Laura Carolina Zavala Medina

Prof. Laura Carolina Zavala Medina


Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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8 January 2026 in Microorganisms
Verified
Journal Article
Open access
PDF file
LMLaura Carolina Zavala Medina
Laura Carolina Zavala Medina
JSJoan Sebastian Salas-Leiva
Joan Sebastian Salas-Leiva
CVCarlos Esteban Villegas-Mercado
Carlos Esteban Villegas-Mercado
JAJuan Antonio Arreguin-Cano
Juan Antonio Arreguin-Cano
USUriel Soto-Barreras
Uriel Soto-Barreras
MBMercedes Bermúdez
Mercedes Bermúdez
Background: Growing evidence indicates that oral microbiome dysbiosis contributes to systemic inflammation, immune activation, and neural dysfunction. These processes may influence the onset and progression of major neuropsychiatric and neurodegenerative disorders. This review integrates clinical, epidemiological, and mechanistic findings linking periodontal pathogens and oral microbial imbalance to Alzheimer’s disease (AD), Parkinson’s disease (PD), depression, and anxiety. Methods: A narrative review was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar to identify recent studies examining alterations in the oral microbiota, microbial translocation, systemic inflammatory responses, blood–brain barrier disruption, cytokine signaling, and neural pathways implicated in brain disorders. Results: Evidence from human and experimental models demonstrates that oral pathogens, particularly Porphyromonas gingivalis, Fusobacterium nucleatum, and Treponema denticola, can disseminate systemically, alter immune tone, and affect neural tissues. Their virulence factors promote microglial activation, cytokine release (IL-1β, IL-6, TNF-α), amyloid-β aggregation, and α-synuclein misfolding. Epidemiological studies show associations between oral dysbiosis and cognitive impairment, motor symptoms in PD, and alterations in mood-related taxa linked to stress hormone profiles. Immunometabolic pathways, HPA-axis activation, and the oral–gut–brain axis further integrate these findings into a shared neuroinflammatory framework. Conclusions: Oral dysbiosis emerges as a modifiable contributor to neuroinflammation and brain health. Periodontal therapy, probiotics, prebiotics, synbiotics, and targeted inhibitors of bacterial virulence factors represent promising strategies to reduce systemic and neural inflammation. Longitudinal human studies and standardized microbiome methodologies are still needed to clarify causality and evaluate whether restoring oral microbial balance can modify the course of neuropsychiatric and neurodegenerative disorders.