Amyloid beta 1–42-induced animal model of dementia

Abstract Nowadays, Alzheimer's disease (AD) presents a high prevalence. One of AD’s hallmarks is the presence of amyloid plaques in the cerebral parenchyma, which are formed by amyloid-beta (Aβ) peptide. However, the pathogeneses of this neurodegenerative disease are still poorly understand. Many transgenic animal models of AD have been proposed and are being used. Nonetheless, genetic animal models represent only the familial AD (i.e., a very small portion of AD cases). Over the years, other approaches have been developed. For instance, Aβ 1–42 aggregated oligomer brain administration (via intracerebroventricular and intrahippocampal injection) has seen good interest since a focus on specific components of AD pathology. Intrahippocampal and intracerebroventricular peptide administration in rodents is useful for studying the acute mechanisms involved in Aβ neurotoxicity—e.g., neuroinflammation. We review evidence about the animal model of dementia, such as AD induced by Aβ 1–42 injection, pointing out its strengths and weaknesses.