1968 papers
This study reveals that tau protein drives neurodegeneration by entering mitochondria and interacting with complex I to induce pathological reverse electron transport, creating a self-perpetuating cycle of oxidative stress and hyperphosphorylation that can be interrupted by blocking this interaction or inhibiting reverse electron transport.
This study demonstrates that in healthy adults, age-related declines in glymphatic system efficiency and processing speed are accompanied by increased meningeal lymphatic vessel volumes, with a combined lymphatic function metric significantly predicting cognitive performance.
This study reveals that rod photoreceptor health critically depends on the cytosolic enzyme GOT1 to prevent toxic NADH accumulation, whereas the mitochondrial enzyme GOT2 is downregulated during stress as a protective mechanism, identifying reductive stress as a key driver of degeneration and GOT2 as a novel therapeutic target.
Using fNIRS hyperscanning in a virtual Minecraft environment, this study demonstrates that successful human group hunting relies on coordinated movement and is characterized by increased prefrontal brain-to-brain synchrony compared to chance levels.
This study demonstrates that acute exposure to beta-sheet-containing tau oligomers reversibly impairs sharp-wave ripple oscillations in both mouse and human hippocampal slices, with species-specific effects on ripple parameters, establishing a high-throughput ex vivo model for investigating Alzheimer's disease mechanisms and screening therapeutics.
Using high-resolution 7 Tesla MRI to overcome previous imaging limitations, this study reconstructs brainstem-augmented connectomes to demonstrate that the 58 brainstem nuclei exhibit diverse structural profiles aligned with a functional spectrum and display heterogeneous structure-function coupling that significantly influences the broader brain network.
This study reveals that SETD5 dysfunction in human astrocytes drives neuronal impairments associated with intellectual disability and autism spectrum disorder by elevating IL-6 levels through the JAK/STAT signaling pathway, a mechanism that can be partially rescued by pharmacological inhibition of JAK/STAT.
This study demonstrates that integrating human iPSC-derived microglia into midbrain organoids creates assembloids where microglia achieve a more mature, inflammation-responsive state and significantly influence the transcriptional profiles of neighboring neurons and astrocytes, offering a superior model for investigating microglia-driven neuroinflammation in Parkinson's disease.
This study introduces a novel data-driven approach to map explicitly nonlinear fMRI connectivity in human infants, revealing that these nonlinear networks uncover complementary developmental trajectories for key brain systems—such as sensorimotor and default mode networks—that remain hidden when relying solely on traditional linear methods.
This study identifies neuronal ELAVL proteins as key substrates of the CDKL5 kinase, demonstrating that CDKL5-mediated phosphorylation of these proteins enhances their mRNA binding and protein synthesis capabilities, which are essential for neuronal viability and the proper formation of cortical circuits in the visual cortex.