Equine Pituitary Pars Intermedia Dysfunction (PPID)

Equine Pituitary Pars Intermedia Dysfunction (PPID), previously known as equine Cushing’s, is a commonly recognized condition in the older horse population.  This disease is estimated to affect 15-30% of horses above the age of 15. Work by Dr. McFarlane and others have demonstrated that PPID is primarily due to a neurodegenerative process in which there is a loss of neurons from the hypothalamus that results in decreased dopamine levels and increased growth of the cells of the pituitary pars intermedia (Figure 1).1 Work in other species, mainly humans, has demonstrated that similar neurodegenerative processes occur in Parkinson’s disease, and are impacted by genetic mutations in genes in one or more key pathways2–12.

PPID Overview

Figure 1. Overview of pathophysiology in PPID.  Image created with Biorender.com.

Some of the common clinical signs include:

  • A long shaggy hair coat (hypertrichosis/hirsutismFigure 2)
  • Loss of muscling (muscle atrophy)
  • Drinking and urinating excessively (polydipsia/polyuria)
  • Change in behavior
  • Recurrent infections
  • Laminitis

Hairy Horse



Figure 2. Long shaggy hair coat (known as hypertrichosis or hirsutism) that is pathognomonic for PPID in horses.




This disease is challenging for veterinarians as it can be difficult to accurately diagnose especially in the early stages.  By the time we see clinical signs, horses may have had the disease for multiple years.   There is no cure for PPID, but it can be managed using medications.  Regular blood work screenings are important to monitor disease progress. 

Our lab is actively investigating a potential genetic component to the development of this condition by identifying mutations in affected PPID horses.  If a genetic component and mutation(s) are recognized, identification of at-risk horses can be performed at an earlier age.  This could improve the ability to accurately diagnose, treat and manage affected horses.  A better understanding of this disease has become even more important as the aged horse population continues to increase due to advances in nutrition, management/husbandry and veterinary care.

PPID Research Team:

Dr. Molly McCue (PI, University of Minnesota)
Dr. Dianne McFarlane (Co-I, University of Florida)
Dr. Lauren Hughes (PhD Student, University of Minnesota)

If you have any questions, please contact the research team at eggl-ppidstudy@umn.edu.

*This project has received funding by Oklahoma State University and the Morris Animal Foundation.

*Additional support has been provided through the ACVIM Advanced Research Training Fellowship, the Foundation for the Horse Research Fellowship, and the National Institutes of Health T32 Training Grant at the University of Minnesota. 



  1. D. McFarlane, Pathophysiology and clinical features of pituitary pars intermedia dysfunction: Pathophysiology of PPID. Equine Veterinary Education, vol. 26, no. 11, pp. 592–598, Nov. 2014, doi: 10.1111/eve.12237.

  2. Hernandez DG, Singleton AB. Movement Disorder Genetics. 2015;(Icm):19-34. doi:10.1007/978-3-319-17223-1

  3. Gollob MH, Seger JJ, Gollob TN, et al. Novel PRKAG2 mutation responsible for the genetic syndrome of ventricular preexcitation and conduction system disease with childhood onset and absence of cardiac hypertrophy. Circulation. 2001;104(25):3030-3033. http://www.ncbi.nlm.nih.gov/pubmed/11748095.

  4. McFarlane D. Advantages and limitations of the equine disease, pituitary pars intermedia dysfunction as a model of spontaneous dopaminergic neurodegenerative disease. Ageing Res Rev. 2007;6(1):54-63. doi:10.1016/j.arr.2007.02.001

  5.  E. Grenblatt et al., “Gene expression profiling of parkinsonian substantia nigra pars compacta; alterations in ubiquitin-proteasome, heat shock protein, iron and oxidative stress regulated proteins, cell adhesion/cellular matrix and vesicle trafficking genes,” J Neural Transm, vol. 111, no. 12, pp. 1543–1573, Dec. 2004, doi: 10.1007/s00702-004-0212-1.

  6. D. G. Hernandez, X. Reed, and A. B. Singleton, “Genetics in Parkinson disease: Mendelian versus non-Mendelian inheritance,” J. Neurochem., vol. 139, pp. 59–74, Oct. 2016, doi: 10.1111/jnc.13593.

  7. E. M. Hill-Burns, W. T. Wissemann, T. H. Hamza, S. A. Factor, C. P. Zabetian, and H. Payami, “Identification of a novel Parkinson’s disease locus via stratified genome-wide association study,” BMC Genomics, vol. 15, no. 1, p. 118, 2014, doi: 10.1186/1471-2164-15-118.

  8. P. A. Lewis and M. R. Cookson, “Gene expression in the Parkinson’s disease brain,” Brain Research Bulletin, vol. 88, no. 4, pp. 302–312, Jul. 2012, doi: 10.1016/j.brainresbull.2011.11.016.

  9. N. Pankratz et al., “Genomewide association study for susceptibility genes contributing to familial Parkinson disease,” Hum Genet, vol. 124, no. 6, pp. 593–605, Jan. 2009, doi: 10.1007/s00439-008-0582-9.

  10. G. T. Sutherland et al., “A Cross-Study Transcriptional Analysis of Parkinson’s Disease,” PLoS ONE, vol. 4, no. 3, p. e4955, Mar. 2009, doi: 10.1371/journal.pone.0004955.

  11. E. C. Schulte et al., “Rare variants in β-Amyloid precursor protein (APP) and Parkinson’s disease,” Eur J Hum Genet, vol. 23, no. 10, pp. 1328–1333, Oct. 2015, doi: 10.1038/ejhg.2014.300.

  12. L. Soreq, Y. Ben-Shaul, Z. Israel, H. Bergman, and H. Soreq, “Meta-analysis of genetic and environmental Parkinson’s disease models reveals a common role of mitochondrial protection pathways,” Neurobiology of Disease, vol. 45, no. 3, pp. 1018–1030, Mar. 2012, doi: 10.1016/j.nbd.2011.12.021.