Beta Amyloid Deposition and Neurofibrillary Tangles Spontaneously Occur in the Brains of Captive Cheetahs (Acinonyx jubatus)

Abstract

Alzheimer disease is a dementing disorder characterized pathologically by Ab deposition, neurofibrillary tangles, and neuronal loss. Although aged animals of many species spontaneously develop Ab deposits, only 2 species (chimpanzee and wolverine) have been reported to develop Ab deposits and neurofibrillary tangles in the same individual. Here, the authors demonstrate the spontaneous occurrence of Ab deposits and neurofibrillary tangles in captive cheetahs (Acinonyx jubatus). Among 22 cheetahs examined in this study, Ab deposits were observed in 13. Immunostaining (AT8) revealed abnormal intracellular tau immunoreactivity in 10 of the cheetahs with Ab deposits, and they were mainly distributed in the parahippocampal cortex and CA1 in a fashion similar to that in human patients with Alzheimer disease. Ultrastructurally, bundles of straight filaments filled the neuronal somata and axons, consistent with tangles. Interestingly, 2 of the cheetahs with the most severe abnormal tau immunoreactivity showed clinical cognitive dysfunction. The authors conclude that cheetahs spontaneously develop age-related neurodegenerative disease with pathologic changes similar to Alzheimer disease.

Tau pathology in aged cynomolgus monkeys is progressive supranuclear palsy/corticobasal degeneration- but not Alzheimer disease-like -Ultrastructural mapping of tau by EDX-

“…Preferential limbic-hippocampal accumulation of tau-positive neurons, similar to human AD pathology, has been described in aged baboons [29], captive cheetahs ( Acinonyx jubatus ) [7], wild Tsushima leopard cats [30], and domestic cats [31]. Moreover, aged domestic cats’ brains exhibit both 3R and 4R tau immunoreactivity in sarkosyl-insoluble brain fractions [31], again consistent with characteristics of AD.…”

“…However, subsequent improvements in rearing prolonged primate life span such that tau-positive lesions could also be observed [5, 6]. It is now known that primates exhibit concomitant Aβ and tau deposits, and this dual pathology has been proposed to occur through AD-like pathogenesis [7]. …”

Pathology of the Aging Brain in Domestic and Laboratory Animals, and Animal Models of Human Neurodegenerative Diseases

“…6). 28,166 In these animals, abundant NFT were found together with Ab deposition and neuronal loss. As is the case in humans, the NFT found in cats were composed of hyperphosphorylated tau.…”

A Mechanism Study of NMDAR1 in A Rat Alzheimer Disease (AD) Model

“…The main pathological features of AD include neuronal loss, amyloid-β deposition, and neurofibrillary tangles in nerve cells. Patients develop memory and cognitive impairment in early stages, and suffer from severe intelligent recession in advanced stages [3]. The pathogenesis of AD is not yet fully elucidated and thus relevant researches have significant clinical importance.…”