FREE SHIPPING over $40
OVER 9000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Home / Equine Research Bank / Vet Sci / A Pilot Study on Blood Concentration of β-Amyloid (40 ...
Veterinary sciences2025; 12(7); 610; doi: 10.3390/vetsci12070610

A Pilot Study on Blood Concentration of β-Amyloid (40 and 42) and Phospho-Tau 181 in Horses.

Abstract: In humans, aging is often accompanied by cognitive decline, as seen in Alzheimer's disease. In contrast, the aging process in horses remains poorly characterized. This study aims to explore the presence of blood-based biomarkers associated with cognitive degeneration in this species. Twenty-three Arabian horses were enrolled, and 5 mL of blood was collected from each to measure serum levels of β-amyloid peptides (Aβ40 and Aβ42) and phosphorylated tau protein (pTau181), both considered reliable indicators of cognitive impairment in other species. Aβ42 was undetectable in all samples, while pTau181 ranged from 5.38 to 54.42 pg/mL and Aβ40 from 67.4 to 743.9 pg/mL. Statistical analysis of the data, performed with the non-parametric Spearman test, did not reveal any correlation between age and the concentrations of Aβ40 and pTau. The pTau/Aβ40 ratio also did not appear to be correlated with the age of the subjects. Interestingly, none of the horses exhibited behavioral changes or clinical signs suggestive of cognitive dysfunction. This absence of symptoms may be related to the undetectable levels of Aβ42, the isoform considered crucial in initiating tau phosphorylation and subsequent neurodegeneration, despite possibly being present at concentrations higher than those typically found in healthy humans.
Get Full Text
Publication Date: 2025-06-23 PubMed ID: 40711270PubMed Central: PMC12300970DOI: 10.3390/vetsci12070610Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research article investigates the presence of certain biomarkers linked to cognitive degeneration in Arabian horses as they age. No evidence of correlation between age and these biomarkers, or observable cognitive impairment, was found.

Research Focus and Methodology

  • This study concentrates on the exploration of neurocognitive changes in horses as they age. The main focus is on certain biomarkers of cognitive degeneration, specifically β-amyloid proteins (Aβ40 and Aβ42) and phosphorylated tau protein (pTau181). These are commonly considered reliable indicators of cognitive impairment in some species.
  • Twenty-three Arabian horses were used for this preliminary research. Five milliliters of blood were collected from each horse to measure serum levels of the aforementioned biomarkers.

Findings

  • Across all samples, Aβ42 was undetectable. The concentration of pTau181 varied from 5.38 to 54.42 pg/mL, and Aβ40 ranged from 67.4 to 743.9 pg/mL.
  • The researchers used the non-parametric Spearman test for statistical analysis and found no correlation between aging and the concentration levels of Aβ40 and pTau181. Equally, the ratio of pTau/Aβ40 didn’t show any association with the age of horses.
  • Interestingly, despite the involvement of these three biomarkers, none of the horses displayed visible symptoms of cognitive dysfunction such as changes in behavior or other clinical signs.

Interpretation and Significance

  • Although the undetectable levels of Aβ42 in all the collected samples can potentially suggest its absence, the researchers argue that it might be present but in concentrations higher than in healthy humans, leading to it being undetected.
  • The Aβ42 isoform is believed to play a critical role in initiating tau phosphorylation and thus neurodegeneration.
  • This research constitutes an initial attempt to investigate aging and cognitive impairment in horses as compared to humans, where aging often presents with some degree of cognitive decline.
  • The findings, while preliminary, suggest that either Arabian horses do not develop cognitive deterioration as they age, or that different biomarkers may need to be studied to reveal any potential cognitive decline.

Cite This Article

APA
Gazzano V, Curadi MC, Capsoni S, Baragli P, Kêdzierski W, Cecchi F, Gazzano A. (2025). A Pilot Study on Blood Concentration of β-Amyloid (40 and 42) and Phospho-Tau 181 in Horses. Vet Sci, 12(7), 610. https://doi.org/10.3390/vetsci12070610

Publication

Veterinary sciences
ISSN: 2306-7381
NlmUniqueID: 101680127
Country: Switzerland
Language: English
Volume: 12
Issue: 7
PII: 610

Researcher Affiliations

Gazzano, Valentina
  • Department of Veterinary Sciences, University of Pisa, 56126 Pisa, Italy.
Curadi, Maria Claudia
  • Department of Veterinary Sciences, University of Pisa, 56126 Pisa, Italy.
Capsoni, Simona
  • Department Neuroscience & Rehabilitation, University of Ferrara, 44124 Ferrara, Italy.
  • Bio@SNS Laboratory of Biology, Scuola Normale Superiore, 56127 Pisa, Italy.
Baragli, Paolo
  • Department of Veterinary Sciences, University of Pisa, 56126 Pisa, Italy.
Kêdzierski, Witold
  • Department of Biochemistry, University of Life Sciences, 20-950 Lublin, Poland.
Cecchi, Francesca
  • Department of Veterinary Sciences, University of Pisa, 56126 Pisa, Italy.
Gazzano, Angelo
  • Department of Veterinary Sciences, University of Pisa, 56126 Pisa, Italy.

Conflict of Interest Statement

The authors declare no conflicts of interest.

References

This article includes 55 references
  1. Zhang X, Guo T, Zhang Y, Jiao M, Ji L, Dong Z, Li H, Chen S, Zheng W, Jing Q. Global Burden of Alzheimer’s Disease and Other Dementias Attributed to Metabolic Risks from 1990 to 2021: Results from the Global Burden of Disease Study 2021. BMC Psychiatry 2024;24:910.
    doi: 10.1186/s12888-024-06375-xpmc: PMC11654253pubmed: 39696219google scholar: lookup
  2. Mohamed S, Rosenheck R, Lyketsos CG, Schneider LS. Caregiver Burden in Alzheimer Disease: Cross-Sectional and Longitudinal Patient Correlates. Am. J. Geriatr. Psychiatry 2010;18:917–927.
    doi: 10.1097/JGP.0b013e3181d5745dpmc: PMC3972419pubmed: 20808108google scholar: lookup
  3. Ciurli L, Casini L, Cecchi F, Baragli P, Macchioni F, Curadi C, Gazzano V, Capsoni S, Gazzano A. The Canine Cognitive Dysfunction Syndrome: Epidemiology, Pathophysiology and Diagnosis. Dog Behav 2023;9:1–8.
    doi: 10.4454/db.v9i2.169google scholar: lookup
  4. Bosch MN, Pugliese M, Gimeno-Bayón J, Rodríguez MJ, Mahy N. Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease. Curr. Alzheimer Res 2012;9:298–314.
    doi: 10.2174/156720512800107546pubmed: 21875411google scholar: lookup
  5. Osella MC, Re G, Odore R, Girardi C, Badino P, Barbero R, Bergamasco L. Canine Cognitive Dysfunction Syndrome: Prevalence, Clinical Signs and Treatment with a Neuroprotective Nutraceutical. Appl. Anim. Behav. Sci 2007;105:297–310.
    doi: 10.1016/j.applanim.2006.11.007google scholar: lookup
  6. Seisdedos Benzal A, Galán Rodríguez A. Recent Developments in Canine Cognitive Dysfunction Syndrome. Pet. Behav. Sci 2016;1:47–56.
    doi: 10.21071/pbs.v0i1.3996google scholar: lookup
  7. American Veterinary Medical Association. Pet Ownership & Demographics Sourcebook. .
  8. Cellai S, Gazzano A, Casini L, Gazzano V, Cecchi F, Macchioni F, Cozzi A, Pageat L, Arroub S, Fratini S. The Memory Abilities of the Elderly Horse. Animals 2024;14:3073.
    doi: 10.3390/ani14213073pmc: PMC11545349pubmed: 39518796google scholar: lookup
  9. Roda A, Serra-Mir G, Montoliu-Gaya L, Tiessler L, Villegas S. Amyloid-Beta Peptide and Tau Protein Crosstalk in Alzheimer’s Disease. Neural Regen. Res 2022;17:1666–1674.
    doi: 10.4103/1673-5374.332127pmc: PMC8820696pubmed: 35017413google scholar: lookup
  10. Karran E, De Strooper B. The Amyloid Cascade Hypothesis: Are We Poised for Success or Failure?. J. Neurochem 2016;139:237–252.
    doi: 10.1111/jnc.13632pubmed: 27255958google scholar: lookup
  11. Selkoe DJ, Hardy J. The Amyloid Hypothesis of Alzheimer’s Disease at 25 Years. EMBO Mol. Med 2016;8:595–608.
    doi: 10.15252/emmm.201606210pmc: PMC4888851pubmed: 27025652google scholar: lookup
  12. Small SA, Duff K. Linking Aβ and Tau in Late-Onset Alzheimer’s Disease: A Dual Pathway Hypothesis. Neuron 2008;60:534–542.
    doi: 10.1016/j.neuron.2008.11.007pmc: PMC2692134pubmed: 19038212google scholar: lookup
  13. He Z, Guo JL, McBride JD, Narasimhan S, Kim H, Changolkar L, Zhang B, Gathagan RJ, Yue C, Dengler C. Amyloid-β Plaques Enhance Alzheimer’s Brain Tau-Seeded Pathologies by Facilitating Neuritic Plaque Tau Aggregation. Nat. Med 2018;24:29–38.
    doi: 10.1038/nm.4443pmc: PMC5760353pubmed: 29200205google scholar: lookup
  14. Elhage A, Cohen S, Cummings J, van der Flier WM, Aisen P, Cho M, Bell J, Hampel H. Defining Benefit: Clinically and Biologically Meaningful Outcomes in the next-Generation Alzheimer’s Disease Clinical Care Pathway. Alzheimer’s Dement 2024;21:e14425.
    doi: 10.1002/alz.14425pmc: PMC11848336pubmed: 39697158google scholar: lookup
  15. Therriault J, Schindler SE, Salvadó G, Pascoal TA, Benedet AL, Ashton NJ, Karikari TK, Apostolova L, Murray ME, Verberk I. Biomarker-Based Staging of Alzheimer Disease: Rationale and Clinical Applications. Nat. Rev. Neurol 2024;20:232–244.
    doi: 10.1038/s41582-024-00942-2pubmed: 38429551google scholar: lookup
  16. Karikari TK, Ashton NJ, Brinkmalm G, Brum WS, Benedet AL, Montoliu-Gaya L, Lantero-Rodriguez J, Pascoal TA, Suárez-Calvet M, Rosa-Neto P. Blood Phospho-Tau in Alzheimer Disease: Analysis, Interpretation, and Clinical Utility. Nat. Rev. Neurol 2022;18:400–418.
    doi: 10.1038/s41582-022-00665-2pubmed: 35585226google scholar: lookup
  17. Hampel H, O’Bryant SE, Molinuevo JL, Zetterberg H, Masters CL, Lista S, Kiddle SJ, Batrla R, Blennow K. Blood-Based Biomarkers for Alzheimer Disease: Mapping the Road to the Clinic. Nat. Rev. Neurol 2018;14:639–652.
    doi: 10.1038/s41582-018-0079-7pmc: PMC6211654pubmed: 30297701google scholar: lookup
  18. Ashton NJ, Hye A, Rajkumar AP, Leuzy A, Snowden S, Suárez-Calvet M, Karikari TK, Schöll M, La Joie R, Rabinovici GD. An Update on Blood-Based Biomarkers for Non-Alzheimer Neurodegenerative Disorders. Nat. Rev. Neurol 2020;16:265–284.
    doi: 10.1038/s41582-020-0348-0pubmed: 32322100google scholar: lookup
  19. Blennow K, Mattsson N, Schöll M, Hansson O, Zetterberg H. Amyloid Biomarkers in Alzheimer’s Disease. Trends Pharmacol. Sci 2015;36:297–309.
    doi: 10.1016/j.tips.2015.03.002pubmed: 25840462google scholar: lookup
  20. Hampel H, Blennow K, Shaw LM, Hoessler YC, Zetterberg H, Trojanowski JQ. Total and Phosphorylated Tau Protein as Biological Markers of Alzheimer’s Disease. Exp. Gerontol 2010;45:30–40.
    doi: 10.1016/j.exger.2009.10.010pmc: PMC2815003pubmed: 19853650google scholar: lookup
  21. Hardy J, Selkoe DJ. The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics. Science 2002;19:353–356.
    doi: 10.1126/science.1072994pubmed: 12130773google scholar: lookup
  22. Selkoe DJ. The genetics and molecular pathology of alzheimer’s disease roles of amyloid and the presenilins. Neurol. Clin 2000;18:903–922.
    doi: 10.1016/S0733-8619(05)70232-2pubmed: 11072267google scholar: lookup
  23. Kang J, Lemaire HG, Unterbeck A, Salbaum JM, Masters CL, Grzeschik KH, Multhaup G, Beyreuther K, Müller-Hill B. The precursor of Alzheimer’s disease amyloid A4 protein resembles a cell-surface receptor. Nature 1987;325:733–736.
    doi: 10.1038/325733a0pubmed: 2881207google scholar: lookup
  24. Müller UC, Deller T, Korte M. Not Just Amyloid: Physiological Functions of the Amyloid Precursor Protein Family. Nat. Rev. Neurosci 2017;18:281–298.
    doi: 10.1038/nrn.2017.29pubmed: 28360418google scholar: lookup
  25. Rice HC, De Malmazet D, Schreurs A, Frere S, Van Molle I, Volkov AN, Creemers E, Vertkin I, Nys J, Ranaivoson FM. Secreted Amyloid-b Precursor Protein Functions as a GABA B R1a Ligand to Modulate Synaptic Transmission. Science 2019;363:143.
    doi: 10.1126/science.aao4827pmc: PMC6366617pubmed: 30630900google scholar: lookup
  26. Younkin SG. The Role of Aβ42 in Alzheimer’s Disease. J. Physiol. Paris 1998;92:289–292.
    doi: 10.1016/S0928-4257(98)80035-1pubmed: 9789825google scholar: lookup
  27. Teng FYH, Tang BL. Widespread γ-Secretase Activity in the Cell, but Do We Need It at the Mitochondria?. Biochem. Biophys. Res. Commun 2005;328:1–5.
    doi: 10.1016/j.bbrc.2004.12.131pubmed: 15670741google scholar: lookup
  28. Thorwald MA, Silva J, Head E, Finch CE. Amyloid Futures in the Expanding Pathology of Brain Aging and Dementia. Alzheimer’s Dement 2023;19:2605–2617.
    doi: 10.1002/alz.12896pmc: PMC10271937pubmed: 36536382google scholar: lookup
  29. Hanseeuw BJ, Betensky RA, Jacobs HIL, Schultz AP, Sepulcre J, Becker JA, Cosio DMO, Farrell M, Quiroz YT, Mormino EC. Association of Amyloid and Tau with Cognition in Preclinical Alzheimer Disease: A Longitudinal Study. JAMA Neurol 2019;76:915–924.
    doi: 10.1001/jamaneurol.2019.1424pmc: PMC6547132pubmed: 31157827google scholar: lookup
  30. Braak H, Braak E. Neuropathological Stageing of Alzheimer-Related Changes. Acta Neuropathol 1991;82:239–259.
    doi: 10.1007/BF00308809pubmed: 1759558google scholar: lookup
  31. Kim J, Onstead L, Randle S, Price R, Smithson L, Zwizinski C, Dickson DW, Golde T, McGowan E. Aβ40 Inhibits Amyloid Deposition in Vivo. J. Neurosci 2007;27:627–633.
    doi: 10.1523/JNEUROSCI.4849-06.2007pmc: PMC6672801pubmed: 17234594google scholar: lookup
  32. Panek WK, Murdoch DM, Gruen ME, Mowat FM, Marek RD, Olby NJ. Plasma Amyloid Beta Concentrations in Aged and Cognitively Impaired Pet Dogs. Mol. Neurobiol 2021;58:483–489.
    doi: 10.1007/s12035-020-02140-9pmc: PMC7855498pubmed: 32970242google scholar: lookup
  33. Smolek T, Madari A, Farbakova J, Kandrac O, Jadhav S, Cente M, Brezovakova V, Novak M, Zilka N. Tau Hyperphosphorylation in Synaptosomes and Neuroinflammation Are Associated with Canine Cognitive Impairment. J. Comp. Neurol 2016;524:874–895.
    doi: 10.1002/cne.23877pubmed: 26239295google scholar: lookup
  34. Ciurli L, Casini L, Cecchi F, Baragli P, Macchioni F, Curadi MC, Gazzano V, Capsoni S, Gazzano A. The Canine Cognitive Dysfunction Syndrome: Rating Scales. Dog Behav 2023;9:23–35.
  35. Iqbal K. Tau and Alzheimer’s Disease: Past, Present and Future. Cytoskeleton 2024;81:116–121.
    doi: 10.1002/cm.21822pmc: PMC10977900pubmed: 38126608google scholar: lookup
  36. Arendt T, Stieler JT, Holzer M. Tau and Tauopathies. Brain Res. Bull 2016;126:238–292.
    pubmed: 27615390
  37. Janelidze S, Mattsson N, Palmqvist S, Smith R, Beach TG, Serrano GE, Chai X, Proctor NK, Eichenlaub U, Zetterberg H. Plasma P-Tau181 in Alzheimer’s Disease: Relationship to Other Biomarkers, Differential Diagnosis, Neuropathology and Longitudinal Progression to Alzheimer’s Dementia. Nat. Med 2020;26:379–386.
    doi: 10.1038/s41591-020-0755-1pubmed: 32123385google scholar: lookup
  38. McLean AN. Short-Term Spatial Memory in the Domestic Horse. Appl. Anim. Behav. Sci 2004;85:93–105.
    doi: 10.1016/j.applanim.2003.09.009google scholar: lookup
  39. Hanggi EB, Ingersoll JF. Long-Term Memory for Categories and Concepts in Horses (Equus Caballus). Anim. Cogn 2009;12:451–462.
    doi: 10.1007/s10071-008-0205-9pubmed: 19148689google scholar: lookup
  40. Wolff A, Hausberger M. Learning and Memorisation of Two Different Tasks in Horses: The Effects of Age, Sex and Sire. Appl. Anim. Behav. Sci 1996;46:137–143.
    doi: 10.1016/0168-1591(95)00659-1google scholar: lookup
  41. Marinier S, Alexander AJ. The Use of a Maze in Testing Learning and Memory in Horses. Appl. Anim. Behav. Sci 1994;39:177–182.
    doi: 10.1016/0168-1591(94)90137-6google scholar: lookup
  42. Ballou ME, Mueller MK, Dowling-Guyer S. Aging Equines: Understanding the Experience of Caring for a Geriatric Horse with a Chronic Condition. J. Equine Vet. Sci 2020;90:102993.
    doi: 10.1016/j.jevs.2020.102993pubmed: 32534771google scholar: lookup
  43. Dong R, Yi N, Jiang D. Advances in Single Molecule Arrays (SIMOA) for Ultra-Sensitive Detection of Biomolecules. Talanta 2024;270:125529.
    doi: 10.1016/j.talanta.2023.125529pubmed: 38091745google scholar: lookup
  44. Tharp WG, Sarkar IN. Origins of Amyloid-β. BMC Genom 2013;14:290.
    doi: 10.1186/1471-2164-14-290pmc: PMC3660159pubmed: 23627794google scholar: lookup
  45. Brothers HM, Gosztyla ML, Robinson SR. The Physiological Roles of Amyloid-β Peptide Hint at New Ways to Treat Alzheimer’s Disease. Front. Aging Neurosci 2018;10:118.
    doi: 10.3389/fnagi.2018.00118pmc: PMC5996906pubmed: 29922148google scholar: lookup
  46. Plant LD, Boyle JP, Smith IF, Peers C, Pearson HA. The Production of Amyloid β Peptide Is a Critical Requirement for the Viability of Central Neurons. J. Neurosci 2003;23:5531–5535.
    doi: 10.1523/JNEUROSCI.23-13-05531.2003pmc: PMC6741264pubmed: 12843253google scholar: lookup
  47. López-Toledano MA, Shelanski ML. Neurogenic Effect of β-Amyloid Peptide in the Development of Neural Stem Cells. J. Neurosci 2004;24:5439–5444.
    doi: 10.1523/JNEUROSCI.0974-04.2004pmc: PMC6729298pubmed: 15190117google scholar: lookup
  48. Li YQ, Tan SS, Wu D, Zhang Q, Wang T, Zheng G. The Role of Intracellular and Extracellular Copper Compartmentalization in Alzheimer’s Disease Pathology and Its Implications for Diagnosis and Therapy. Front. Neurosci 2025;19:1553064.
    doi: 10.3389/fnins.2025.1553064pmc: PMC11936913pubmed: 40143849google scholar: lookup
  49. Carrillo-Mora P, Luna R, Colín-Barenque L. Amyloid Beta: Multiple Mechanisms of Toxicity and Only Some Protective Effects?. Oxid. Med. Cell Longev 2014;2014:795375.
    doi: 10.1155/2014/795375pmc: PMC3941171pubmed: 24683437google scholar: lookup
  50. Koudinov A, Koudinova N. Amyloid Beta Protein Restores Hippocampal Long Term Potentiation: A Central Role for Cholesterol?. Neurobiol. Lipids 2003;1:45–56.
  51. Puzzo D, Privitera L, Leznik E, Fà M, Staniszewski A, Palmeri A, Arancio O. Picomolar Amyloid-β Positively Modulates Synaptic Plasticity and Memory in Hippocampus. J. Neurosci 2008;28:14537–14545.
    doi: 10.1523/JNEUROSCI.2692-08.2008pmc: PMC2673049pubmed: 19118188google scholar: lookup
  52. Zhang Y, Wu KM, Yang L, Dong Q, Yu JT. Tauopathies: New Perspectives and Challenges. Mol. Neurodegener 2022;17:28.
    doi: 10.1186/s13024-022-00533-zpmc: PMC8991707pubmed: 35392986google scholar: lookup
  53. Bloom GS. Amyloid-β and Tau: The Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA Neurol 2014;71:505–508.
    doi: 10.1001/jamaneurol.2013.5847pubmed: 24493463google scholar: lookup
  54. Sperling RA, Mormino EC, Schultz AP, Betensky RA, Papp KV, Amariglio RE, Hanseeuw BJ, Buckley R, Chhatwal J, Hedden T. The Impact of Amyloid-Beta and Tau on Prospective Cognitive Decline in Older Individuals. Ann. Neurol 2019;85:181–193.
    doi: 10.1002/ana.25395pmc: PMC6402593pubmed: 30549303google scholar: lookup
  55. Zetterberg H, Wilson D, Andreasson U, Minthon L, Blennow K, Randall J, Hansson O. Plasma Tau Levels in Alzheimer’s Disease. Alzheimers Res. Ther 2013;5:9.
    doi: 10.1186/alzrt163pmc: PMC3707015pubmed: 23551972google scholar: lookup

Citations

This article has been cited 0 times.
Subscribe to our newsletter
Join 99,001 horse owners like you who receive our email updates on horse health and nutrition.