Senile plaques in aged squirrel monkeys
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Cited by (74)
Aging African green monkeys manifest transcriptional, pathological, and cognitive hallmarks of human Alzheimer's disease
2018, Neurobiology of AgingCitation Excerpt :Hyperphosphorylated tau is even less frequently observed in the brains of aged rhesus and cynomolgus macaque (Hartig et al., 2000; Oikawa et al., 2010), and no evidence of tangles have been published for these species. Similar findings have been reported in squirrel monkeys with regard to Aβ and tau pathologies (Selkoe et al., 1987; Walker et al., 1987, 1990). Thus, within old- and new-world monkeys, the AGM appears rather unique with respect to the high prevalence of dense-core plaques, as well as the occurrence, albeit still rather infrequent, of hyperphosphorylated tau tangle-like structures later in life (Lemere et al., 2004, 2006).
Aged chimpanzees exhibit pathologic hallmarks of Alzheimer's disease
2017, Neurobiology of AgingCitation Excerpt :In addition, aged primates demonstrate cognitive deficits in working memory, learning tasks, long-term retention, and cognitive flexibility similar to elderly humans (Joly et al., 2014; Lacreuse et al., 2014; Nagahara et al., 2010; Picq et al., 2015). Previous studies in aged monkeys and great apes confirmed the presence of diffuse and neuritic amyloid plaques as well as vascular amyloid (Gearing et al., 1994, 1996, 1997; Geula et al., 2002; Heuer et al., 2012; Kimura et al., 2003; Lemere et al., 2004, 2008; Martin et al., 1991; Mufson et al., 1994; Oikawa et al., 2010; Perez et al., 2013, 2016; Poduri et al., 1994; Rosen et al., 2008; Walker et al., 1987). The presence of abnormally phosphorylated tau has been reported in neurons and glia in rhesus monkeys (Macaca mulatta) and squirrel monkeys (Saimiri sciureus) as well as baboons (Papio anubis) (Elfenbein et al., 2007; Hartig et al., 2000; Oikawa et al., 2010; Schultz et al., 2000; Selkoe et al., 1987).
Comparative pathobiology of β-amyloid and the unique susceptibility of humans to Alzheimer's disease
2016, Neurobiology of AgingCitation Excerpt :The paradoxical existence of extensive cerebral Aβ-amyloidosis without overt neurodegeneration and dementia in animal models (and possibly humans) might be reconciled by differences in the post-translational characteristics of Aβ, such as species-specific populations of Aβ isoforms or the formation of structurally and functionally distinct proteopathic “strains” (Fritschi et al., 2014; Hatami et al., 2014; Heilbronner et al., 2013; Levine and Walker, 2010; Lu et al., 2013; Mehta et al., 2013; Meyer-Luehmann et al., 2006; Petkova et al., 2005; Rosen et al., 2010a, 2011; Stohr et al., 2014; Watts et al., 2014). To gain insight into the comparative pathobiology of Aβ in a species proximal to humans, we analyzed the properties of Aβ in the brains of humans with AD and aged squirrel monkeys (Saimiri sciureus), a New World primate that develops senile plaques and CAA with advancing age (Elfenbein et al., 2007; Walker et al., 1987, 1990). We found that the populations of Aβ and its post-translationally variant isoforms are remarkably similar in humans and squirrel monkeys, and that Aβ-rich cortical extracts from aged squirrel monkeys effectively seed the deposition of Aβ in an APP-transgenic mouse model.
Early Alzheimer's disease-type pathology in the frontal cortex of wild mountain gorillas (Gorilla beringei beringei)
2016, Neurobiology of AgingCitation Excerpt :Although neurofibrillary tangles (NFTs) are a major pathological feature in human neurodegenerative conditions (Bouras et al., 1994; Braak and Braak, 1991; Jackson and Lowe, 1996), mainly beta amyloid (Aβ) deposits (neuritic and diffuse plaques), and Aβ angiopathy have been reported in several nonhuman primate species. Most non-human primate studies have been carried out in captive rhesus monkeys (Gearing et al., 1996; Martin et al., 1991; Mufson et al., 1994; Norvin et al., 2015; Poduri et al., 1994), long-tailed macaques (Kimura et al., 2003), Caribbean vervets (Lemere et al., 2004), squirrel monkeys (Walker et al., 1987), and cotton-top tamarins (Lemere et al., 2008), and a few in great apes (Edler et al., 2015; Gearing et al., 1994, 1996, 1997; Kimura et al., 2001; Perez et al., 2013; Rosen et al., 2008). Great apes, which include common chimpanzees, bonobos, gorillas, and orangutans, are of significant interest in aging and AD research because they are the closest living relatives of humans and therefore could provide clues to the evolutionary changes underlying the onset of AD pathology.
Should Alzheimer's disease be equated with human brain ageing?: A maladaptive interaction between brain evolution and senescence
2012, Ageing Research ReviewsCitation Excerpt :Amyloid plaques similar to Alzheimer's type NP have been detected in the cortex of some aged non-human mammalian species (Struble et al., 1985; Wisniewski et al., 1970; Selkoe et al., 1987) however this generally occurs in the absence of NFT formation. It is highly significant that primate relatives such as orangutans (Gearing et al., 1997), rhesus monkeys (Poduri et al., 1994; Uno et al., 1996), squirrel monkeys (Walker et al., 1987) and our closest relative the chimpanzee (Gearing et al., 1994), whilst developing NP with age, do not develop NFT with age. This is despite having similar tau sequence and expression profiles to humans (Holzer et al., 2004; Janke et al., 1999).
Alzheimer-type tau pathology in advanced aged nonhuman primate brains harboring substantial amyloid deposition
2010, Brain ResearchCitation Excerpt :Distinct from Tg mice, both the production of Aβ and expression of tau are likely within physiological ranges in nontransgenic animals; thus, the natural spatiotemporal profiles of Aβ and tau pathologies should be presented in the brains of these animals. To date, it has been reported that a lot of mammalian species exhibit cerebral Aβ-amyloidosis, such as parenchymal Aβ deposition and amyloid angiopathy, and intraneuronal tau accumulation (Bons et al., 2006; Braak et al., 1994; Cummings et al., 1996a,b; Gearing et al., 1994; Geula et al., 2002; Härtig et al., 2000; Lemere et al., 2004, 2008; Podlisny et al., 1991; Roertgen et al., 1996; Schultz et al., 2000a,b; Selkoe et al., 1987; Walker et al., 1987). Among those animals, we paid particular attention to cynomolgus monkey because of the similarity of Aβ pathology as follows.