Abstract

β-amyloid deposition and tau phosphorylation are present in human cases of Alzheimer’s disease, clinically producing a decline in cognitive function. These changes have previously been identified in domestic felids, associated with clinical cognitive decline in some animals.^1,2 This present study was performed to determine if similar β-amyloid and tau lesions can occur in non-domestic felid species.

Postmortem brain specimens were collected from 15 non-domestic felids with specific focus on Asiatic lions (Panthera leo persica, n=7) that ranged in age from 3 days to 20 years (mean 6 years). Two animals—Pallas cat, Felis manul, 5 years, and Asiatic lion, 7 years—had neurologic clinical signs ante-mortem that were associated with infectious encephalitis. Mild degenerative changes (neuronal lipofuscinosis and vacuolar change with gliosis) were detected in two other animals—Persian leopard, Panthera pardus saxicolor, 20 years, and cheetah, Acinonyx jubatus, 8 years.

From these specimens, multiple brain sections (n=66) were assessed by application of monoclonal mouse anti-human β-amyloid (Clone 6F/3D, Dako, Glostrup, Denmark) and monoclonal mouse anti-human PHF-tau (Clone AT8, Innogenetics, Autogen Bioclear, Nottingham, UK) primary antibodies. Positive and negative controls were included in each batch processed.

β-amyloid deposition was detected in animals across the age range; however, as with previous studies in domestic cats, plaques were more diffuse than those seen typically in human Alzheimer’s disease. Staining for tau phosphorylation was less definitive and only a few sections presented small positive foci. No association was seen between age and either β-amyloid or tau detection.

Literature Cited

1.  Gunn-Moore DA, McVee J, Bradshaw JM, Pearson GR, Head E, Gunn-Moore FJ. Ageing changes in cat brains demonstrated by β-amyloid and AT8-immunoreactive phosphorylated tau deposits. J Feline Med Surg. 2006;8:234–242.

2.  Head E, Moffat K, Das P, Sarsoza F, Poon WW, Landsberg G, et al. β-Amyloid deposition and tau phosphorylation in clinically characterized aged cats. Neurobiol Aging. 2005;26:749–763.