Tau, synapse loss and gliosis progress in an Alzheimer's mouse model after amyloid-β immunotherapy.

ABSTRACT: Preclinical studies assessing drugs for Alzheimer's disease (AD) are conducted in animal models that usually display only one neuropathological feature of AD, whereas patients present with a complex combination of comorbidities and neuropathologies. Importantly, it is well established that amyloid-β (Aβ) plaque and tau tangle accumulation interact in a phase-dependent manner, making it difficult to predict how targeting one might influence the other, as well as downstream degeneration. We developed a transgenic mouse model, APP/PS1xTau22, with progressive cortical Aβ deposition and hippocampal tau neurofibrillary inclusions, to investigate how both neuropathologies act jointly to bring about neural degeneration, synapse loss and glial phenotypes. We then assessed whether applying murine ch

SUBMITTER: Welikovitch LA 

PROVIDER: S-EPMC11967717 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature