integrity and disrupt homeostatic control of its components. This review provides a synopsis of the known neurological adverse reactions linked to four major antibiotic classes routinely used in UTI management and the mechanistic pathways underlying CNS toxicity. An overall clearer understanding of these risks may help clinicians balance therapeutic benefit against potential harm, optimize antimicrobial selection, and improve prevention and management strategies for antibiotic‐associated neurotoxicity.