Importantly, AβOs lead to similar dendritic spine loss to that observed in normal aging in monkeys, but so far without detection of amyloid plaques or tau pathology. AβOs infused into the monkey brain target a specific population of spines in the prefrontal cortex, induce neuroinflammation, and increase AD biomarkers in the cerebrospinal fluid to similar levels observed in patients with AD. We describe here the development of a rhesus monkey model of AD using soluble oligomers of the amyloid beta (Aβ) peptide (AβOs). Aging is the leading risk factor for developing AD and understanding neurobiological changes that affect synaptic integrity with aging will help clarify why the aged brain is vulnerable to AD. There is a translational gap in AD research, with promising drugs based on work in rodent models failing in clinical trials. Despite significant investment in research over the last decades, there is no effective treatment to prevent or delay AD progression. As the average age of the population continues to rise, the number of individuals affected with age-related cognitive decline and Alzheimer’s disease (AD) has increased and is projected to cost more than $290 billion in the United States in 2019.
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