Raja Sekhar Nirujogi

The paper uses spatial single-cell proteomics to analyze tangle-bearing neurons in Alzheimer's disease, revealing a continuum of proteomic changes associated with tau pathology.

This study uses mouse models with tau mutations to show two distinct pathogenic mechanisms in tauopathies, with different progression patterns and responses to amyloid.

This study identifies differentially expressed micro-RNAs in LRRK2 G2019S mutation carriers using induced pluripotent stem cell-derived neurons, showing no linear correlation with LRRK2 activity.

This paper reports the crystal structures of TMEM55B and its complex with a RILPL1 peptide, revealing a conserved TBM motif that mediates adaptor recruitment to lysosomes.

The paper identifies splicing dysregulation in Parkinson's disease linked to TDP-43 loss of function and shows its association with genetic mutations and cellular models.

This study creates (GA)400 knock-in mice to model C9orf72 polyGA expression, finding mild motor dysfunction and proteomic changes in the spinal cord.

The paper develops a tagless LysoIP method to isolate lysosomes from clinical samples and human cell lines, revealing glycerophosphodiesters as potential biomarkers for lysosomal storage disorders.

CURTAIN and CURTAIN-PTM are web-based tools for exploring and sharing MS-based proteomics data, enabling non-experts to analyze and visualize results through interactive features and shareable links.

This study shows that the VPS35[D620N] mutation causes lysosomal dysfunction, activates LRRK2, and promotes the lysosomal association of RILPL1 and TMEM55B through phosphorylation of Rab proteins.

The paper generates C9orf72 DPR knock-in mice and identifies an extracellular matrix signature in C9ALS/FTD that is conserved across species and protected by TGF-β1 and COL6A1.

This study shows that C9orf72 mutations disrupt autophagy in microglia, leading to immune dysfunction and increased motor neuron death in ALS/FTD.

This study uses hiPSCs with SNCA mutations to identify early molecular events in synucleinopathy, showing protein aggregation precedes functional impairments in midbrain dopaminergic neurons.

The paper identifies complement and coagulation cascade pathways as significantly altered in two Parkinson's disease mouse models through proteome analysis.

The paper develops and validates a multiplexed mass spectrometry assay to quantify LRRK2-phosphorylated Rab proteins and biomarker sites, showing VPS35[D620N] enhances Rab1 phosphorylation in Parkinson's disease.