About

Dr. Carrie Finno is a veterinarian and researcher with a veterinary degree from the University of Minnesota. She completed a one-year internship in Large Animal Medicine and Surgery at Minnesota, followed by a three-year residency in Large Animal Medicine and Surgery at UC Davis. She earned a PhD in Comparative Pathology at UC Davis and subsequently joined the faculty at the University of Minnesota as an Assistant Professor. Dr. Finno later returned to UC Davis as a faculty member in genetics and a clinical role with the Equine Medicine Service. Her research focuses on companion animal genetics, particularly the genetic and environmental risk factors associated with equine neuromuscular diseases. Her laboratory investigates the molecular basis for genetic diseases in horses and other companion animals, with translational research on vitamin E in neurodegeneration using mouse models and naturally-occurring models like neuroaxonal dystrophy in horses. Dr. Finno has received numerous awards, including the 2022 Chancellor’s Fellow and the 2021 Zoetis Excellence in Research Award, and is a member of professional societies such as the American College of Veterinary Internal Medicine.

Research topics

• Biology
• Genetics
• Evolutionary biology
• Pathology
• Medicine
• Sociology
• Surgery
• Computational biology
• Physiology
• Gastroenterology
• Endocrinology
• Cell biology
• Internal medicine

Selected publications

• Evidence of occipitoatlantoaxial malformations independent of the HOXD3 mutation in an Arabian horse

  Journal of Equine Veterinary Science · 2026-04-12

  article
  PublisherDOI

• Additional Evidence Fails to Associate Variation in <scp> <i>KCNE4</i> </scp> With Equine Anhidrosis

  Animal Genetics · 2026-04-26

  articleOpen accessSenior author

  ABSTRACT A prior genome‐wide association (GWA; N = 200) including Thoroughbreds and stock horses implicated chromosome 6 (NC_009149.3) in owner‐reported equine anhidrosis. A missense variant in KCNE4 (NC_009149.3:g.11813731A&gt;G) was proposed as a risk allele, although its association with anhidrosis was not reported. Variant annotation and protein modelling in the original study suggested the G allele conferred risk. We reported no association of the G allele with anhidrosis in 50 horses phenotyped by an intradermal terbutaline sweat test (ITST); all horses produced sweat regardless of genotype. It later appeared the A allele was instead suggested to confer disease risk. To reassess this, we genotyped 20 ITST‐tested Thoroughbreds including 9 with partial or complete anhidrosis. The KCNE4 A allele was not associated with phenotype when analyzed as a binary trait ( p = 0.16) or when classifying affected horses as having either partial or complete anhidrosis ( p = 0.21). The locus was also uninformative in four clinical cases (AA = 1, AG = 1, GG = 2). Reasoning that a true risk allele should be in linkage disequilibrium (LD) with the associated GWA SNV (AX‐103822151; rs68656009), we evaluated whole‐genome sequence ( N = 2) from the initial publication. Both case and control were homozygous AA at the putative risk locus; the case was heterozygous at the GWA SNV. In public data ( N = 897), LD between loci was low (r 2 = 0.19). In 369 Thoroughbreds, LD was 0.58. Restricting to Thoroughbreds in the original GWA ( N = 85), we found no association of chromosome 6 with anhidrosis. Collectively, these data do not support a role of the KCNE4 variant or the GWA SNV in equine anhidrosis.

  PublisherDOI

• Author response for "Cardiac arrhythmia prevalence and risk factors in 24-h electrocardiograms of sedentary horses"

  2025-04-12

  peer-review
  PublisherDOI

• Genetics of Muscle Disease

  Veterinary Clinics of North America Equine Practice · 2025-01-28 · 1 citations

  reviewOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Identification of a cryptic exon in FDXR associated with equine juvenile spinocerebellar ataxia in Quarter Horses

  Journal of Equine Veterinary Science · 2025-05-01

  articleSenior author
  PublisherDOI

• Evaluating the extent to which ataxia and responsiveness to stimuli reflect the efficacy of xylazine sedation using pharmacokinetics

  Journal of Equine Veterinary Science · 2025-07-15

  articleOpen access

  BACKGROUND: Clinical assessments of equine sedation typically rely on subjective observations, the accuracy of which is paramount to the safety of equine veterinary procedures. METHODS: To assess the degree in which subjective clinical sedative evaluations reflect pharmacokinetic measurements of equine drug metabolism, xylazine hydrochloride, an alpha-2 adrenoreceptor agonist, was administered to 36 horses of varying breed and age at a dosage of 0.5 mg/kg body weight. Subjective clinical parameters were scored at 5-, 15-, 30-, 45- and 60-minutes post xylazine administration and included responsiveness to sound, touch, visual stimuli, and observed degree of ataxia. Blood samples were collected at each time interval and liquid chromatography tandem mass spectrometry was performed to determine serum plasma concentrations of xylazine (XC) and 4-OH-xylazine (OHXC). Spearman's and Kendall's rank correlations assessed associations between subjective and objective measures of xylazine sedation. RESULTS: Ataxia demonstrated the strongest association, showing moderate positive correlation with both XC and OHXC (r = 0.63 and r = 0.58 respectively). Whilst all individual stimuli measures were significantly (p < 0.05) associated with both XC and OHXC, correlation for each was classified as negligible, ranging from r = -0.158 to -0.247. Combined stimuli responsiveness scores marginally improved the correlation with both XC and OHXC over that of individual stimuli measures yet remained classified as negligible correlation (XC r = -0.29, OHXC r = -0.28). CONCLUSIONS: This study highlights the limited correlation between stimuli-based sedation assessments and xylazine plasma concentrations, underscoring the importance of multifactorial evaluations with the inclusion of ataxia when assessing sedation for clinical procedures.

  PublisherDOI

• The role of vitamin E deficiency in equine neuromuscular disorders

  UK-Vet Equine · 2025-01-02

  articleSenior author

  Horses obtain vitamin E, an essential nutrient for neuromuscular health, through green pasture. Vitamin E dietary deficiencies can lead to neuromuscular diseases such as equine neuroaxonal dystrophy/equine degenerative myeloencephalopathy, equine motor neuron disease and vitamin E deficient myopathy. Some horses are genetically susceptible to developing these neuromuscular diseases, but not all horses that are vitamin E deficient exhibit clinical signs. Vitamin E supplementation is effective at slowing or halting clinical signs of some of these diseases, but the neuromuscular damage is usually irreversible, except in the case of vitamin E deficient myopathy. Adequate access to vitamin E early in life is essential to preventing these conditions.

  PublisherDOI

• Annotation of cis-regulatory-associated histone modifications in the genomes of two Thoroughbred stallions

  Frontiers in Genetics · 2025-02-27 · 1 citations

  articleOpen access

  The Functional Annotation of Animal Genomes (FAANG) consortium aims to annotate animal genomes across species, and work in the horse has substantially contributed to that goal. As part of this initiative, chromatin immunoprecipitation with sequencing (ChIP-seq) was performed to identify histone modifications corresponding to enhancers (H3K4me1), promoters (H3K4me3), activators (H3K27ac), and repressors (H3K27me3) in eight tissues from two Thoroughbred stallions: adipose, parietal cortex, heart, lamina, liver, lung, skeletal muscle, and testis. The average genome coverage of peaks identified by MACS2 for H3K4me1, H3K4me3, and H3K27ac was 6.2%, 2.2%, and 4.1%, respectively. Peaks were called for H3K27me3, a broad mark, using both MACS2 and SICERpy, with MACS2 identifying a greater average number of peaks (158K; 10.4% genome coverage) than SICERpy (32K; 24.3% genome coverage). Tissue-unique peaks were identified with BEDTools, and 1%-47% of peaks were unique to a tissue for a given histone modification. However, correlations among usable reads, total peak number, and unique peak number ranged from 0.01 to 0.92, indicating additional data collection is necessary to parse technical from true biological differences. These publicly available data expand a growing resource available for identifying regulatory regions within the equine genome, and they serve as a reference for genome regulation across healthy tissues of the adult Thoroughbred stallion.

  PublisherOA PDFDOI

• How nutrigenomics impacts equine health - A case study of vitamin E

  Journal of Equine Veterinary Science · 2025-03-22

  reviewOpen access1st authorCorresponding

  • Nutrigenomics defines the interaction between the genome, nutrition and overall health. • Response to vitamin E supplementation varies from horse to horse and may be due to genetic variations in genes related to vitamin E transport and metabolism. • This review includes a case study of a horse with vitamin E responsive myopathy. Nutrigenomics defines the interaction between the nutrients in our food and the genes in our body. Examples from human medicine of diseases and associated genes include lactose intolerance (genetic variants in LCT lactase ), hypercholesteremia ( low density lipoprotein receptor, LDLR ) and caffeine sensitivity ( adenosine A2A receptor, ADORA2A ). In horses, examples include Hyperkalemic Periodic Paralysis (HYPP), where clinical signs of disease are managed through maintaining a diet low in potassium and Polysaccharide Storage Myopathy Type 1 (PSSM1), where low starch and high fat diets are recommended to prevent episodes of rhabdomyolysis. Personalized nutrition tailors nutrition advice for an individual based on their genetic makeup. In humans and in horses, there is a wide range of individual response to vitamin E supplementation. Some horses obtain very high serum vitamin E concentrations with minimal intake, whereas others require high doses of supplementation to remain in the normal range. In humans, the efficiency of vitamin E absorption is widely variable and is affected by dietary factors, such as food matrix, and genetic polymorphisms in genes related to vitamin E intake, distribution and metabolism. In horses, the efficiency of vitamin E absorption is also related to diet; however, genetic variation has not been yet evaluated. With over 200 genetic variants identified in and surrounding vitamin E candidate genes in horses, future genetic profiling of vitamin E response in horses should be performed.

  PublisherDOI

• Identification of the role of SEL1L in platelet function through a multi-species genetic investigation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-06

  preprintOpen accessSenior author

  Abstract SEL1L is a well-known protein in the endoplasmic reticulum associated degradation (ERAD) pathway. While it is known to be expressed in platelets, SEL1L has never been shown to play an active role. Here we find evidence that SEL1L regulates platelet function. We first identified SEL1L through the study of Atypical Equine Thrombasthenia (AET), an autosomal recessive platelet disorder found in Thoroughbred horses. A missense variant in SEL1L (c.1810A&gt;G p.Ile604Val) was found in AET-affected horses, which we show is associated with decreased protein expression. SEL1L is intracellular in equine platelets and localizes to the surface upon activation with thrombin. Platelets from homozygous horses exhibit significant decreases in spreading on immobilized collagen. Human megakaryocytes were found to have two SEL1L protein isoforms that increase in expression during megakaryopoiesis, although only one is delivered to mature platelets. Studies using inducible mouse and constitutive zebrafish knockouts demonstrate that SEL1L is necessary for efficient platelet or thrombocyte (fish equivalent) adhesion to sites of endothelial injury. These data reveal a previously undescribed and conserved role for the ERAD pathway in the etiology of AET and platelet function, which may play a role in human platelet disorders as well. Brief Summary Using a multi-species approach, SEL1L was determined to have a role in platelet function, specifically in helping platelets properly adhere to sites of injury,

  PublisherOA PDFDOI

Recent grants

• NIH Grant K01OD01513401A1

  NIH · $101k · 2014

• NIH Grant K01OD015134

  NIH · $498k · 2018

Frequent coauthors

• Stephanie J. Valberg

  Michigan State University

  60 shared

• Rebecca R. Bellone

  University of California, Davis

  53 shared

• Jessica L. Petersen

  University of Nebraska–Lincoln

  45 shared

• Theodore S. Kalbfleisch

  University of Kentucky

  40 shared

• Sichong Peng

  University of California, Davis

  34 shared

• Monica Aleman

  University of California, Davis

  25 shared

• Danika L. Bannasch

  University of California, Davis

  24 shared

• Callum G. Donnelly

  University of California, Davis

  21 shared

Education

• DVM, School of Veterinary Medicine

  University of Minnesota

  2014

Awards & honors

• 2022 Chancellor’s Fellow
• 2021 Zoetis Excellence in Research Award
• 2012 James M. Wilson Award, Center for Equine Health, UC Dav…
• 2011 Merial/NIH National Veterinary Scholars Symposium Young…
• 2010-2011 Ann Bowling Scholarship for Equine Genetics