Inflammation and Neurological Outcomes in Cardiac Arrest - a Narrative Review of Serum Biomarker Investigations.

Background: Hypoxic-ischemic brain injury (HIBI) is a significant cause of disability following cardiac arrest (CA). Activation of the inflammatory cascade is central to HIBI pathophysiology and drives post-cardiac arrest syndrome (PCAS), which can induce further secondary brain injury. Although numerous studies have described this mechanism in preclinical models, translating this knowledge to therapeutic targets and neurological outcomes in humans is variable and incomplete.

Corrigendum: Neurological history both twinned and queried by generative artificial intelligence.

[This corrects the article DOI: 10.3389/fmed.2024.

Neurological history both twinned and queried by generative artificial intelligence.

Background And Objectives: We propose the use of GPT-4 to facilitate initial history-taking in neurology and other medical specialties. A large language model (LLM) could be utilized as a digital twin which could enhance queryable electronic medical record (EMR) systems and provide healthcare conversational agents (HCAs) to replace waiting-room questionnaires.

Methods: In this observational pilot study, we presented verbatim history of present illness (HPI) narratives from published case reports of headache, stroke, and neurodegenerative diseases.

Amyloid pathology-produced unexpected modifications of calcium homeostasis in hippocampal subicular dendrites.

Introduction: Alzheimer's disease (AD) is linked to neuronal calcium dyshomeostasis, which is associated with network hyperexcitability. Decreased expression of the calcium-binding protein cal- bindin-D (CB) might be a susceptibility factor for AD. The subiculum is affected early in AD, for unknown reasons.

Genetic underpinnings in Alzheimer's disease - a review.

In this review, we discuss the genetic etiologies of Alzheimer's disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations.