Topic: AppNL-G-F mice

Alzheimer's disease (AD) is a progressive neurological disorder characterized by amyloid accumulation and behavioral changes across preclinical and clinical stages. Although AD is currently incurable, emerging machine-learning (ML) approaches are facilitating novel insights into disease etiology and treatment mechanisms. Our study utilized and built upon two open-source ML platforms, DeepLabCut (Mathis et al. 2018) and Variational Animal Motion Encoding (VAME) (Luxem et al. 2022), to track and analyze naturalistic behavior in App knock-in (KI) and 5xFAD transgenic mouse models of AD. New human

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterised by the gradual deterioration of executive functions and memory. Its primary pathophysiological hallmarks are amyloid plaques and neurofibrillary tangles. Promising humanised knock-in AD mouse models have been developed that exhibit Aβ pathology, neuroinflammation, synaptic dysfunction, and behavioural impairment. A rigorous battery of behavioural tests and analyses was utilised to further our knowledge of Alzheimer's disease.Our study comprised young (6-months), middle-aged (12-months), and old (22-months) AppNL-G-F

Alzheimer's disease (AD) exhibits sex-specific prevalence rates, yet the molecular mechanisms underlying these differences remain elusive. Neuroinflammation, specifically the microglia response, is thought to have a prominent role in AD pathogenesis. This study seeks to understand how sex chromosomes influence human microglia response to amyloid accumulation and how this may contribute to sexual dimorphisms in AD pathology. Inducible pluripotent stem cells (iPSCs) were generated from a donor with Klinefelter’s syndrome (XXY) and modified to express one or 2 sex chromosomes (XX, XY, XO). Microg

Identification of Alzheimer's disease (AD) risk loci highlighted the role of microglia in the pathogenies of AD. Nevertheless, whether microglia are beneficial or detrimental in AD is still debated. Several studies tested the contribution of microglia to amyloid pathology by microglia depletion, resulting in seemingly contradictory results. Here, we aimed to unify these conflicting findings by systematically testing microglia depletion at various stages of disease progression in mice.Depletion of microglia by PLX3397 treatment before the onset of amyloid plaques in AppNL-G-F mice resulted in a