Genetic factors The degu, a small caviomorph rodent endemic to central Chile, some of which spontaneously develop AD-like neuropathology, including neuroinflammation, amyloid and tau indicators in brain and plasma, all in conjunction with deficits in rodent equivalents of activities of daily living and cognition (Altimiras et al., 2017; Ardiles et al., 2012; Deacon et al., 2015; Du et al., 2015; Inestrosa et al., 2005).
In addition, degu frequently develop type 2 diabetes, insulin resistance, altered lipid metabolism, atherosclerosis and circadian rhythm disturbances (see below). These are all factors that can drive the onset and/or progression of AD. Based on the premise that the causes of non-familial AD are multi- factorial and age related, we will review the suitability of the degu as a non-genetic long-lived model of AD, based on the findings that a proportion of degu spontaneously develop AD-like brain pathology, cognitive dysfunction and systemic comorbid diseases, which distinguish this species from transgenic mouse models of AD.are likely to play a common underlyingrole in the peripheral and central dysfunction associated with AD, although the functional actions of many of the risk genes for AD are not fully known (Lane et al., 2017).
The degu is also used as a model of circadian activity. The body's circadian clock system maintains physiological functions in 24-hour rhythms, including the sleep-wake cycle, and synchronizes them to the light-dark cycle. Disturbances of both sleep and the underlying circadian rhythms have long been associated with many neurological and psychiatric diseases, including AD (Musiek, Xiong & Holtzman, 2015).
