Salvatore Spina

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

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.

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

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 identifies genetic risk factors for FTLD-TDP subtypes using whole-genome sequencing and meta-analysis across multiple cohorts.

This study examines neuronal loss and tau pathology in the hypothalamic intermediate nucleus of AD and PSP patients, linking these changes to distinct sleep disturbances.

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 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 identifies molecular signatures of selectively vulnerable neurons in Alzheimer's Disease using single-nucleus RNA sequencing and validates findings with neuropathological methods.

The paper links neuron type-specific TDP-43 pathology in the frontoinsular cortex to salience network atrophy and loss of empathy in frontotemporal dementia.

This study analyzes the lateralization and progression of atrophy in the anterior temporal lobe in TDP-43-C pathology, finding that right-predominant atrophy is common and that atrophy patterns are similar in left and right variants.