Histochemical characteristics and distribution of lipofuscin and polyglucosan bodies in the brain of dogs more than 10 years old

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Sladjan Nesic
Ivana Vučićević
Darko Marinković
Vladimir Kukolj
Trpe Ristoski
Sonja Nikolić
Sanja Aleksić-Kovačević


The ageing process is accompanied by numerous changes in the brain of dogs, such as accumulation of amyloid, fibrosis of blood vessel walls and meninges, accumulation of lipofuscin, and the presence of polyglucosan bodies (PGBs), satellitosis and neuronophagia. In this study, the presence of lipofuscin and PGBs in various parts of the brain in dogs of different sexes and ages was examined. For this purpose, brain samples were stained using haematoxylin eosin, modified Ziehl Neelsen and Periodic acid Schiff (PAS) methods. Lipofuscin was visualised by Ziehl Neelsen and PAS methods of specific staining on the same brain tissue segments. Lipofuscin had accumulated in 93% of old (more than 10 years old) dog brains, mostly in neurons of the medulla oblongata. The percentage of age-related lipofuscin pigment in other examined brain tissue segments was lower than in the medulla oblongata. There was a small difference in the percentage of lipofuscin-positive individuals between the two staining methods. The presence of PGBs was established by the PAS method for the vast majority (about 93%) of the old dogs (more than 10 years old), while PGBs were not detected in the group of young dogs (up to 5 years old). However, PGBs occurred in all examined segments of the dog’s brain tissues (for each of the tissue types, from 90% to 93% of dogs were positive for PGBs). The results obtained the oldest dogs (15 years old) harboured PGBs both extracellularly and intracellularly, while in other dogs, only extracellular PGBs were seen. Lipofuscin was accumulated mostly in large neurons of olivary nuclei of the medulla oblongata. PGBs were confirmed in all examined segments of the brain tissue of dogs more than 10 years old. This is one of the numerous indications that old dogs could be a very good animal model for studying the normal ageing process or neurodegenerative diseases.


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Nesic, S., Vučićević, I., Marinković, D., Kukolj, V., Aničić, M., Ristoski, T., Nikolić, S., & Aleksić-Kovačević, S. (2021). Histochemical characteristics and distribution of lipofuscin and polyglucosan bodies in the brain of dogs more than 10 years old. Veterinarski Glasnik, 75(1), 57-68. https://doi.org/10.2298/VETGL201002001N
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Benavides S.H., Monserrat A.J., Fariña S., Porta E.A. 2002. Sequential histochemical studies of neuronal lipofuscin in human cerebral cortex from the first to the ninth decade of life. Archives of Gerontology and Geriatrics, 34(3):219-231. http://dx.doi.org/10.1016/s0167-4943(01)00223-0

Borras D., Ferrer I., Pumarola M. 1999. Age-related changes in the brain of the dog. Veterinary Pathology, 36:202-211. http://dx.doi.org/10.1354/vp.36-3-202

Brunk U.T., Terman A. 2002a. Lipofuscin: mechanisms of age-related accumulation and influence on cell function. Free Radical Biology and Medicine, 33(5):611-619. http://dx.doi.org/10.1016/s0891-5849(02)00959-0

Brunk U.T., Terman A. 2002b. The mitochondrial-lysosomal axis theory of aging: accumulation of damaged mitochondria as a result of imperfect autophagocytosis. European Journal of Biochemistry, 269(8):1996-2002. http://dx.doi.org/10.1046/j.1432-1033.2002.02869.x

Cavanagh J.B. 1999. Corpora-amylacea and the family of polyglucosan diseases. Brain Research. Brain Research Reviews, 29(2-3):265-295. http://dx.doi.org/10.1016/s0165-0173(99)00003-x

Double L.K., Dedov N.V., Fedorov H., Kettle E., Halliday M.G., Garner B. Brunk T.U. 2008. The comparative biology of neuromelanin and lipofuscin in the human brain. Cellular and Molecular Life Sciences, 65(11):1669-1682. http://dx.doi.org/10.1007/s00018-008-7581-9

Gilissen E.P., Leroy K., Yilmaz Z., Kövari E., Bouras C., Boom A., Poncelet L., Erwin J.M., Sherwood C.C., Hof P.R., Brion J.P. 2016. A neuronal aging pattern unique to humans and common chimpanzees. Brain Structure and Function, 221(1):647-664. http://dx.doi.org/10.1007/s00429-014-0931-5

Gray D.A., Woulfe J. 2005. Lipofuscin and aging: a matter of toxic waste. Science of Aging Knowledge Environment, 2005(5):re1. http://dx.doi.org/10.1126/sageke.2005.5.re1

Gredal H., Berendt M., Leifsson P.S. 2003. Progressive myoclonus epilepsy in a beagle. Journal of Small Animal Practice, 44(11):511-514. http://dx.doi.org/10.1111/j.1748-5827.2003.tb00113.x

Jung T., Bader N., Grune T. 2007. Lipofuscin – formation distribution and metabolic consequences. Annals of the New York Academy of Sciences, 1119:97-111. http://dx.doi.org/10.1196/annals.1404.008

Jung T., Höhn A., Grune T. 2010. Lipofuscin: detection and quantification by microscopic techniques, Methods in Molecular Biology, 594:173-193. http://dx.doi.org/10.1007/978-1-60761-411-1_13

Kurz T., Eaton J.W., Brunk U.T. 2010. Redox activity within the lysosomal compartment: implications for aging and apoptosis. Antioxidants and Redox Signaling. 13(4):511-523. http://dx.doi.org/10.1089/ars.2009.3005

Kurz T., Terman A., Brunk U.T. 2007. Autophagy, ageing and apoptosis: the role of oxidative stress and lysosomal iron. Archives of Biochemistry and Biophysics. 462(2):220-230. http://dx.doi.org/10.1016/j.abb.2007.01.013

Lohi H., Ianzano L., Zhao X.C., Chan E.M., Turnbull J., Scherer S.W., Ackerley C.A., Minassian B.A. 2005. Novel glycogen synthase kinase 3 and ubiquitination pathways in progressive myoclonus epilepsy. Human Molecular Genetics, 14:2727-2736. http://dx.doi.org/10.1093/hmg/ddi306

Márquez M., Pérez L., Serafín A., Teijeira S., Navarro C., Pumarola M. 2010. Characterisation of Lafora-like bodies and other polyglucosan bodies in two aged dogs with neurological disease. Veterinary Journal, 183(2):222-225. http://dx.doi.org/10.1016/j.tvjl.2008.10.002

Nešić S., Kukolj V., Marinković D., Vučićević I., Jovanović M. 2017. Histological and immunohistochemical characteristics of cerebral amyloid angiopathy in elderly dogs. Veterinary Quarterly, 37(1):1-7. http://dx.doi.org/10.1080/01652176.2016.1235301

Papaioannou N. 2014. Principles of age-related changes in the canine and feline brain. Acta Veterinaria-Beograd, 64(1):1-9. http://dx.doi.org/10.2478/acve-2014-0001

Porta E.A. 2002. Pigments in aging: an overview. Annals of the New York Academy of Sciences, 959:57-65. http://dx.doi.org/10.1111/j.1749-6632.2002.tb02083.x

Rofina J., Van Andel I., Van Ederen A.M., Papaioannou N., Yamaguchi H., Gruys E. 2003. Canine counterpart of senile dementia of the Alzheimer type: amyloid plaques near capillaries but lack of spatial relationship with activated microglia and macrophages. Amyloid, 10:86-96. http://dx.doi.org/10.3109/13506120309041730

Terman A., Gustafsson B., Brunk U.T. 2007. Autophagy, organelles and ageing. Journal of Pathology, 211(2):134-143. http://dx.doi.org/10.1002/path.2094

Torp R., Head E., Cotman C.W. 2000. Ultrastructural analyses of β-amyloid in the aged dog brain: neuronal β-amyloid is localized to the plasma membrane. Progress in Neuro-psychopharmacology and Biological Psychiatry, 24(5):801-10. http://dx.doi.org/10.1016/s0278-5846(00)00107-x

Youssef S.A., Capucchio M.T., Rofina J.E., Chambers J.K., Uchida K., Nakayama H., Head E. 2016. Pathology of the aging brain in domestic and laboratory animals, and animal models of human neurodegenerative diseases, Veterinary Pathology: 53(2)327-348, DOI: 10.1177/0300985815623997.

Bancroft J.D., Cook H.C. 1984. Manual of Histological Techniques. Churchill Livingstone, New York, USA.

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