Maureen Hanson

Maureen R. Hanson, PhD., is the Liberty Hyde Bailey Professor in the Department of Molecular Biology & Genetics, Cornell University, Ithaca, New York, USA. In addition to her research on genome-containing organelles of plants, chloroplasts and mitochondria, she is exploring the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Research goals include examining the gut and blood microbiome in healthy vs. ill subjects and identifying differences in gene expression before and after exercise in subjects diagnosed with CFS/ME compared to healthy subjects.

Dr. Hanson, together with Dr. Betsy Keller at Ithaca College are collaborating to create a new ME/CFS research center called the Center for Enervating NeuroImmune Disease (CEND).

Dr. Hanson's strong desire to research and advocate for ME/CFS is motivated by her having a family member with chronic fatigue syndrome.

Education

 * B.S. degree at Duke University
 * Ph.D. in Cell and Developmental Biology from Harvard University
 * NIH postdoctoral fellowship at Harvard

Notable studies

 * 2016, A Pair of Identical Twins Discordant for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Differ in Physiological Parameters and Gut Microbiome Composition"'BACKGROUND: Patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) present with profound fatigue, flu-like symptoms, pain, cognitive impairment, orthostatic intolerance, and post-exertional malaise (PEM), and exacerbation of some or all of the baseline symptoms. CASE REPORT: We report on a pair of 34-year-old monozygotic twins discordant for ME/CFS, with WELL, the non-affected twin, and ILL, the affected twin. Both twins performed a two-day cardiopulmonary exercise test (CPET), pre- and post-exercise blood samples were drawn, and both provided stool samples for biochemical and molecular analysis. At peak exertion for both CPETs, ILL presented lower VO2peak and peak workload compared to WELL. WELL demonstrated normal reproducibility of VO2@ventilatory/anaerobic threshold (VAT) during CPET2, whereas ILL experienced an abnormal reduction of 13% in VAT during CPET2. A normal rise in lactate dehydrogenase (LDH), creatine kinase (CK), adrenocorticotropic hormone (ACTH), cortisol, creatinine, and ferritin content was observed following exercise for both WELL and ILL at each CPET. ILL showed higher increases of resistin, soluble CD40 ligand (sCD40L), and soluble Fas ligand (sFasL) after exercise compared to WELL. The gut bacterial microbiome and virome were examined and revealed a lower microbial diversity in ILL compared to WELL, with fewer beneficial bacteria such as Faecalibacterium and Bifidobacterium, and an expansion of bacteriophages belonging to the tailed dsDNA Caudovirales order. CONCLUSIONS: Results suggest dysfunctional immune activation in ILL following exercise and that prokaryotic viruses may contribute to mucosal inflammation and bacterial dysbiosis. Therefore, a two-day CPET and molecular analysis of blood and microbiomes could provide valuable information about ME/CFS, particularly if applied to a larger cohort of monozygotic twins.'"
 * 2016, Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome
 * 2016, Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome(FULL TEXT)"Abstract - 'Background: Mitochondrial dysfunction has been hypothesized to occur in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a disease characterized by fatigue, cognitive difficulties, pain, malaise, and exercise intolerance. We investigated whether haplogroup, single nucleotide polymorphisms (SNPs), or heteroplasmy of mitochondrial DNA (mtDNA) were associated with health status and/or symptoms. Methods: Illumina sequencing of PCR-amplified mtDNA was performed to analyze sequence and extent of heteroplasmy of mtDNAs of 193 cases and 196 age- and gender-matched controls from DNA samples collected by the Chronic Fatigue Initiative. Association testing was carried out to examine possible correlations of mitochondrial sequences with case/control status and symptom constellation and severity as reported by subjects on Short Form-36 and DePaul Symptom Questionnaires. Results: No ME/CFS subject exhibited known disease-causing mtDNA mutations. Extent of heteroplasmy was low in all subjects. Although no association between mtDNA SNPs and ME/CFS vs. healthy status was observed, haplogroups J, U and H as well as eight SNPs in ME/CFS cases were significantly associated with individual symptoms, symptom clusters, or symptom severity. Conclusions: Analysis of mitochondrial genomes in ME/CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to ME/CFS of individuals carrying particular mitochondrial genomes or SNPs was observed.'"

Talks & interviews

 * 1 September 2016, Solve ME/CFS Initiative Webinar with Maureen Hanson, Ph.D., "Current and Previous Research on ME/CFS at Cornell University"
 * 3 June 2016, Speaker at the 11th Invest in ME International ME Conference on "The Search for Biomarkers for Myalgic Encephalomyelitis" DVD available
 * 2014, Speaker at the 9th Invest in ME International ME Conference DVD available(no speech title given)]

Articles

 * 10 Oct 2016,The Real Story About Chronic Fatigue Syndrome
 * 30 Sept 2016,Millions Are Missing: Will The World Finally Notice?
 * 20 May 2016,Aware and Beware: Chronic Fatigue Syndrome Is an Equal Opportunity Disease'' by Maureen Hanson
 * 10 May 2016, When the Hoofbeats are Zebras by Maureen Hanson

Online presence

 * PubMed
 * Twitter
 * Facebook
 * Cornell University - Professor Maureen Hanson Website
 * Cornell University - Faculty page, Maureen Hanson
 * Scholar Google