Calcium signaling in astrocytes and gliotransmitter release – The sooner electric brain goes away, the sooner we move forward. If only they had measurable zaps, we’d put some respect on their name.
Are cytoskeleton changes observed in astrocytes functionally linked to aging? – It’s an interesting question, is this the functional equivalent to the Sinclair-esque “epigenetic” conceit? Especially since those cytoskeletal features are literally behavioral/memory information?
Receptor-receptor interactions and microvesicle exchange as mechanisms modulating signaling between neurons and astrocytes – It’s kind of funny, neurons are unidirectional except for the bidirectional glial endpoints. Does this imply neurons are doing primary calculation or transfer? (dumb rhetorical question)
Disrupting cortical astrocyte Ca2+ signaling in developing brain induces social deficits and depressive-like behaviors – Disrupting glial signalling disrupts behavioral responsiveness to stimuli.
Spinal astrocyte dysfunction drives motor neuron loss in late-onset spinal muscular atrophy – There’s no difference between “brains” and the rest of the nervous system. It’s all the same thing. Disrupt glial function and behavioral/memory encoding goes with it.
Connexin 43 regulates astrocyte dysfunction and cognitive deficits in early life stress-treated mice – I hate work like this, which tries to assert subjective internal experience by using subjective external observation, but the idea of condensing all of these markers down into a western blot (or other biomarker appropriate blot) is really intriguing. This reduces a big chunk of work necessary to deploy biomarker based health assessment mainstream.
Neurochemical effects of sepsis on the brain – It’s like red asphalt but for dentists to get people to brush and floss. (Heh, didn’t realize Red Asphalt was a California thing, they are driving trauma movies inflicted on students during Driver’s Ed courses).
Nrf2 regulates glucose uptake and metabolism in neurons and astrocytes – Wow, nervous systems (information systems) prioritize astrocyte survival over neurons! This is expected, but I don’t think I’ve ever seen work so clearly imply it!
Multiplex translaminar imaging in the spinal cord of behaving mice – Wow in a lot of different contexts.
Deletion of CaMKIIα disrupts glucose metabolism, glutamate uptake and synaptic energetics in the cerebral cortex – Not surprising for anyone paying attention, but when astrocytes die, the information system dies.
Rescue of astrocyte activity by the calcium sensor STIM1 restores long-term synaptic plasticity in female mice modelling Alzheimer’s disease – Again, astrocytes are required for adaptive information processing. As dementia progresses, we lose the ability to (“correctly”) integrate current state information with prior encoded information.
Molecular cascades and cell-type specific signatures in ASD revealed by single cell genomics – Starting to see the word “cascade” come up a lot more frequently in the pre-prints, getting the sense that this will heat up by the end of the year.
Cellular dynamics across aged human brains uncover a multicellular cascade leading to Alzheimer’s disease – I swear cascade is not a search term.
Whole-body vibration ameliorates glial pathological changes in the hippocampus of hAPP transgenic mice, but does not affect plaque load – Hah, this came up in the sleepless apology thread regarding whether vibration could help improve glymphatic clearance rates. This suggests that no, particularly for accumulated particles (e.g. once it reaches the tangle/body stage the particles are simply to big to clear without blowing open astrocytic endfoot cohesion like the *cab AD drugs do). It does suggest that it can however reduce the harm of the accumulation by clearing the metabolic zone around astrocytes, increasing their function. Wonder if this will work for “healthy” individuals for extended stress situations? E.g. instead of a pomodoro, a shake-a-doro?
Now We Can Tame the Wild West of Controlling Astrocytes for Treating Neocortical Epilepsy – Wow, what an inspiring bit of work, we may be able to completely eliminate cortical resection surgeries and longitudinal drug therapies by figuring out which circuits are causing the cascades and stimulating the astrocytes directly to control them.
Lipid-accumulated reactive astrocytes promote disease progression in epilepsy – How much of dementia related degeneration is subacute epileptiform activity?
Purkinje cell dopaminergic inputs to astrocytes regulate cerebellar-dependent behavior – I hate single knockout work as a rule, but this is slightly new territory (and mostly conformant to expectations).
Loss of fatty acid degradation by astrocytic mitochondria triggers neuroinflammation and neurodegeneration – Okay, the mechanics with regard to dementia we’ve been talking about the last year have been vetted and should be abundantly clear by now. We need to urgently start moving toward standardized testing for astrocytic biomarkers in blood as part of the yearly physical.
Disruption of Astrocyte-Dependent Dopamine Control in the Developing Medial Prefrontal Cortex Leads to Excessive Grooming in Mice – Breaking dorsal feedback causes ventral loops. It’s weird that lab thinking so fucking rigid that no one ever tries the obverse of this and see if the mice stop grooming altogether. We don’t have a form to record that though!1!
Transcriptomic atlas and interaction networks of brain cells in mouse CNS demyelination and remyelination – Critical work. Cycles like this are required for the formation of “memory”, or storing stimuli responses.
Astrocytes actively support long-range molecular clock synchronization of segregated neuronal populations – So right and so wrong at the same time. Yes, astrocytes negotiate CPG signals between themselves over neuronal pipes. Organism dominant CPG cells exist in the lower brainstem however.
MicroRNA‑124: an emerging therapeutic target in central nervous system disorders – In our search for non-invasive early biomarkers, this is a pretty interesting target, especially with regard to dementia class disorders. m124 is an information processing signal, and changes here indicate changes in information processing cascade.