Abstract
Neurons with histopathological changes consistent with granulovacuolar degeneration (GVD) were found in brain sections from aged cynomolgus monkeys (Macaca fascicularis) with clinical and pathological signs of cognitive aging. To our knowledge, this is the first reported description of GVD in non-human primates. GVD-like lesions were found also in age-matched cognitively healthy subjects, albeit in lower numbers, suggesting that they may relate to aging and the increase may have tendency to increase with the memory deficits. The increased incidence of GVD-like lesions in memory-impaired subjects with pahological backgrounds of senile plaques (SPs) and tauopathy is, however, an interesting observation of relevance to the characterization of pathologies in the spontaneous cynomolgus monkey model of human Alzheimer’s type of brain pathology.
Highlights
Non-human primates (NHPs) with spontaneous pathological lesions similar to those found in human Alzheimer’s disease (AD) are promising models for neurodegenerative studies (Verdier et al, 2015; Perez et al, 2016; Edler et al, 2017)
Based on human’s granulovacuolar degeneration (GVD) criteria and by comparing our histopathology samples with images of GVD in AD patients (Yamazaki et al, 2011), the lesion indicative of GVD were found in all aged subjects (Figure 1)
The lesions indicative of GVD in the brains of aged cynomolgus monkeys appear similar to human GVD with respect to size, shape, and morphology of the granules and vacuoles (Funk et al, 2011; Yamazaki et al, 2011)
Summary
Non-human primates (NHPs) with spontaneous pathological lesions similar to those found in human Alzheimer’s disease (AD) are promising models for neurodegenerative studies (Verdier et al, 2015; Perez et al, 2016; Edler et al, 2017). These include delayed response tasks (DRTs), where delays of various durations are imposed between the presentation of a stimulus and a desired response (Rodriguez and Paule, 2009; Nagahara et al, 2010) These types of memory tests are appropriate for assessing cognitive aging in NHPs. Some of the earliest cerebral lesions in the etiology of AD are typically located in the hippocampus (Deiana et al, 2010), making spatial memory tests of particular interest when designing comparative NHP studies to explore cross-species similarities in age-related memory impairments. Regional specificity of hippocampal circuit-patterns suggested that a decline in the fidelity of input to the hippocampus from the entorhinal cortex plays a critical role in spatial learning (Smith et al, 2000)
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