Stefan F. Lichtenthaler

IgLON5 autoimmune antibodies activate Tau via neuronal hyperactivity

This study shows that IgLON5 autoantibodies cause neuronal hyperactivity and Tau pathology by clustering cell surface proteins, linking them to neurodegeneration.

VMAT2 dysfunction impairs vesicular dopamine uptake, driving its oxidation and α-synuclein pathology in DJ-1-linked Parkinson's disease neurons

This study shows that DJ-1 deficiency impairs VMAT2 function and vesicle dynamics, leading to dopamine oxidation and α-synuclein pathology in Parkinson's disease neurons.

TREM2 expression level is critical for microglial state, metabolic capacity and efficacy of TREM2 agonism

This study investigates how TREM2 expression levels affect microglial function, metabolism, and response to TREM2 agonists in a mouse model of Alzheimer's disease.

A reproducible human brain tissue model to study physiological and disease-associated microglia phenotypes

This paper develops a 3D cortical brain tissue model with mature microglia that recapitulates Alzheimer's disease hallmarks and enables study of microglia phenotypes.

BACE1 regulates sleep-wake cycle through both enzymatic and non-enzymatic actions.

This study investigates BACE1's role in sleep-wake cycles through enzymatic and non-enzymatic actions using mouse models, finding altered sleep patterns and EEG characteristics in mutants.

Loss of the Parkinson's disease-associated protein DJ-1 impacts dopamine metabolism in astrocytes

This study shows that DJ-1 mutations impair astrocytic dopamine metabolism, leading to disrupted detoxification and potential contribution to Parkinson's disease pathogenesis.

Neuronal compartmentalization results in impoverished axonal mitochondria

The paper uses proteomics to compare mitochondrial diversity in somatodendritic and axonal compartments across neurons, finding axonal mitochondria are 'impoverished' with reduced mtDNA expression and impaired oxidative phosphorylation.

Multiomic profiling reveals aberrant immunomodulatory signature in β-propeller protein-associated neurodegeneration patient iPSC-derived microglia

The paper uses iPSC-derived microglia from BPAN patients to identify immune-related alterations and immunomodulatory signaling changes, revealing a shift to a reactive, disease-associated state.

Anti-Aβ immunotherapy-mediated amyloid clearance attenuates microglial activation without inducing exhaustion at residual plaques

This study shows that long-term anti-Aβ treatment reduces amyloid plaques and microglial activation but leaves residual plaques with persistent immune activity.

The late onset Alzheimer's disease risk factor iRhom2/RHBDF2 is a modifier of microglial TREM2 proteolysis

This study identifies iRhom2 as a modifier of ADAM17-mediated TREM2 proteolysis in microglia, linking it to Alzheimer's disease risk.

Loss of CLN3 in microglia leads to impaired lipid metabolism and myelin turnover

This study shows that loss of CLN3 in microglia causes lipid metabolism defects and impaired myelin turnover, leading to early neuroinflammation in a mouse model of CLN3 disease.

Protective variant in PLCgamma2 mitigates Alzheimer's disease associated pathology via enhancing beneficial microglia functions

This study shows that the PLCgamma2-P522R variant reduces beta-amyloid pathology and enhances microglial function in AD models, suggesting an anti-ageing mechanism.

Cleavage site-directed antibodies reveal the prion protein in humans is shed by ADAM10 at Y226 and associates with misfolded protein deposits in neurodegenerative diseases

This study identifies ADAM10-mediated shedding of human PrP at Y226 and shows sPrP associates with misfolded protein aggregates in neurodegenerative diseases.

An improved method for sampling and quantitative protein analytics of cerebrospinal fluid of single mice

The paper introduces an improved method for collecting and analyzing murine cerebrospinal fluid, enabling quantitative proteomics and revealing proteome changes in Alzheimer's disease models.

Deciphering sources of PET signals in the tumor microenvironment of glioblastoma at cellular resolution

The paper identifies cellular sources of PET signals in glioblastoma by combining radiotracer uptake with 3D-histology and proteomics, showing tumor cells mainly contribute to TSPO enrichment while TAMs have specific PET targets.

A MICROGLIAL ACTIVITY STATE BIOMARKER PANEL DIFFERENTIATES FTD-GRANULIN AND AD FROM CONTROL CASES

The paper identifies a microglial activity biomarker panel that differentiates FTD-GRN and AD cases from controls using proteomic analysis in mouse models and human samples.

Endogenous retroviruses promote prion-like spreading of proteopathic seeds

This study shows endogenous retroviruses enhance prion-like spreading of protein aggregates between cells, suggesting antiviral drugs could inhibit disease progression.

Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions

The paper shows that TCA cycle dysfunction contributes to axonal energy deficiency in neuroinflammatory lesions and that restoring TCA enzymes can alleviate this deficit.

LncRNA RUS shapes the gene expression program towards neurogenesis

This study identifies RUS, a lncRNA that promotes neurogenesis by regulating gene expression and epigenetic interactions during neuronal differentiation.

Highly efficient intercellular spreading of protein misfolding mediated by viral ligand - receptor interactions

The paper shows viral ligand-receptor interactions enhance the spread of protein misfolding via extracellular vesicles and direct cell contact.

Amyloid-beta mediates homeostatic synaptic plasticity

This study shows that amyloid-beta, not APP or its secreted fragments, mediates homeostatic synaptic plasticity in the absence of APP.

Loss of NPC1 enhances phagocytic uptake and impairs lipid trafficking in microglia

This study shows that loss of NPC1 in microglia increases phagocytic uptake and impairs lipid trafficking, leading to myelin accumulation and potential therapeutic implications.

Quantitative secretome analysis establishes the cell type-resolved mouse brain secretome

The paper develops a method to analyze the secretome of mouse brain cells and identifies cell type-specific secreted proteins, revealing proteolytic cleavage of membrane proteins.

Fibrillar Aβ triggers microglial proteome alterations and dysfunction in Alzheimer mouse models

This study identifies proteomic changes in microglia during Alzheimer's disease progression in mouse models, showing fibrillar Aβ drives microglial dysfunction.

CNTNAP2 ectodomain, detected in neuronal and CSF sheddomes, modulates Ca2+ dynamics and network synchrony