Pathogenic LRRK2 mutations cause loss of primary cilia and Neurturin in striatal Parvalbumin interneurons
By onLRRK2 mutations in Parkinson's disease inhibit primary cilium formation in specific brain cells, affecting movement control. Parvalbumin interneurons lose cilia, impacting response to signals and neuroprotection for dopamine neurons.
Restoration of striatal neuroprotective pathways by kinase inhibitor treatment of Parkinson’s linked-LRRK2 mutant mice
By onParkinson's disease mutations in LRRK2 inhibit cilia formation in brain cells, reducing neuroprotective factors. Treatment with LRRK2 inhibitor restores cilia and promotes neuron health, offering potential therapy for Parkinson's patients.
State-of-the-art review of the clinical research on menopause and hormone replacement therapy association with Parkinson’s disease: What meta-analysis studies cannot tell us
By onStudies have shown varying effects of menopause on Parkinson's disease in part due to differences in study design. This review provides an overview of the clinical literature thus far and provides considerations for future studies.
scNAT: a deep learning method for integrating paired single-cell RNA and T cell receptor sequencing profiles
By onThe authors developed scNAT, a deep learning method that integrates paired scRNA-seq and scTCR-seq data to represent data in a unified latent space for downstream analysis.
Gut instincts in neuroimmunity from the eighteenth to twenty-first centuries
By onIn this review, the authors revisit the history of gut-brain interactions in science and medicine, which dates back to at least the eighteenth century, and outline how concepts in this field have shifted and evolved across eras.
Nigrostriatal tau pathology in parkinsonism and Parkinson’s disease
By onStudy focuses on mild motor deficits not meeting Parkinson's criteria. Nigrostriatal system changes occur regardless of alpha-synuclein presence, hinting at tau-mediated dopaminergic neurodegeneration initiation. Tau pathology seen in affected groups
Motor Cortical Neuronal Hyperexcitability Associated with α-Synuclein Aggregation
By onOur results documented motor cortical neuronal hyperexcitability associated with αSyn aggregation and provided a novel mechanistic understanding of cortical circuit dysfunction in PD
Distributed dopaminergic signaling in the basal ganglia and its relationship to motor disability in Parkinson’s disease
By onDegeneration of dopaminergic neurons in the brain causes PD motor symptoms. Recent research shows dopamine's role in basal ganglia regions beyond striatum impact movement control. Restoring dopamine signaling outside the striatum can alleviate PD.
Movement-related increases in subthalamic activity optimize locomotion
By onWe found most neurons in the STN exhibit increased activity during locomotion. Furthermore, optogenetic inhibition of this activity rapidly dysregulated gait. Thus, the STN facilitates movement and may drive locomotor activity in at-risk DA neurons.
A neurocomputational view of the effects of Parkinson’s disease on speech production
By onThis article reviews the role of cortico-basal ganglia circuits in speech motor learning and execution in Parkinson's disease.
Visualizing chaperone-mediated multistep assembly of the human 20S proteasome
By onAssembly factors guide proteasome core particle (CP) formation. Cryo-EM shows chaperones and propeptides aiding in subunit addition order, stabilization and activation, shedding light on proteasome biogenesis and functions of assembly factors.
Combinatorial selective ER-phagy remodels the ER during neurogenesis
By onThe endoplasmic reticulum (ER) is crucial for various cellular functions. ER proteome is modified by autophagy, especially in neurons. Specific receptors target ER components for degradation, impacting neuronal health.
Global cellular proteo-lipidomic profiling of diverse lysosomal storage disease mutants using nMOST
By onNanoflow-based nMOST workflow quantifies proteins and lipids in LSD mutants, revealing autophagy defects and mitochondrial abnormalities in NPC1/NPC2 mutants.
α-Synuclein aggregation decreases cortico-amygdala connectivity and impairs social behavior in mice
By onThe study suggests that early circuit modulation could be an effective approach to alleviate symptoms associated with α-Syn pathology, necessitating studies of functional consequences of α-Syn aggregation.
Motor cortical circuit adaptations in parkinsonism
By onPerspective article on the publication (Chen et al. (2023), Sci Adv). It summarizes the major findings of this research paper and highlights a few potential future directions regarding the motor cortical circuit changes in parkinsonism.
Immune Senescence, Immunosenescence and Aging.
By onThis review focuses on age-related immune dysfunction, cellular senescence and the impaired immune response to pathogens.
Cellular Senescence: A Key Therapeutic Target in Aging and Diseases
By onThis paper discusses cellular senescence as a therapeutic target in aging and age-related diseases, as well as strategies and recent advances in the development of senotherapeutics targeting senescent cells to treat age-related diseases.
Genetically Encoded and Modular SubCellular Organelle Probes (GEM SCOPe) reveal lysosomal and mitochondrial dysfunction driven by PRKN
By onLysosomal and mitochondrial dysfunction are implicated in many diseases. GEM-SCOPe, a modular toolbox of fluorescent markers, helps visualize these organelles. In a PRKN-knockout model of PD, GEM-SCOPe identified disease-associated changes.
Development and characterization of a non-human primate model of disseminated synucleinopathy
By onThe intraputaminal delivery of AAV9-SynA53T resulted in a widespread synucleinopathy throughout the cerebral cortex and substantia nigra in the non-human primate brain.
Functional efficacy of the MAO-B inhibitor safinamide in murine substantia nigra pars compacta dopaminergic neurons in vitro: a comparative study with tranylcypromine
By onSafinamide (SAF) is used for PD by enhancing dopamine signal. SAF prolongs recovery from dopamine-mediated firing inhibition in SNpc DAergic neurons, mildly compared to tranylcypromine, suggesting multiple sites of action for SAF's therapeutics.
