Dr. Umar

Organophosphates are cholinesterase-inhibiting chemicals widely used as pesticides. Beyond neurotoxicity, evidence links chronic exposure to gut microbiome changes, barrier disruption, and metabolic effects. Microbiome medicine integrates exposure biomarkers and microbiome signatures to support personalized risk assessment.

Ambient long-term organophosphorus pesticide exposure gut microbiome signatures were associated with specific genus-level shifts and predicted functional changes (cell-wall/respiration pathways, reduced B1/B6 synthesis), despite no differences in overall microbiome diversity, in an older California cohort enriched for Parkinson’s disease.

This paper uses NHANES urinary dialkyl phosphate metabolites to estimate cumulative organophosphate exposure and compares results with EPA models, finding major model conservatism and key limitations of non-specific metabolites. Clinically, DAPs are best treated as screening biomarkers and exposure confounders in microbiome studies.

This mechanistic toxicology study shows that AChE inhibition explains most acute lethality from highly toxic organophosphorus agents. Steep dose–response slopes across species and strong correlations between enzyme inhibition/reactivation kinetics and survival support AChE inhibition as the dominant mechanism.

This review explains how AChE inhibition triggers respiratory failure and SE after organophosphate exposure, and how SE drives excitotoxic, oxidative, and inflammatory brain injury. Chronic low-dose effects may occur without SE. No microbiome signatures or microbial biomarkers are reported.

Calprotectin is a neutrophil-derived protein complex measured in stool to detect intestinal inflammation. It helps distinguish IBD from functional bowel disorders and reflects mucosal immune activity that can reshape microbiome composition through antimicrobial metal sequestration.

In older adults, higher fecal calprotectin tracked with fecal calprotectin gut dysbiosis: more pro-inflammatory taxa, fewer SCFA producers, increased IL-17C/CCL19, and markedly higher indoxyl sulfate (microbiome-mediated), alongside higher BMI/obesity and more heart attack history.

This meta-analysis supports fecal calprotectin relapse prediction in adult IBD remission, identifying an optimal FC threshold of 152 µg/g with pooled sensitivity 0.72 and specificity 0.74. FC helps stratify relapse risk and can complement microbiome profiling by anchoring host inflammatory activity.

This meta-analysis shows faecal calprotectin to distinguish IBD from IBS has high pooled sensitivity (85.8%) and specificity (91.7%). It performs best as a rule-out test, with NPV 99.8% at 1% IBD prevalence. Optimal sensitivity appears at cut-offs ≤50 μg/g

Calprotectin-limits-Aspergillus-hyphal-growth by chelating zinc and manganese, restricting invasive hyphae in murine fungal keratitis. Protection is restored with recombinant calprotectin and depends on intact Zn/Mn binding, while conidial killing is calprotectin-independent. Fungal ZafA-mediated zinc uptake confers resistance and virulence.

This study shows that manganese sequestration by calprotectin is essential for maximal inhibition of multiple bacterial pathogens. A unique six-histidine Mn²⁺-binding site (enabled by the S100A9 tail) explains calprotectin’s broad antimicrobial activity and its suppression of Mn-dependent oxidative stress defenses.

This review summarizes evidence that fecal calprotectin is a stable, noninvasive stool biomarker reflecting neutrophilic intestinal inflammation, reliably distinguishing IBD from IBS, correlating with endoscopic/histologic activity, predicting relapse, and detecting pouchitis—useful for inflammation phenotyping alongside microbiome signatures.

What was studied? This study investigated whether the gut microbiome harbors a distinct microbial signature associated with mild cognitive impairment (MCI) in individuals with Parkinson’s disease (PD). Prior research has established significant differences in the gut microbiome between PD patients and healthy controls, but the question of whether specific gut microbiome changes are linked to […]

This study identified a taurine-based microbiome-metabolism axis in Parkinson’s disease, showing that gut dysbiosis impairs taurine metabolism and exacerbates PD pathology. Restoring taurine levels or beneficial microbes alleviates disease features, highlighting potential microbiome-targeted interventions.

This multi-omics meta-analysis identifies depletion of Blautia as a robust microbiome signature linked to Parkinson’s disease across feces, blood, and brain, highlighting its potential diagnostic value and mechanistic ties to neurodegeneration via mitochondrial and inflammatory pathways.

This study revealed a PD-specific oral-gut microbiome axis, with increased oral Lactobacillus linked to gut dysbiosis and reduced glutamate/arginine biosynthesis. Shotgun metagenomics identified superior functional microbial signatures for PD, underscoring the importance of functional profiling in clinical microbiome research.

This study links increased Desulfovibrio and Parkinson’s disease severity, identifying a Desulfovibrio MAG with strong hydrogen sulfide–producing potential and suggesting Desulfovibrio as both a biomarker and mechanistic contributor to PD progression via gut–brain axis disruption.

Cross-sectional metagenomic profiling shows that the gut microbiome in Parkinson’s disease differs from age-matched controls via selective loss of butyrate-producing taxa, especially Butyricimonas synergistica, with links to non-motor symptoms, ageing-related Bifidobacterium decline, and sleep-associated Roseburia in older adults.

This study links specific gut microbiome dysbiosis signatures in Parkinson’s disease to reduced brain NMNAT2 expression and worsening neurobehavioral and oxidative stress outcomes, highlighting FMT and NMNAT2 restoration as promising therapeutic avenues.

This large, prospective study found that gut microbiome alterations—particularly loss of anti-inflammatory, SCFA-producing bacteria—precede Parkinson’s disease, offering promising early biomarkers and highlighting microbial pathways linked to PD pathogenesis.

FGF21 modulates gut microbiota in Parkinson’s disease, reversing motor and cognitive deficits in PD mice while restoring brain and colon metabolic homeostasis. Key microbial shifts include enrichment of Ruminococcaceae and Lachnospiraceae, highlighting the microbiota–gut–brain axis as a therapeutic target.

This study reveals gender-specific gut microbiota alterations in Parkinson’s disease, linking distinct microbial signatures to brain activity differences via the gut-brain axis. Findings suggest sex-dependent microbial influences on PD pathology, emphasizing the importance of personalized approaches to diagnosis and treatment.

Differences in gut microbiota between Parkinson’s disease patients and controls seem to depend on multiple-frequently unmeasured-confounders. Monozygotic twins offer a unique model for controlling several factors responsible for interpersonal variation in gut microbiota.

This study reveals that gut microbiome alterations, especially reduced Lachnospiraceae taxa, are evident in treatment-naive, de novo Parkinson’s disease patients, supporting early involvement of the microbiome in PD pathogenesis, but highlights limited reproducibility of taxonomic biomarkers across cohorts.