The gut microbiota has emerged as a central regulator of the gut–brain axis, profoundly influencing neural, immune, and metabolic homeostasis. Increasing evidence indicates that disturbances in microbial composition and function contribute to the onset and progression of neurodegenerative diseases (NDs) through mechanisms involving neuroinflammation, oxidative stress, and impaired neurotransmission. Gut dysbiosis is characterized by a loss of microbial diversity, a reduction in beneficial commensals, and an enrichment of pro-inflammatory taxa. These shifts alter intestinal permeability and systemic immune tone, allowing microbial metabolites and immune mediators to affect central nervous system (CNS) integrity. Metabolites such as short-chain fatty acids (SCFAs), tryptophan derivatives, lipopolysaccharides (LPS), and trimethylamine N-oxide (TMAO) modulate blood–brain barrier (BBB) function, microglial activation, and neurotransmitter synthesis, linking intestinal imbalance to neuronal dysfunction and cognitive decline. Disruption of this gut–brain communication network promotes chronic inflammation and metabolic dysregulation, key features of neurodegenerative pathology. SCFA-producing and tryptophan-metabolizing bacteria appear to exert neuroprotective effects by modulating immune responses, epigenetic regulation, and neuronal resilience. The aim of this work was to comprehensively explore the current evidence on the bidirectional communication between the gut microbiota and the CNS, with a focus on identifying the principal molecular, immune, and metabolic mechanisms supported by the strongest and most consistent data. By integrating findings from recent human studies, this review sought to clarify how microbial composition and function influence neurochemical balance, immune activation, and BBB integrity, ultimately contributing to the onset and progression of neurodegenerative processes. Collectively, these findings position the gut microbiota as a dynamic interface between the enteric and CNS, capable of influencing neurodegenerative processes through immune and metabolic signaling.

Musculoskeletal ultrasonography (MSKUS) is increasingly used to assess masticatory-muscle morphology and mechanical properties, but its clinical interpretability in temporomandibular disorders (TMDs) and bruxism remains uncertain. We systematically reviewed quantitative B-mode, elastographic, functional, diagnostic, and measurement-property evidence. The final pre-submission search combined PubMed/MEDLINE, Scopus, Embase, and Web of Science Core Collection, with supplementary discovery in Europe PMC and Lens, through 20 August 2026 (PROSPERO CRD420261481058). Random-effects meta-analyses used restricted maximum likelihood (REML) with Hartung-Knapp inference. Resting masseter thickness showed no consistent case-control difference (k=14; MD -0.19 mm, 95% CI -0.78 to 0.40; I²=88.9%), nor did contracted masseter thickness (k=11; MD -0.06 mm, 95% CI -1.16 to 1.03; I²=95.9%). Anterior temporalis thickness remained inconclusive at rest (k=5; MD 0.33 mm, 95% CI -0.59 to 1.25; I²=83.4%) and during contraction (k=5; MD -0.05 mm, 95% CI -1.59 to 1.49; I²=94.5%). Resting masseter stiffness measured by shear-wave elastography remained higher in clinical/bruxism groups (k=4; Hedges' g 1.80, 95% CI 0.15 to 3.44; I²=83.5%). Certainty was very low for all pooled outcomes. MSKUS is currently better supported for adjunctive phenotyping and longitudinal monitoring than as a stand-alone diagnostic test.