Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia
Background Genetic mutations underlying familial Alzheimer's disease (AD) were identified
decades ago, but the field is still in search of transformative therapies for patients. While …
decades ago, but the field is still in search of transformative therapies for patients. While …
Altered metabolic pathways in a transgenic mouse model suggest mechanistic role of amyloid precursor protein overexpression in Alzheimer's disease
Introduction The mechanistic role of amyloid precursor protein (APP) in Alzheimer's disease
(AD) remains unclear. Objectives Here, we aimed to identify alterations in cerebral …
(AD) remains unclear. Objectives Here, we aimed to identify alterations in cerebral …
Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse models
L Sebastian Monasor, SA Müller, AV Colombo… - Elife, 2020 - elifesciences.org
Microglial dysfunction is a key pathological feature of Alzheimer's disease (AD), but little is
known about proteome-wide changes in microglia during the course of AD and their …
known about proteome-wide changes in microglia during the course of AD and their …
Mitochondrial hypermetabolism precedes impaired autophagy and synaptic disorganization in App knock-in Alzheimer mouse models
Accumulation of amyloid β-peptide (Aβ) is a driver of Alzheimer's disease (AD). Amyloid
precursor protein (App) knock-in mouse models recapitulate AD-associated Aβ pathology …
precursor protein (App) knock-in mouse models recapitulate AD-associated Aβ pathology …
Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer's disease
Background Knock-in (KI) mouse models of Alzheimer's disease (AD) that endogenously
overproduce Aβ without non-physiological overexpression of amyloid precursor protein …
overproduce Aβ without non-physiological overexpression of amyloid precursor protein …
APP mouse models for Alzheimer's disease preclinical studies
H Sasaguri, P Nilsson, S Hashimoto, K Nagata… - The EMBO …, 2017 - embopress.org
Animal models of human diseases that accurately recapitulate clinical pathology are
indispensable for understanding molecular mechanisms and advancing preclinical studies …
indispensable for understanding molecular mechanisms and advancing preclinical studies …
Human Alzheimer's disease gene expression signatures and immune profile in APP mouse models: a discrete transcriptomic view of Aβ plaque pathology
Background Alzheimer's disease (AD) is a chronic neurodegenerative disease with
pathological hallmarks including the formation of extracellular aggregates of amyloid-beta …
pathological hallmarks including the formation of extracellular aggregates of amyloid-beta …
Oligomeric amyloid-beta induces MAPK-mediated activation of brain cytosolic and calcium-independent phospholipase A2 in a spatial-specific manner
JP Palavicini, C Wang, L Chen, K Hosang… - Acta neuropathologica …, 2017 - Springer
Alzheimer's disease (AD) is histopathologically characterized by the build-up of fibrillar
amyloid beta (Aβ) in the form of amyloid plaques and the development of intraneuronal …
amyloid beta (Aβ) in the form of amyloid plaques and the development of intraneuronal …
An App knock-in rat model for Alzheimer's disease exhibiting Aβ and tau pathologies, neuronal death and cognitive impairments
A major obstacle in Alzheimer's disease (AD) research is the lack of predictive and
translatable animal models that reflect disease progression and drug efficacy. Transgenic …
translatable animal models that reflect disease progression and drug efficacy. Transgenic …
Generation of App knock-in mice reveals deletion mutations protective against Alzheimer's disease-like pathology
K Nagata, M Takahashi, Y Matsuba… - Nature …, 2018 - nature.com
Although, a number of pathogenic mutations have been found for Alzheimer's disease (AD),
only one protective mutation has been identified so far in humans. Here we identify possible …
only one protective mutation has been identified so far in humans. Here we identify possible …