Astrocytic uptake of neuronal corpses promotes cell-to-cell spreading of tau pathology – This is interesting if it confirms out and tweaks things a bit. My prior assumption was that tau aggregates accumulated due to bad folds, I didn’t realize tau isn’t native to astrocytes at all. That was a huge miss on my part. Reconstituting all this, it looks like neurons start getting “bad” inputs and start going tits up, then astrocytes attempt to phagocytose the junk but can’t digest it either. This normally wouldn’t be a problem except astrocytes synapse against many different neurons, meaning the higher levels of tau clump. Think of an organism being okay processing regular “expired” products in the blood, but a blood clot can be fatal to cells both at the point of the clot and down stream. So either bad metabolic products from astrocyte->neuron, induces toxicity, induces tau, astrocytes/microglia try to clear the tau production but get overwhelmed producing tangles, which turn into a game of Katamari Damacy.
Antidiabetic agents as a novel treatment for Alzheimer’s and Parkinson’s disease – There’s gotta be longitudinal data somewhere we can see rates of dementia against these treatments already in stream right?
An Electric Light Orchestra in the Brain: Optogenetics for Controlling Seizures via Modulation of Astrocyte Activity – This seems interesting, and somehow less invasive than lobectomies.
Differential usage of DNA modifications in neurons, astrocytes, and microglia – A system of systems, working in tension with each other.
Astrocyte store-operated calcium entry is required for centrally mediated neuropathic pain – Astrocytes are signalling “gate keepers”.
Astrocytic modulation of neuronal signalling – LOL, very next article in the feed!
Lactate as a determinant of neuronal excitability, neuroenergetics and beyond – And where again does the lactate come from?
Dissociation Between Neuronal and Astrocytic Calcium Activity in Response to Locomotion in Mice – Wow, very cool work! This is something that should either replicate well or not. Astrocytes provide “internal” modification to calculations, neurons are relays of stimuli.
High-intensity interval training ameliorates Alzheimer’s disease-like pathology by regulating astrocyte phenotype-associated AQP4 polarization – I’m always skeptical of research regarding “exercise”, particularly when it’s based around any modality other than aerobic vs anaerobic, but the MOA for this could be the intense shaking. Eventually we gotta try making the bass seat.
Astrocytic α4-containing nAChR signaling in the hippocampus governs the formation of temporal association memory – Sort of. Acetylcholine pathways represent a global valence calculation, turn it off and it’s going to impact the ability of astrocytes to make the necessary calculations, which require valence and salience signals.