The term ‘dementia’ encompasses a diverse group of progressive neurodegenerative disorders, the common feature of which is the deterioration of higher cortical functions. This process not only involves memory deficits and language communication disorders, but also executive dysfunction and loss of emotional control, which ultimately leads to a complete loss of the patient’s independence. Within this group of disorders, Alzheimer’s disease (AD) presents the most serious clinical challenge, characterized by a unique neuropathological triad: the presence of extracellular β-amyloid plaques, intracellular neurofibrillary tangles of tau protein, and widespread dysfunction of cholinergic transmission. The cholinergic hypothesis remains the cornerstone of the current understanding of cognitive impairment in AD. It posits that progressive dementia is caused by the selective degeneration of neurons in the anterior basal forebrain, resulting in a drastic reduction in acetylcholine (ACh) levels in the synaptic cleft. In the absence of a causal treatment, acetylcholinesterase inhibitors (AChEIs) remain the standard of care. Their pharmacological action is based on the inhibition of the AChE enzyme, which allows neurotransmission deficits to be compensated for by prolonging the half-life of acetylcholine at the synapse. This literature review presents a synthesis of the efficacy and safety of classic and novel AChEIs. A comprehensive search of the PubMed, Scopus, and Cochrane Library databases was conducted for clinical data published up to 2026. Evidence from key trials indicates that standard AChEIs induce significant cognitive stabilization compared to placebo, with rivastigmine maximizing daily living parameters via transdermal delivery. However, their therapeutic impact remains strictly symptomatic without arresting neurodegeneration. Conversely, emerging agents like huperzine A and the translation-blocker Posiphen demonstrate disease-modifying potential by modulating CSF biomarkers associated with amyloid and tau proteins. Clinically, while traditional regimens are limited by gastrointestinal toxicities, transitioning toward innovative multi-target structures represents a necessary shift to address both cognitive decline and neurodegeneration.

Small intestinal bacterial overgrowth (SIBO) is an increasingly recognized condition that influences immune responses. It may be linked to atopic disorders such as bronchial asthma (BA), food allergies (FA), chronic spontaneous urticaria (CSU), and mast cell activation syndrome (MCAS). The aim of our study was to perform a structured literature search to assess the possible correlation between SIBO and the presentation of atopic disorders. The prevalence of SIBO was highest in patients with BA (60–100%) and FA (50–87.5%), followed by MCAS (30.9%) and CSU (27.9%). The diagnosis of SIBO was based on lactulose or glucose breath tests. SIBO exacerbated symptoms of atopic diseases, and treating it within BA and MCAS improved the symptoms, in contrast to CSU. The present evidence suggests a possible crosslink between SIBO and atopic manifestations. Bacterial overgrowth appears to trigger the Th2 immune response via the mucosal pathway and low-grade endotoxemia. These result in the increased synthesis of interleukins involved in allergic reactions (IL-4, IL-5, IL-13). Further studies are essential to confirm the clinical significance of this association. The “gut–allergy axis” may offer new therapeutic options and possibly improve quality of life in patients with atopy.

Background: Dexmedetomidine is a highly selective α₂-adrenergic receptor agonist increasingly used in neonatal and pediatric intensive care and anesthesia. Its central mechanism of action and experimental evidence suggesting anti-inflammatory, anti-apoptotic, antioxidant, and antiexcitotoxic effects have raised interest in its influence on the developing central nervous system. At the same time, uncertainty remains regarding its long-term neurodevelopmental consequences and the clinical relevance of reported neurological safety signals. Objective: This review aimed to critically evaluate the neurological and neurodevelopmental effects of dexmedetomidine in neonatal and pediatric populations, with particular emphasis on potential neuroprotective effects, acute neurological safety signals, and long-term neurodevelopmental outcomes. Methods: A structured literature review of publications from 1989 to 2026 was conducted. Evidence included primary clinical studies, prospective and retrospective cohorts, randomized controlled trials, follow-up studies, case reports, and secondary evidence syntheses, including systematic reviews and meta-analyses. Long-term neurodevelopmental and cognitive outcomes were analyzed separately from acute neurological effects and neurological safety signals. Secondary evidence was evaluated independently from primary studies to avoid double counting of participants. Preclinical and surrogate evidence of neuroprotection was distinguished from direct evidence of long-term human neurodevelopmental benefit. Results: Dexmedetomidine was associated with measurable effects on the developing central nervous system, although their clinical significance varied across populations and study designs. In neonates with hypoxic-ischemic encephalopathy undergoing therapeutic hypothermia, secondary evidence suggested a lower pooled seizure risk with dexmedetomidine compared with conventional sedatives, although substantial heterogeneity and observational study designs limited causal interpretation. In pediatric anesthesia, dexmedetomidine reduced sevoflurane-related emergence agitation, but this short-term behavioral endpoint does not constitute evidence of long-term neuroprotection. Preclinical studies demonstrated attenuation of sevoflurane-associated neuronal migration delay, restoration of dendritic spine density, and improvement of transient somatosensory dysfunction, supporting a potential synaptic and developmental neuroprotective effect. However, clinical studies did not consistently demonstrate improvements in cognition, behavior, or long-term neurodevelopment. Reported neurological safety signals included altered cerebral activity, seizure-related events, abnormal movements, and posterior reversible encephalopathy syndrome following abrupt dexmedetomidine withdrawal with rebound hypertension. Conclusions: Dexmedetomidine exerts measurable effects on the developing central nervous system, but current evidence is insufficient to classify it as either a clinically proven neuroprotective agent or as directly neurotoxic to the developing human brain. Available data support short-term neurological effects and preclinical neuroprotective potential, whereas long-term human neurodevelopmental consequences remain uncertain. Further prospective studies using validated longitudinal neurodevelopmental outcomes are required to determine its long-term neurological safety and potential neuroprotective benefit. Anesthetic agents and method of discontinuation. Further prospective, adequately powered studies with standardized dosing and long-term neurodevelopmental follow-up are required.