Alissa L. Nana

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.

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

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

The paper confirms the presence of myelinated inhibitory axons in all layers of human neocortex, similar to findings in mice, and identifies their distinctive features and potential implications for neurological disorders.