18 results for “Neuron-Glia Interactions”. Showing 18 of 39,449.
CRISPRi-based screens in iAssembloids to elucidate neuron-glia interactions.
allows for the unbiased identification of mechanisms of neuron-glia cell interactions.
Immune imbalance in the human hippocampus in PTSD revealed by single-nucleus transcriptomics.
neuron-glia communication. Our study provides a comprehensive single-cell atlas of the hippocampal neuroimmune landscape in PTSD and highlights dysfunctional glial-neuronal interactions
Axo-glial interactions between midbrain dopamine neurons and oligodendrocyte lineage cells in the anterior corpus callosum.
neuron-glia interactions with important implications for myelin plasticity by identifying
Neuron-Glial Interactions: Implications for Plasticity, Behavior, and Cognition.
neuron-glia interactions, the impact of these interactions on brain
Alzheimer's disease protective allele of Clusterin modulates neuronal excitability through lipid-droplet-mediated neuron-glia communication.
into how CLU confers resilience to AD through neuron-glia interactions.
NF$\kappa$B-Activated Astroglial Release of Complement C3 Compromises Neuronal Morphology and Function Associated with Alzheimer's Disease
neuron-glia interaction through NFκB/C3/C3aR signaling may contribute
GABA-dependent microglial elimination of inhibitory synapses underlies neuronal hyperexcitability in epilepsy.
Neuron-glia interactions underlie this process but the detailed mechanisms
Proteomic analysis identifies HSP90AA1, PTK2B, and ANXA2 in the human entorhinal cortex in Alzheimer's disease: Potential role in synaptic homeostasis and Aβ pathology through microglial and astroglial cells.
Neuron-glia interactions have recently come into focus; however, the role
Tunnelling nanotubes between neuronal and microglial cells allow bi-directional transfer of α-Synuclein and mitochondria.
neuron-glia interactions. TNT-like structures were also reported between
Neurotoxic Microglial Activation via IFNγ-Induced Nrf2 Reduction Exacerbating Alzheimer's Disease.
neuron-glia interactions. Here, the mechanism of detrimental microgliosis in AD by employing
The immune system in Parkinson's disease: what we know so far.
neuron-glia crosstalk as well as the central-peripheral immune interaction
Single-Nucleus Transcriptomics Reveals Glial Metabolic-Immune Rewiring and Intercellular Signaling Disruption in Chronic Migraine.
interactions (e.g., CSF1-CSF1R) alongside enhanced proinflammatory signaling (e.g., FGF1-FGFR2, PTN-SDC4), particularly affecting neuron-glia
Tau pathology epigenetically remodels the neuron-glial cross-talk in Alzheimer's disease.
neuron-glia cross-talk is critical to brain homeostasis and is particularly affected by neurodegenerative diseases. How neurons manipulate the neuron-astrocyte interaction
Altered glia-neuron communication in Alzheimer's Disease affects WNT, p53, and NFkB Signaling determined by snRNA-seq.
neuron-glia and glial cell crosstalk. Many signaling pathways have been proposed to be dysregulated in Alzheimer's disease, including WNT, TGFβ, p53, mTOR, NFkB, and Pi3k/Akt signaling. Here
Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq.
neuron-glia and glial cell crosstalk. Many signaling pathways have been proposed to be dysregulated in Alzheimer's disease, including WNT, TGFβ, p53, mTOR, NFkB, and Pi3k/Akt signaling. Here
Astroglial contribution to tau-dependent neurodegeneration.
interact actively via glutamine-glutamate cycle (GGC) that supports neuronal metabolic demands and neurotransmission. GGC deficiency may be involved in different diseases of the brain, where impaired astrocytic control
Neuronal DAMPs exacerbate neurodegeneration via astrocytic RIPK3 signaling.
interacting protein kinase-3 (RIPK3) signaling has recently been described as a key regulator of neuroinflammation, but whether this kinase mediates astrocytic responsiveness to neuronal death has not yet been
Two lysosomal genes ATP13A2 and GBA1 interact to drive neurodegeneration.
interaction screen of lysosomal storage disorder (LSD) genes to identify dominant modifiers of Gba1b (fly homolog of GBA1). Age-dependent locomotor assessments, electroretinograms (ERG), transmission electron microscopy (TEM) analyses