Mathias Jucker

This study evaluates how biomarker variability affects individualized amyloid time estimation in Alzheimer's disease, finding that inter-individual variability is the main source of error.

The paper identifies the Pgb1 locus as controlling glycogen aggregation in aged hippocampal astrocytes without affecting cognitive function.

This paper compares Aβ fibril structures in three mouse models of Alzheimer's disease, finding age-dependent differences in plaque morphology and polymorph maturation.

This study shows hub disruption in ADAD follows a targeted attack pattern, detectable pre-clinically and linked to amyloid beta changes and neuronal activity.

The paper quantifies Aβ production from PSEN1 variants and links it to clinical and biomarker progression in ADAD, showing strong associations with disease trajectories.

This study shows LAG3 is not expressed in human and mouse neurons and does not worsen α-synuclein pathology in vitro or in vivo.

This study shows that SERF2 deletion changes amyloid fibril structure in Alzheimer's mouse models, suggesting SERF's role in modifying amyloid aggregation.

This study shows that PITRM1 deficiency in human cerebral organoids leads to Alzheimer's-like pathology, including protein aggregates and tau pathology, while 2D cultures do not show these features.

The paper develops a model to predict brain aging from resting state fMRI and finds accelerated brain aging in preclinical Alzheimer's disease, independent of amyloid-beta pathology.

This paper models prion-like spreading of Alzheimer's disease by integrating misfolding kinetics with a brain connectivity network derived from the Human Connectome Project, showing accurate predictions of neuropathology and simulating therapeutic strategies.