William W. Seeley

The paper identifies potential diagnostic biomarkers for frontotemporal lobar degeneration subtypes using cerebrospinal fluid proteomics.

The paper determines cryo-EM structures of low-twist α-synuclein filaments from Lewy bodies and shows they share a structural core with high-twist forms.

The paper identifies PQLC2 as a lysosomal pH regulator that affects tau homeostasis through a CRISPRi screen in iPSC-derived neurons.

This study shows that tau regulates mitochondrial reverse electron transport, leading to ROS production and neurodegeneration, and identifies potential therapeutic targets.

This study shows that transplanting wild-type human iPSC-derived microglia into progranulin-deficient mice reduces neuropathology, circuit dysfunction, and behavioral issues in a FTD model.

The paper identifies molecular subtypes of neurons in the frontoinsular cortex and links specific gene expression patterns to neuronal vulnerability in FTD.

This study shows TAF15 forms amyloid fibrils and propagates prion-like between cells, identifying specific motifs that drive its aggregation in vitro and in cells.

The paper identifies shared lipid and proteomic alterations in frontotemporal lobar degeneration and Alzheimer's disease, with greater changes in FTLD frontal cortex.

This paper identifies a posterior predominant amyloid PET binding pattern in multiple cohorts, showing its clinical and biological relevance and suggesting the need for more nuanced analysis methods.

This study identifies TDP-43-dependent cryptic splicing events in synaptic and membrane excitability genes and shows they drive neuronal dysfunction in ALS and FTD.

The paper identifies glial cell-specific regulatory elements and genetic risk modifiers in tau-related dementias using single-nucleus epigenomic profiling.

This study identifies distinct tau filament structures in FTLD-tau caused by the MAPT S305I mutation, revealing a unique 4-layer architecture and potential RNA-like polyanion binding.

This study identifies functional network changes in neurodegenerative diseases using MRI data, linking brain atrophy to specific connectivity patterns and cognitive deficits.

This study shows that β-amyloid induces microglial GPC4 and APOE, which increases neuronal tau pathology and toxicity.

This study uses snRNA-seq and spatial transcriptomics to show PitNETs exhibit transcriptional continuity and originate from different developmental pathways, influenced by stromal interactions.

This study identifies plasma proteomic signatures associated with repetitive head impact exposure and CTE, linking them to immune, mitochondrial, and metabolic pathways and cognitive decline.

This study shows that ADGRG1 in microglia helps protect against Alzheimer's disease by improving amyloid clearance and reducing pathology.

The paper examines molecular and pathological changes in the suprachiasmatic nucleus across Alzheimer's disease stages, finding SCN-specific tau pathology and immune dysregulation.

This study examines the differential degeneration of wake- and sleep-modulating neurons in Alzheimer's disease, finding significant loss of orexinergic neurons and relative preservation of MCHergic neurons.

This study identifies and characterizes lysosomal, glial, and neurodegenerative biomarkers in cerebrospinal fluid and plasma from FTD patients, revealing their correlation with disease severity and tissue changes.

This study shows that CT-KIBRA repairs synaptic plasticity and memory in tauopathy models by stabilizing PKMζ, without altering tau levels or preventing synapse loss.

The paper uses single-cell genomics to identify shared and disease-specific cell states and gene regulatory networks in three dementias, revealing distinct neuroimmune mechanisms and potential therapeutic targets.

The paper investigates C9orf72 expansion carriers using radiogenomics to link peripheral blood transcriptomics with thalamic atrophy and clinical impairment, finding global transposable element de-repression and associations between C9orf72 expression and disease severity.

The paper uses scRNA-seq to analyze peripheral blood mononuclear cells from MAPT carriers and controls, finding reduced CX3CR1 and nonclassical monocytes associated with tau pathology.

This study uses deep learning to analyze fMRI data and identifies dynamic spatial gradients that underlie brain activity states and functional connectivity.

This study shows that microglial NF-κB signaling drives tau spreading and toxicity in a mouse model of tauopathy, with inhibition reducing tau pathology and cognitive deficits.

This study shows that TDP-43 represses a cryptic exon in UNC13A, and genetic variants associated with FTD/ALS increase cryptic exon inclusion when TDP-43 is dysfunctional.