Electroencephalography (EEG) has been providing a window into human brain activity for nearly a century, yet its interpretation often remains empirical rather than mechanistic. This review revisits the cellular and biophysical foundations of EEG through a modern perspective, integrating advances from neurophysiology, computational modeling, and cellular neuroscience. We examine the fundamental physics of EEG generation, from transmembrane currents and dipole formation to the spatial summation. Electroencephalography results from coordinated cellular and network activity, reflecting the integrated contributions of excitatory and inhibitory synaptic events, intrinsic conductances, and tissue geometry, with pyramidal neurons acting as dominant generators, while interneurons play a role in rhythmogenesis and oscillatory coupling. Expanding beyond traditional Berger frequencies, we highlight the significance of high-frequency oscillations and the underlying cellular and network mechanisms that generate the high-frequency component of the EEG signal. Conversely, infra-slow fluctuations and direct current shifts reveal the roles of glial networks, ionic homeostasis, and spreading depolarizations in health and disease. Across these domains, EEG uniquely captures neural activity from submillisecond events to long-term state changes spanning days or years, offering an unparalleled temporal range for studying the human brain. Clinically, this multiscale capacity underpins the emergence of EEG-based biomarkers for epilepsy, psychiatric disorders, and disorders of consciousness, while guiding development of closed-loop neuromodulation and precision medicine strategies. With technological advances and the expanding field of machine learning, the role of EEG will continue to expand as we will gain deeper insights into its underlying mechanisms.

Marked by protein aggregation, impaired proteostasis, organelle stress, and chronic neuroinflammation, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) form a clinically, genetically, and pathologically overlapping disease spectrum. Increasing evidence indicates that innate immune activation is not merely a secondary response to neuronal injury, but an active driver of disease progression. In this review, we elaborate on how ALS/FTD-associated genetic lesions and pathogenic protein aggregates, including TDP-43, SOD1, FUS, and C9orf72-derived dipeptide repeat proteins, engage three interconnected innate immune pathways: cGAS-STING, NLRP3 inflammasomes, and TREM2-DAP12 signaling. We further highlight emerging crosstalk among these pathways, in which cGAS-STING and NLRP3 reinforce inflammatory signaling, while NLRP3-driven TREM2 shedding may impair microglial clearance and perpetuate proteostatic failure. Understanding this immune network may help define disease subtypes, identify biomarkers, and guide combinatorial therapeutic strategies that suppress harmful inflammation while preserving protective microglial functions.

Percutaneous endoscopic gastrostomy (PEG) is commonly used for long-term enteral nutrition in patients unable to feed orally. The cut-and-push technique, where the internal bolster is left to pass spontaneously, is generally safe, but complications are uncommon. We report an 88-year-old bed-bound female with multiple comorbidities, including type 2 diabetes mellitus, chronic kidney disease, dementia, and a prior lower midline laparotomy, who underwent PEG replacement using the cut-and-push method. Three weeks later, she developed a small bowel obstruction. Imaging revealed the retained PEG bolster lodged in the terminal ileum, causing proximal dilatation and distal collapse. Following a 48-hour trial of conservative management without clinical improvement, minimally invasive intervention was attempted. Diagnostic laparoscopy with adhesiolysis was initially performed, followed by an attempted colonoscopic retrieval; however, colonoscopy was unsuccessful because of inadequate bowel preparation. Definitive management required open surgical retrieval through enterotomy via the previous laparotomy scar, which was completed successfully. Postoperatively, the patient required prolonged ventilatory support via tracheostomy and was transferred to a long-term care facility. This case illustrates a rare delayed obstruction from a retained PEG bolster, highlighting the importance of careful patient selection, close follow-up to confirm spontaneous passage, and timely intervention when excretion fails.

A large share of assisted living (AL) residents have a diagnosis of dementia or cognitive impairment, and these individuals can benefit from person-centered care and family-involved care. This study examines whether and how states' AL licenses address these topics.

Patients with Dementia with Lewy Bodies (DLB) typically experience attentional deficits. Understanding these deficits and the underlying neural correlates is crucial as sustained attention supports higher level cognitive functions. The objective of this study was to investigate the patterns of brain connectivity during a functional magnetic resonance imaging (fMRI) sustained attention task in a DLB group compared with healthy controls (HC).

Vascular cognitive impairment (VCI) encompasses a spectrum of cerebrovascular diseases ranging from mild clinical cognitive impairment to advanced vascular dementia and is recognized as a major contributor to the global dementia burden. Frequently coexisting with Alzheimer's Disease (AD), VCI represents a complex, mixed-pathology neurodegenerative process driven by chronic cerebral hypoperfusion (CCH), white matter (WM) injury and volume loss, neurovascular dysfunction, and progressive cognitive decline. While numerous animal models have been developed to characterize the underlying mechanisms and identify therapeutic targets, the field is presently limited by the absence of a distinct framework to guide model selection based on unique pathophysiological features of recently delineated VCI subtypes. Surgical VCI models, including transient and permanent occlusion, stenosis, or gradual occlusion approaches, differ substantially in the duration of ischemic injury, severity of hypoperfusion, and mechanism of cerebral blood flow (CBF) reductions, generating diverse downstream effects on cerebral tissue damage, neuroinflammation, neurometabolic dysfunction, functional integrity, and, ultimately, memory function. No single model completely captures the heterogeneity of VCI pathology; however, each selectively captures unique aspects of disease subtypes. As such, this review aims to establish a clear, pathophysiology-driven framework to guide the selection of appropriate surgical VCI models for investigating specific VCI subtypes. To do so, we evaluate common models of carotid artery manipulation, integrating histological, neuroenergetic, and cognitive outcomes with clinically relevant imaging and patient data. This review provides practical guidance for model selection, enhancing the specificity and translational relevance of preclinical VCI investigation.