Kristine Freude

This study identifies BNIP3L/NIX-mediated mitophagy as a critical pathway that limits Alzheimer's disease pathology and preserves neuronal function by maintaining mitochondrial health and reducing proteotoxicity.

This study shows simvastatin reduces PD-related phenotypes in iPSC-derived neurons by inhibiting RhoA, with RhoA activity varying across PD subtypes.

This study uses forebrain organoids to show that schizophrenia involves sex-specific protein-state dysregulation, with changes in post-translational modifications and proteomic pathways rather than transcript levels.

This study uses patient-derived organoids to identify synaptic protein and phospho-regulatory deficits in schizophrenia.

This study uses brain organoids to show that miRNA dysregulation in schizophrenia leads to premature GABAergic maturation and neurodevelopmental defects.

This study develops a centrifugation protocol to isolate growth cones and immature synapses from human organoids, capturing synaptic development stages and enabling models for studying synaptic function and dysfunction.

The paper identifies sex-specific changes in the tRNA epitranscriptome in Alzheimer's disease models and human tissue, and develops a tRNA modification score linked to disease severity.

This study uses a multidisciplinary approach to identify age-dependent expression patterns in porcine experimental wounds to improve objective wound age estimation in forensic cases.

This study compares guided and unguided forebrain organoids using multi-omic analyses, revealing differences in cellular composition, metabolic profiles, and post-translational modifications.

This study identifies NINJ1 as a mediator of plasma membrane rupture in Mtb-infected macrophages, showing it operates independently of canonical cell death pathways and requires the ESX-1 secretion system.

The paper assesses metabolic and oxidative stress in NTG by analyzing skin fibroblasts, finding no significant differences compared to controls.

This study shows that human iPSC-derived pericyte-like cells with the APP Swedish mutation overproduce beta-amyloid and exhibit CAA-like features in vitro.

The paper identifies Golgi fragmentation as an early AD phenotype in neurons using stem cell and mouse models, showing its link to SORL1 variants and glycosylation changes.

The paper shows USP30 inhibition enhances mitophagy and reduces oxidative stress in parkin-deficient neurons, with non-dopaminergic neurons being the main受益者.

This study shows APOE4 disrupts calcium homeostasis in neurons, leading to sustained translation inhibition and impaired NMDAR signaling, while APOE3 causes a transient calcium response with recovery.