The bridge-like lipid transport protein VPS13C/PARK23 mediates ER-lysosome contacts upon lysosome damage
By onGenetic studies link lysosome dysfunction to Parkinson's disease. VPS13C, a PD gene, relocates to damaged lysosomes, aiding in membrane repair. This process involves Rab7 and suggests early lipid transport as a protective response.
Skip Nav Destination Tools|July 30 2025 AI-directed voxel extraction and volume EM identify intrusions as sites of mitochondrial contact
By onThe AI-directed Voxel Extraction (AIVE) segmentation strategy combines AI predictions with image electron signals to confidently segment membrane boundaries. Authors identify a new category of Membrane contact Sites named Mitochondrial Intrusions.
Mitophagy in Neurons: Mechanisms Regulating Mitochondrial Turnover and Neuronal Homeostasis
By onAuthors discuss the current understanding of mitophagy mechanisms operating in neurons to govern mitochondrial homeostasis and summarize progress on our understanding of the links between mitophagic dysfunction and neurodegeneration.
Development of a simplified smell test to identify Parkinson’s disease using multiple cohorts, machine learning and item response theory
By onReduced olfaction is a common feature of typical Parkinson disease (PD) and dementia with Lewy bodies (DLB). We have created a simplified smell test based on seven specific odorants that can distinguish PD/DLB patients from healthy controls.
Reply to: Is Gauchian genotyping of GBA1 variants reliable?
By onSummarizing a study by N. Tayebi et al. in Communications Biology, published in 2025.
Neuromelanin and selective neuronal vulnerability to Parkinson’s disease
By onNeuromelanine (NM), a pigment in human catecholamine neurons, plays a crucial role in PD. We review the development of NM in dopamine versus noradrenaline neurons and focus on previously overlooked cellular organelles in NM format and function.
Allosteric regulation of the Golgi-localized PPM1H phosphatase by Rab GTPases modulates LRRK2 substrate dephosphorylation in Parkinson’s disease
By onPPM1H phosphatase reverses LRRK2-mediated Rab GTPase phosphorylation, with Golgi localization facilitated by an amphipathic helix. PPM1H binds Rab8A and Rab10 at an allosteric site, inhibiting phosphatase activity.
Defect in hematopoiesis and embryonic lethality at midgestation of Vps13a/Vps13c double knockout mice
By onVPS13 proteins facilitate lipid transfer at membrane contact sites. VPS13A and VPS13C double knockout causes embryonic death due to impaired erythropoiesis and innate immunity activation.
How Membrane Contact Sites Shape the Phagophore
By onPhagophores form membrane contact sites with organelles like the vacuole, ER, and lipid droplets. In situ imaging techniques, such as cryo-CLEM, provide valuable insights into these interactions, aiding in understanding autophagosome biogenesis.
Microinvasive Probes for Monitoring Electrical and Chemical Neural Activity in Nonhuman Primates
By onWe designed carbon fiber sensors that enable long-term simultaneous recording of both neurochemical and electrical neural activity in deep brain structures of nonhuman primates.
Aseptic, semi-sealed cranial chamber implants for chronic multi-channel neurochemical and electrophysiological neural recording in nonhuman primates
By onWe developed an implantable neural interface in monkeys that allows dual monitoring of electrical and chemical neural activity for long-term studies.
The human autophagy-initiating complexes ULK1C and PI3KC3-C1
By onULK1C and PI3KC3-C1 are crucial for macroautophagy initiation. Recent research focuses on their structural organization, activation mechanisms, and roles in autophagy initiation's protein interaction network for potential therapeutic targeting.
Generation of knock-in Cre and FlpO mouse lines for precise targeting of striatal projection neurons and dopaminergic neurons
By onTo enable precise genetic targeting of key neuronal populations in the basal ganglia, we generated and characterized five knock-in mouse lines: Drd1-Cre, Adora2a-Cre, Drd1-FlpO, Adora2a-FlpO, and DAT-FlpO.
Autophagic stress activates distinct compensatory secretory pathways in neurons
By onNeurodegenerative diseases are linked to autophagy dysfunction causing harmful build-up of cellular waste. Neurons with Parkinson's mutation increase release of autophagic vesicles and exosomes, suggesting a protective response to chronic stress.
Derailed degradation: LRRK2-dependent exocytosis in Parkinson’s disease
By onFerguson discusses new data on LRRK2 mutations increasing neuronal exocytosis of vesicles enriched in endosomal components. LRRK2 may promote lysosome exocytosis through interactions with GABARAP and Rab GTPases.
Lrrk2 G2019S mutation incites increased cell-intrinsic neutrophil effector functions and intestinal inflammation in a model of infectious colitis
By onUsing single cell RNA sequencing, we demonstrate that LRRK2 G2019S is associated with an increased neutrophil presence in the colonic lamina propria during infection, Th17 skewing, upregulated Il17a, and greater colonic pathology.
LRRK2, lysosome damage, and Parkinson’s disease
By onRecent research has uncovered how LRRK2 kinase activity is regulated by recruitment to endolysosomal membranes, involving interactions with small GTPases and GABARAP. This sheds light on its role in lysosomal damage and Parkinson's disease.
Tackling a disease on a global scale, the Global Parkinson’s Genetics Program, GP2: A new generation of opportunities
By onThis perspective describes the vision and progress of the Global Parkinson's Genetics Program toward a more genetically representative understanding of Parkinson's disease.
