Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
Kimberly Eyer, a Registered Nurse with 30 years of nursing experience across diverse settings, including Home Health, ICU, Operating Room Nursing, and Research. Her roles have encompassed Operating Room Nurse, RN First Assistant, and Acting Director of a Same Day Surgery Center. Her specialty areas include Adult Cardiac Surgery, Congenital Cardiac Surgery, Vascular Surgery, and Neurosurgery.
Parkinson’s disease (D) is a neurodegenerative disorder primarily characterized by the degeneration of dopaminergic neurons in the nigrostriatal pathway, leading to progressive hypokinetic movements [1], and a range of non-motor symptoms, including gastrointestinal (I) dysfunction [2]. However, Parkinson’s disease involves complex interactions that extend beyond neuronal degeneration, with growing evidence highlighting the roles of the […]
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
Kimberly Eyer, a Registered Nurse with 30 years of nursing experience across diverse settings, including Home Health, ICU, Operating Room Nursing, and Research. Her roles have encompassed Operating Room Nurse, RN First Assistant, and Acting Director of a Same Day Surgery Center. Her specialty areas include Adult Cardiac Surgery, Congenital Cardiac Surgery, Vascular Surgery, and Neurosurgery.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
Kimberly Eyer, a Registered Nurse with 30 years of nursing experience across diverse settings, including Home Health, ICU, Operating Room Nursing, and Research. Her roles have encompassed Operating Room Nurse, RN First Assistant, and Acting Director of a Same Day Surgery Center. Her specialty areas include Adult Cardiac Surgery, Congenital Cardiac Surgery, Vascular Surgery, and Neurosurgery.
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
Parkinson’s disease (PD) is a neurodegenerative disorder primarily characterized by the degeneration of dopaminergic neurons in the nigrostriatal pathway, leading to progressive hypokinetic movements [1], and a range of non-motor symptoms, including gastrointestinal (GI) dysfunction [2]. However, Parkinson’s disease involves complex interactions that extend beyond neuronal degeneration, with growing evidence highlighting the roles of the gut microbiome, metabolomic signals, and metallomics. The gut-brain axis is a crucial bidirectional communication pathway implicated in PD pathogenesis, where gut dysbiosis, inflammation, and alpha-synuclein aggregation are linked to disease progression. [2][3][4]Alterations in the gut microbiota, including reduced diversity and shifts in bacterial populations, contribute to increased intestinal permeability and neuroinflammation, potentially influencing alpha-synuclein misfolding and its spread from the gut to the brain via the vagus nerve. [5][6][7]
Causes
Parkinson’s disease is increasingly understood as the clinical endpoint of converging pathogenic processes rather than a single linear pathway, with genetic susceptibilities intersecting with mitochondrial dysfunction, oxidative stress, alpha-synuclein misfolding, neuroinflammation, and environmental toxicant exposure. These mechanistic frameworks are tightly interconnected, since mitochondrial impairment and redox imbalance can promote protein aggregation and microglial activation, while gut-derived inflammatory signals and endotoxins amplify neuronal injury through the gut–brain axis. In parallel, dysregulated metal homeostasis and chronic exposure to pesticides and heavy metals further destabilize dopaminergic neurons by exacerbating oxidative stress, disrupting proteostasis, and impairing organellar function, particularly within the substantia nigra. Together, these processes create self-reinforcing cycles of bioenergetic failure, proteotoxic stress, and inflammatory signaling that progressively erode nigrostriatal integrity, driving the characteristic motor and non-motor manifestations of PD.
What are the major causative theories of Parkinson's Disease
Mitochondrial Dysfunction and Oxidative Stress Hypothesis
Mitochondria are crucial for cellular energy production, and their dysfunction is consistently implicated in PD. This dysfunction can lead to increased generation of reactive oxygen species (ROS), resulting in oxidative stress—an imbalance between oxidants and antioxidants. [8][9] The brain, particularly the substantia nigra, is highly vulnerable to oxidative stress due to its high metabolic activity, rich dopamine content (which can generate oxyradicals through oxidation), and relatively weak antioxidant defenses. [10][11] Oxidative stress can damage critical biological molecules, trigger inflammation, and ultimately lead to the death of dopaminergic neurons. [12][13] Studies have shown increased lipid peroxidation and decreased levels of protective antioxidants like glutathione in PD patients [14] This theory is further supported by the observation that neurotoxins capable of selectively destroying dopaminergic neurons, such as 6-hydroxydopamine and MPTP, appear to act by inducing oxidative stress. [15]
Alpha-Synuclein Misfolding and Aggregation
Another significant causal theory revolves around a key pathological hallmark of PD: the abnormal accumulation and aggregation of alpha-synuclein protein within affected neurons, forming Lewy bodies and Lewy neurites. [16][17] This misfolding is believed to spread in a prion-like manner through specific brain regions, contributing to neurodegeneration and progressive neurological impairment.[18] Alpha-synuclein abnormalities can be triggered by various factors, including mitochondrial dysfunction and oxidative stress, creating a vicious cycle that exacerbates neuronal damage. [19][20] The theory also suggests that this aggregation might initiate in the gastrointestinal system, with misfolded alpha-synuclein then transported to the central nervous system via the vagus nerve, supporting the “gut-first” hypothesis of PD.[21][22]
Neuroinflammation Hypothesis
This hypothesis proposes that chronic inflammation in the brain plays a critical role in the initiation and progression of Parkinson’s disease. Neuroinflammation can be triggered by various factors, including genetic predispositions, mitochondrial dysfunction, and gut microbiome dysbiosis. [23] Microglial activation, a hallmark of neuroinflammation, can lead to the production of pro-inflammatory cytokines that contribute to dopaminergic neuronal degeneration. [24][25]
The gut-brain axis is central to this hypothesis, as gut dysfunction and alterations in the microbiome can promote a peripheral inflammatory response that communicates with the brain, leading to neuroinflammation and spreading pathology. [26][27] Bacterial endotoxins, like lipopolysaccharides (LPS) from Gram-negative bacteria in the gut, are thought to contribute to this inflammatory cascade, inducing alpha-synuclein aggregation and microglial activation. [28]
Environmental Factors and Metal Dyshomeostasis Theory
The Environmental Factors and Metal Dyshomeostasis Theory highlights the impact of external elements on PD development. Only 5-10% of PD cases are purely genetic, suggesting a significant role for environmental factors. [29] Exposure to environmental toxicants, such as pesticides (e.g., rotenone, paraquat) and heavy metals (e.g., mercury, lead, manganese, copper, iron, aluminum), is associated with an increased risk of PD.[30][31][32] These metals can accumulate abnormally in the brain, particularly in the substantia nigra, and disrupt cellular homeostasis. [33][34]
Metal dyshomeostasis can lead to oxidative stress, protein aggregation (especially of alpha-synuclein), and mitochondrial dysfunction, thus contributing to neuronal loss.[35][36][37] For example, iron accumulation in the substantia nigra is a consistent feature of PD and is believed to cause neurodegeneration through redox-active mechanisms. [38] This theory underscores how environmental exposures can synergize with genetic susceptibilities to trigger the disease. [39]
Research Feed
The therapeutic role of minocycline in Parkinson’s disease
Did you know? The gut microbiome produces over 90% of the body’s serotonin, a key neurotransmitter that regulates mood, sleep, and cognition.
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Did you know? Short-chain fatty acids produced by gut microbes supply up to seventy percent of the energy used by colonocytes, making them fundamental regulators of intestinal barrier integrity and inflammation.
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Gut microbiome is not associated with mild cognitive impairment in Parkinson’s disease
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Metagenome-assembled microbial genomes from Parkinson’s disease fecal samples
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Oral and gut microbiome profiles in people with early idiopathic Parkinson’s disease
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Gut microbiota-associated taurine metabolism dysregulation in a mouse model of Parkinson’s disease
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Integrated Multi-Cohort Analysis of the Parkinson’s Disease Gut Metagenome
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Altered gut microbiota in patients with idiopathic Parkinson’s disease: an age-sex matched case-control study
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Integrated Microbiome and Host Transcriptome Profiles Link Parkinson’s Disease to Blautia Genus: Evidence From Feces, Blood, and Brain
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Oral and gut dysbiosis leads to functional alterations in Parkinson’s disease
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The link between increased Desulfovibrio and disease severity in Parkinson’s disease
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Differences in the gut microbiome across typical ageing and in Parkinson’s disease
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Dysbiosis of gut microbiota inhibits NMNAT2 to promote neurobehavioral deficits and oxidative stress response in the 6-OHDA-lesioned rat model of Parkinson’s disease
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Metagenomics of the Gut Microbiome in Parkinson’s Disease: Prodromal Changes
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Fibroblast growth factor 21 ameliorates behavior deficits in Parkinson’s disease mouse model via modulating gut microbiota and metabolic homeostasis
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Exploring the alteration of gut microbiota and brain function in gender-specific Parkinson’s disease based on metagenomic sequencing
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Fecal microbiome alterations in treatment-naive de novo Parkinson’s disease
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Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms
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Parkinson’s Disease and the Gut Microbiome in Rural California
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Altered gut microbiota in Parkinson’s disease patients with motor complications
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Nutritional Intake and Gut Microbiome Composition Predict Parkinson’s Disease
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The Gut Microbiome in Parkinson’s Disease: A Longitudinal Study of the Impacts on Disease Progression and the Use of Device-Assisted Therapies
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Clinical Phenotypes of Parkinson’s Disease Associate with Distinct Gut Microbiota and Metabolome Enterotypes
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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson’s disease
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Systematic analysis of gut microbiome reveals the role of bacterial folate and homocysteine metabolism in Parkinson’s disease
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Evaluation of fecal microbiota transplantation in Parkinson’s disease patients with constipation
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Altered Actinobacteria and Firmicutes Phylum Associated Epitopes in Patients With Parkinson’s Disease
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Cross-Sectional Study on the Gut Microbiome of Parkinson’s Disease Patients in Central China
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Association between Parkinson’s disease and the faecal eukaryotic microbiota
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Deep nasal sinus cavity microbiota dysbiosis in Parkinson’s disease
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Differences in the Composition of Gut Microbiota between Patients with Parkinson’s Disease and Healthy Controls: A Cohort Study
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An analysis of the characteristics of the intestinal flora in patients with Parkinson’s disease complicated with constipation
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Short-Chain Fatty Acid-Producing Gut Microbiota Is Decreased in Parkinson’s Disease but Not in Rapid-Eye-Movement Sleep Behavior Disorder
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A Pilot Microbiota Study in Parkinson’s Disease Patients versus Control Subjects, and Effects of FTY720 and FTY720-Mitoxy Therapies in Parkinsonian and Multiple System Atrophy Mouse Models
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Gut Microbiota Altered in Mild Cognitive Impairment Compared With Normal Cognition in Sporadic Parkinson’s Disease
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Parkinson’s disease-associated alterations of the gut microbiome predict disease-relevant changes in metabolic functions
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Characterizing dysbiosis of gut microbiome in PD: evidence for overabundance of opportunistic pathogens
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Acupuncture inhibits neuroinflammation and gut microbial dysbiosis in a mouse model of Parkinson’s disease
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Gut metagenomics-derived genes as potential biomarkers of Parkinson’s disease
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Gut Microbiota and Metabolome Alterations Associated with Parkinson’s Disease
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Changes in Gastrointestinal Microbiome Composition in PD: A Pivotal Role of Covariates
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The impact of intestinal microbiota on weight loss in Parkinson’s disease patients: a pilot study
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Gut microbiota in Parkinson’s disease: Temporal stability and relations to disease progression
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The oral microbiome of early stage Parkinson’s disease and its relationship with functional measures of motor and non-motor function
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Gut Microbiota Differs Between Parkinson’s Disease Patients and Healthy Controls in Northeast China
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Altered Gut Microbiome in Parkinson’s Disease and the Influence of Lipopolysaccharide in a Human α-Synuclein Over-Expressing Mouse Model
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Effect of Parkinson’s disease and related medications on the composition of the fecal bacterial microbiota
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Analysis of the Gut Microflora in Patients With Parkinson’s Disease
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Unraveling gut microbiota in Parkinson’s disease and atypical parkinsonism
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Dysbiosis of gut microbiota in a selected population of Parkinson’s patients
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Alteration of the fecal microbiota in North-Eastern Han Chinese population with sporadic Parkinson’s disease
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The nasal and gut microbiome in Parkinson’s disease and idiopathic rapid eye movement sleep behavior disorder
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Alteration of the fecal microbiota in Chinese patients with Parkinson’s disease
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Gut microbiota in patients with Parkinson’s disease in southern China
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Parkinson’s disease and Parkinson’s disease medications have distinct signatures of the gut microbiome
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Analysis of Gut Microbiota in Patients with Parkinson’s Disease
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Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson’s disease
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Changes in the Gut Microbiome and Predicted Functional Metabolic Effects in an Australian Parkinson’s Disease Cohort
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Altered gut microbiota in Parkinson’s disease patients/healthy spouses and its association with clinical features
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Gut microbiota are related to Parkinson’s disease and clinical phenotype
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Colonic bacterial composition in Parkinson’s disease
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Gut microbiota in Parkinson disease in a northern German cohort
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Structural changes of gut microbiota in Parkinson’s disease and its correlation with clinical features
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Short chain fatty acids and gut microbiota differ between patients with Parkinson’s disease and age-matched controls
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Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease
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Functional implications of microbial and viral gut metagenome changes in early stage L-DOPA-naïve Parkinson’s disease patients
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Transition metals like iron, zinc, copper, and manganese are crucial for the enzymatic machinery of organisms, but their imbalance can foster pathogenic environments within the gastrointestinal tract.
Lipopolysaccharide (LPS)
Lipopolysaccharide (LPS), a potent endotoxin present in the outer membrane of Gram-negative bacteria that causes chronic immune responses associated with inflammation.
Copper (Cu)
Copper serves as both a vital nutrient and a potential toxin, with its regulation having profound effects on microbial pathogenesis and immune responses. In the body, copper interacts with pathogens, either supporting essential enzyme functions or hindering microbial growth through its toxicity. The gastrointestinal tract, immune cells, and bloodstream are key sites where copper plays a crucial role in controlling infection and maintaining microbial balance. Understanding copper’s interactions with the microbiome and host defenses allows for targeted clinical strategies.
Brain Health
Brain health encompasses the overall functioning and well-being of the brain, including cognitive function, emotional and psychological well-being, neurological integrity, behavioral health, neurodevelopmental health, age-related brain health, and brain resilience and plasticity.
Short-chain Fatty Acids (SCFAs)
Short-chain fatty acids are microbially derived metabolites that regulate epithelial integrity, immune signaling, and microbial ecology. Their production patterns and mechanistic roles provide essential functional markers within microbiome signatures and support the interpretation of MBTIs, MMAs, and systems-level microbial shifts across clinical conditions.
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Class)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Family)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Genus)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Kingdom)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Order)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Relative Abundance (Phylum)
A microbiome signature is defined through a comprehensive approach that integrates differential abundance analysis across multiple datasets, followed by interpretation for biological relevance. This rigorous process ensures that the identified signature is both statistically robust and biologically meaningful. Associations that do not meet statistical significance or lack mechanistic relevance are excluded from the final signature.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study. 
Kimberly Eyer, a Registered Nurse with 30 years of nursing experience across diverse settings, including Home Health, ICU, Operating Room Nursing, and Research. Her roles have encompassed Operating Room Nurse, RN First Assistant, and Acting Director of a Same Day Surgery Center. Her specialty areas include Adult Cardiac Surgery, Congenital Cardiac Surgery, Vascular Surgery, and Neurosurgery. 
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Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study. 
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