OPCs eat in response to sensory experiences.

Oligodendrocytes are derived from a subtype of glia called oligodendrocyte precursor cells (OPCs). The potential functions of OPCs beyond oligodendrogenesis however, have remained elusive. In their latest study, Auguste et al.

Beta-amyloid production in neurons is regulated by astrocyte-derived cholesterol.

The accumulation of amyloid β (Aβ) in the brain is an established feature of Alzheimer’s disease, however mechanisms that regulate Aβ accumulation are not fully understood. In a recent study, Wang et al show that Aβ accumulation in neurons is tightly regulated by cholesterol production in astrocytes. This finding paves the way for future work that will establish whether the selective removal of Aβ by targeting this mechanism has therapeutic potential.

A DNA origami-based nanoscale molecular transport railway.

Origami, the Japanese art of paper folding, has taken on new meaning for the fields of chemistry and biology. DNA origami describes the folding of DNA strands to form nanoscale structures. The ability to design and form complex structures at a nanoscale level has fuelled new ambitions of nanostructure applications in life science.

Glycans housed by a bacteriophage enable rapid identification of glycan recognition patterns.

Glycans are a major composition of the cell surface that interacts with the surrounding environment. The ability to carry out glycan-binding profile studies has been mainly done with glycan arrays. However, glycan arrays are not easily adaptable for cell surface and in vivo glycan recognition assays.

Identifying therapeutic targets for schizophrenia.

There is a continual need to develop new therapies for neuropsychiatric disorders such as Schizophrenia, and identifying the underlying molecular processes remains challenging. Chadha et al. recently discovered a potential role for mTOR kinase activity disruption in Schizophrenia and further uncover the precise pathomechanism.

Changes in blood-spinal cord barrier permeability and neuroimmune interactions in the underlying mechanisms of chronic pain.

Advancing our understanding of the underlying mechanisms of chronic pain is instrumental to the identification of new potential therapeutic targets. Neuroimmune communication throughout the pain pathway is of crucial mechanistic importance and has been a major focus of preclinical chronic pain research over the last 2 decades. In the spinal cord, not only do dorsal horn neurons partake in mechanistically important bidirectional communication with resident immune cells such as microglia, but in some cases, they can also partake in bidirectional crosstalk with immune cells, such as monocytes/macrophages, which have infiltrated into the spinal cord from the circulation.

Teasing apart the cell death pathways in HIV pathogenesis.

The progressive loss of CD4 + T cells has been recognised as being central to HIV-1 pathogenesis, however a precise understanding of the underlying mechanisms and, consequently, improved therapies have yet to be achieved. Zhang et al. have recently shown in HIV-1 patients that the NLRP3 inflammasome pathway, which plays a key role in innate immunity, is a crucial mediator of the loss of CD4 + T cells.

T cells in the brain may contribute to attenuation of sepsis-associated depression.

Sepsis-associated encephalopathy, as well as increasing mortality, has been associated with long-lasting depressive behaviour, which is thought to be caused by infection-induced neuroinflammation in the brain. Saito et al. have recently demonstrated in a mouse model of sepsis that infiltrated regulatory T cells in the cerebral cortex mediate the resolution of neuroinflammation and alleviate anxious/depressive behaviour.

Cellular proteostasis decline in human senescence.

A huge amount of intrigue surrounds the aging process. Senescence—the decreased likelihood of reproduction and the increased chance of mortality—is a hallmark of aging. The reduced ability of senescent cells to maintain protein homeostasis (proteostasis) has been well-established in nematodes but this phenomenon had yet to be directly demonstrated in human cells.

Sleep-wake cycles are disrupted by diseases that result in cytoplasmic crowding.

It doesn’t take much to disrupt our sleep. Whilst we are aware of environmental factors that can disturb our circadian rhythms, the precise mechanisms that control molecular time cues have remained elusive. Beesley and co-workers demonstrate that diseases associated with cytoplasmic crowding affect the sleep-wake cycle.

Cathepsin S as a potential therapeutic target for chronic pain.

Chronic pain is a distressing yet poorly-treated condition that can arise as a result of diseases and injuries to the nervous system. The development of more efficacious therapies for chronic pain is essential and requires advances in our understanding of its underlying mechanisms. Clinical and preclinical evidence has demonstrated that immune responses play a crucial role in chronic pain.

The role of microRNAs in neurons and neuroimmune communication in the dorsal root ganglia in chronic pain.

Despite being a life-restricting condition, chronic pain remains poorly treated. A better understanding of the underlying mechanisms of chronic pain and thence development of innovative targets is therefore essential. Recently we have started to elucidate the importance of the role of microRNAs (miRs) in preclinical chronic pain.

Imbalance of proresolving lipid mediators in persistent allodynia dissociated from signs of clinical arthritis.

Rheumatoid arthritis-associated pain is poorly managed, often persisting when joint inflammation is pharmacologically controlled. Comparably, in the mouse K/BxN serum-transfer model of inflammatory arthritis, hind paw nociceptive hypersensitivity occurs with ankle joint swelling (5 days after immunisation) persisting after swelling has resolved (25 days after immunisation). In this study, lipid mediator (LM) profiling of lumbar dorsal root ganglia (DRG), the site of sensory neuron cell bodies innervating the ankle joints, 5 days and 25 days after serum transfer demonstrated a shift in specialised proresolving LM profiles.

Changes in vascular permeability in the spinal cord contribute to chemotherapy-induced neuropathic pain.

Chemotherapy-induced neuropathic pain is a dose-limiting side effect of many cancer therapies due to their propensity to accumulate in peripheral nerves, which is facilitated by the permeability of the blood-nerve barrier. Preclinically, the chemotherapy agent vincristine (VCR) activates endothelial cells in the murine peripheral nervous system and in doing so allows the infiltration of monocytes into nerve tissue where they orchestrate the development of VCR-induced nociceptive hypersensitivity. In this study we demonstrate that VCR also activates endothelial cells in the murine central nervous system, increases paracellular permeability and decreases trans endothelial resistance.