Juan Carlos Troncoso

This study shows that loss of TDP-43 function leads to increased cryptic circular RNAs in neurodegenerative diseases.

This study shows that TDP-43 dysfunction accelerates tauopathy, which primes co-filament assembly and dysfunction of TDP-43, exacerbating neuron loss in AD-LATE.

This study identifies a mechanism by which reactive astrocytes drive neurodegeneration in synucleinopathies through extracellular acidification and neuronal ASIC1a activation.

This study identifies a molecular pathway involving TRIM32, UBQLN2, and p62 that forms condensates promoting TDP-43 aggregation in neurodegenerative diseases.

The paper identifies sense and antisense RAN proteins as a common mechanism in CAG-SCAs, showing their accumulation and toxicity in brain regions and demonstrating metformin's ability to reduce RAN protein levels.

This study shows that PARIS in neurons activates STAT3, leading to tau pathology and glial activation in Alzheimer's disease, and identifies the PARIS-STAT3 pathway as a therapeutic target.

This study uses bulk RNA-seq to analyze transcriptional changes in the middle temporal gyrus across Alzheimer's disease and aging, identifying distinct gene expression patterns and pathways associated with each condition.

The paper identifies molecular programs coordinated with NPTX2 that distinguish cognitive resilience in AD pathology from non-pathological cognition and AD.

This study shows that LINE1 RNA dysregulation impairs chromatin accessibility in ALS/FTD, leading to transcriptional changes and neuronal dysfunction.

The paper screens a kinase inhibitor library in HD iPSC-derived neurons to identify PKC alpha and beta1 inhibition as neuroprotective against mutant huntingtin toxicity.

This study identifies UNC-45A as an ATP-independent microtubule severing protein that inhibits repair of defects, leading to microtubule loss and neurite dystrophy in Alzheimer's disease.

The paper identifies distinct protein interactors of Tau-seed in AD across species and brain regions, highlighting functional differences in Tau propagation.

This study identifies DCPS as a genetic modifier of TDP-43 loss-of-function neurotoxicity by restoring P-body integrity and RNA turnover in human neurons.

This study uses HiF-snRNA-seq to analyze the cingulate cortex in Parkinson's disease and Parkinson's disease dementia, identifying cell-type-specific gene expression changes and disease-stage-related pathways.

This study identifies differentially expressed genes and pathways in Alzheimer's disease brain tissue from African American donors, highlighting potential targets for treatment.

This study shows that elevated nuclear TDP-43 causes species-specific exon skipping, which differs from exon skipping seen in TDP-43 loss-of-function, highlighting the need for careful interpretation of TDP-43 overexpression models.

This study uses MD-MRI to map cortical astrogliosis and distinguishes cognitive resilience from dementia in Alzheimer's disease despite significant neuropathology.

This paper identifies NOD2/RIPK2 signaling as a key driver of neuroinflammation in Parkinson's disease, showing that pathological α-synuclein activates this pathway in microglia, leading to neurodegeneration and that targeting NOD2 or RIPK2 protects dopamine neurons.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

This study examines postmortem brains of AsymAD cases to identify mechanisms of cognitive resilience, finding enhanced microglial dynamics and reduced tau seeding in the amyloid plaque microenvironment.

The paper characterizes extracellular vesicles (EVs) from different brain regions, revealing regional differences in EV yield, surface markers, and RNA content.

This paper performs a large meta-analysis of GWAS in dementia with Lewy bodies, identifying sex-specific genetic risk signals and highlighting the need for larger cohorts.

The paper identifies differentially enriched proteins in brain-derived extracellular vesicles from Parkinson's disease, PSP, and control samples using surface phenotyping and proteomics.

This study identifies that pathological α-synuclein destabilizes the TSC1-TSC2 complex, activates mTORC1, and enhances protein translation, contributing to neurodegeneration in Parkinson's disease.

This study identifies JADE1 as a novel genetic factor in tauopathy through genome-wide association and functional validation in human and Drosophila models.

The paper identifies stage-specific microglia subtypes in Alzheimer's disease using single-cell RNA-sequencing, showing both amyloid-beta and tau pathologies are required for their induction.

This paper identifies five new genetic risk loci for Lewy body dementia through whole-genome sequencing and shows shared risk profiles with Alzheimer’s and Parkinson’s disease.

This study evaluates the impact of species and processing parameters on the recovery and content of brain tissue-derived extracellular vesicles using modified protocols.

The paper identifies de-novo SPTLC1 mutations in juvenile ALS patients and suggests serine supplementation may alleviate symptoms.

This study identifies 114 proteins and 5 modules linked to cerebral atherosclerosis in the brain, with 23 proteins and 2 modules also associated with Alzheimer’s dementia, highlighting shared mechanisms involving synaptic signaling and myelination.