Characterization of Cellular Pathological Signatures in a Mouse Model of Alzheimer's Disease
Although Alzheimer’s Disease (AD) is an extremely common form of dementia, treatment options are limited and many pathological signatures of the disease are not fully understood. The goal of this research was to review the presence of amyloid-β plaques in a mouse with AD and to see if these amyloid-β plaques lead to neuronal loss in important brain structures related to memory and cognition. Two strains of mice, hAPP-J20 and its age matched wild-type control, were used to collect histological data in order to compare the AD mouse to the control mouse, respectively. Due to the overexpression of mutant human amyloid precursor protein (hAPP), transgenic J20 mice act as an adequate model when studying the features and effects of AD (Gulbranson et al., 2021). Staining with multiple antibodies was done in order to detect the presence of multiple pathological signatures associated with AD. Bright-field (BF) and fluorescent microscopes were used to obtain qualitative data of brain slices, followed by image analysis with particle counting via ImageJ computer software. A significant presence of amyloid-β plaques were found in the hippocampal formation and neocortex in the hAPP-J20 mouse. However, there was no significant neuronal loss discovered in these areas between the wild-type control (wild-type) and AD (hAPP-J20) mice, despite extremely old age of the hAPP-J20 animal (nearly 77 weeks). This finding challenges the dogma that amyloid-β alone is responsible for neuronal death and demonstrates the importance of continued research relating to AD and its pathological signatures in order to find an effective treatment.
PublisherUniversity of Wyoming. Libraries
- Zoology and Physiology - ZOO