The placenta epigenome–brain axis: placental epigenomic and transcriptomic responses that preprogram cognitive impairment – Genes are important, but it’s expression that matters. I dunno about the “placenta-brain” axis thing though.
Human white matter myelinates faster in utero than ex utero – Heh, white matter is white because of myelination (and fibrous cell types).
A new diagnostic tool for brain disorders: extracellular vesicles derived from neuron, astrocyte, and oligodendrocyte – /u/Hopere, what’s up?
Glial-derived mitochondrial signals impact neuronal proteostasis and aging – There’s just a lot of “holy shit” in this one, including discovering that astrocytes have discrete channels for neurons and peripheral signalling.
Accelerated aging in mice with astrocytic redox imbalance as a consequence of SOD2 deletion – I have a love/hate relationship with stuff like this, SOD2 itself is probably irrelevant in the “big picture”, it doesn’t appear to be a low level part of the chain. But it does give us an idea of “what happens when redox imbalance occurs”. Some distant place in the future, we’ll hopefully be talking about more about biochemical interactions with classes of chemicals rather than more of this hunt and peck type of stuff.
General cognitive ability, as assessed by self-reported ACT scores, is associated with reduced emotional responding: Evidence from a Dynamic Affect Reactivity Task – Decades of MRI work am cry. “High IQ” is demonstrated by lower activation (and almost certainly has fuck all to do with brain volume or the other measures CogSci has been dry humping for awhile).
Regeneration of the cerebral cortex by direct chemical reprogramming of macrophages into neuronal cells in acute ischemic stroke – In vivo cellular reprogramming. Whoa.
Hierarchical differences in the encoding of sound and choice in the subcortical auditory system – This is the first time I’ve ever seen work which outright states that the entire map of functions necessary to generate behavior exists in the brain stem. One of my mini-rants is trying to get people to realize that all sensory processing starts in the brain stem, and our cortical/limbic/DCN circuitry are “enhancers” or “modifiers” of that initial salience.
Heralding a new era of oxytocinergic research: New tools, new problems? – Same problems mostly.
Retinal astrocyte morphology predicts integration of vascular and neuronal architecture – Wow a lot of cool stuff in this one. Also, I’m taking offense at the whole s100b/GFAP biomarkers are wimpy dog, even though they are almost certainly right. Crazy that they had to discard most of their cells because astrocytes overlap so much. Heh, the whole process of describing cells according to the visual impressions of someone over 100 years ago has turned into a pretty interesting roadblock for neuroscience.
Cortical astrocytes modulate dominance behavior in male mice by regulating synaptic excitatory and inhibitory balance – Explainer Piece: Control of social hierarchy beyond neurons. Remember the whole “astrocytes (or similar class) are necessary for adaptive behavior” thing? Doesn’t matter how complex or “simple”.
Mechanical stimuli activate gene expression via a cell envelope stress sensing pathway – Hey, here’s a crazy idea, what if nervous systems communicated via chemical methods and used mechanical forces to physically push those chemical products between cells in some cells using an electro-chemical “pump”. And other cells do the same thing without the electro-chemical pump. But it’s always mechanical. Hey, what if there were organisms that didn’t use “electricity” at all, but still had predictable adaptive behavior using purely mechanical interactions? What if we could manipulate the function, differentiation, and transport of cells purely by mechanical means?
Thyroid hormone rewires cortical circuits to coordinate body-wide metabolism and exploratory drive – What if manipulating chemical elements could result in coordinated system function shifts?
What Does Physiological Mean? – I’m pretty sure 5 packs of cigarettes a day is physiological right?
Isolation of Splenic Microvesicles in a Murine Model of Intraperitoneal Bacterial Infection – Explainer: Methods of Isolation and Purification of Extracellular Vesicles from Different Biological Matrixes: Special Issue at a Glance (for reference).
Intercellular communication atlas reveals Oprm1 as a neuroprotective factor for retinal ganglion cells – One of the things that I’m pretty excited about is work which is picking away at intercellular communication processes, particularly focusing on miRNA/peptide interactions which are universal to all cells. This change in thinking has brought a pretty significant wave of new therapies for the previously incurable, particularly thinking about conditions like juvenile cystic fibrosis. One of the coolest things we are coming to realize is that genetic “expression” is an artifact of RNA, and RNA expression is an artifact of environment in physiological conditions.
Engineered 3D Immuno-Glial-Neurovascular Human Brain Model – This gave context to a question I couldn’t translate well into words! It’s been my impression that multiple discrete interdependent whole organism signalling methods exist, but there’s not a huge amount of guidance on where each begins and ends. I really like this triad as all three are capable of independently storing data specific to system itself. For example, memory B/T cells write information in a really similar way as synaptic storage, just designed for transport throughout the body. Viewing these three as interdependent systems with independent memory seems like a really good fit for observations.
Prenatal Antidepressant Exposure and Offspring Brain Morphologic Trajectory – Oh psychiatry you rascal. How do we disguise the harmful effects of low SES? By prescribing SSRIs! The common caveat applies here, MRI volumetric studies are a compost pile ready to explode on top of a raging dumpster fire. The crazy thing about this study is that it really doesn’t support the asserted conclusions at all, it’s a careful selection of data to produce the desired output (and even then it needed some statistical massaging to achieve the desired result). The underlying principle is probably correct though. taking anticholinergic medications during pregnancy and breast feeding is probably a bad idea.
Specialized astrocytes mediate glutamatergic gliotransmission in the CNS – The amount of “Well we thought this was a neuron exclusive function, but actually it’s the other side of a glial interaction” coming out over the last year is really encouraging.
Synaptic phagocytosis by multiple glial cell types – It’s in Japanese so you’ll need to translate it, but “eat me signals” alone merits inclusion in any serious neuroscience discussion. Haha, I wish I could get away with calling some phenotypes of “autism” a lack of “eat me signals”.
General anesthesia alters CNS and astrocyte expression of activity-dependent and activity-independent genes – I think this is my current kick, it’s not about the genes themselves, it’s about the expression.
Astrocytes Transplanted during Early Postnatal Development Integrate, Mature, and Survive Long Term in Mouse Cortex – Heh, these guys out here trying to cure paralysis or something down the road.
Complete human day 14 post-implantation embryo models from naïve ES cells – Wow. Turns out the chicken or egg question was dumb all along, the correct answer is “expression”.
An ex vivo model of Toxoplasma recrudescence reveals developmental plasticity of the bradyzoite stage – Inter-species developmental interactions is a super fascinating subject IMO, and a pretty strong bit of evidence demonstrating just how agnostic organisms can be to external stimuli/inputs. Toxoplasmosis in particular has a lot of evidence demonstrating the variation in this space, a toxo colony in the right place at the right time and you’re a “genius”, a toxo colony in the wrong place or wrong time and, well you aren’t.
Human in vivo evidence of reduced astrocyte activation and neuroinflammation in patients with treatment-resistant depression following electroconvulsive therapy – ECT apparently has a very similar mechanic to ketamine, it causes astrocytes to “dump” certain types of information, reducing the “harmful” protein signals being produced and allowing some level of “relearning” in the effected astrocytes. Unfortunately most of the time this means relearning exactly the same types of “harmful” information that resulted in ECT being necessary in the first place. How do these treatments break/suppress/disrupt signals?
Astrocytes on steroids binge on synapses to cope with stress – Early developmental stress results in over-pruning of circuits, degrading the nuance/granularity of behavior capable when processing certain stimuli.
Astrocytes in functional recovery following central nervous system injuries – Glia are the Rodney Dangerfield of cells, even in a review like this it leads with lines like “Microglia, astrocytes and oligodendrocytes are collectively known as glial cells. They provide physical, functional and metabolic support to neurons.”
Astrocyte Responses Influence Local Effects of Whole-Brain Magnetic Stimulation in Parkinsonian Rats – Super cool that the last few months have seen a lot more attempts to model astrocytes.