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In this issue, Min et al. (p 1154) identify acetylation of tau at site K174 as an early pathological change in human Alzheimer's Disease (AD) brain tissue and show that this acetylation exacerbates tau-mediated neurodegeneration and memory impairments in mice. Furthermore, pharmacological inhibition of tau acetylation can ameliorate these phenotypes in a mouse model of AD/FTD (frontotemporal dementia). The cover image depicts immunostaining for AC312-positive acetylated tau (red and magenta) and MC1-positive pathological tau (blue and green) in the hippocampus of the PS19 transgenic mouse model of AD/FTD. Image credit: the original image is by Chao Wang, and the artwork is by Connor Ludwig.
The proposed 21st Century Cures Act is a potential boon to the funding woes faced by the US National Institutes of Health and the Food and Drug Administration. But a careful look at the provisions within the bill is warranted to avoid enacting policies that could undermine the progressive translation of research into clinical products.
The Canadian Institutes of Health Research (CIHR) recently terminated its MD/PhD training program without clear alternative funding in place. This misguided decision must urgently be reversed, as it has the potential to diminish a unique pool of graduates at the forefront of translational research.
The role of CD47—often expressed on tumor cells—as a 'don't eat me' signal that inhibits macrophage phagocytosis is well established. But new work reveals a major role for other immune cell types—T cells and dendritic cells—in the anti-tumor effects of therapeutic CD47 blockade.
During viral infections, antigen-presenting cells (APC) have traditionally been thought to recruit and activate CD4+ T cells by presenting fragments of viral proteins captured from the extracellular environment. A new study indicates that the material the APCs need to present is much closer: in fact, APCs need to make it themselves.
Depression is mechanistically not well understood. A new study investigates the expression of chromatin-remodeling complexes in a mouse model for depression and describes an epigenetic pathway that may explain why some individuals are more susceptible to stress-induced depression than others.
Several independent groups question the reliability of an antibody-based method that is used to isolate oogonial stem cells from the ovaries of adult humans, nonhuman primates and mice.
Morgane Rolland and colleagues report that in HIV infection, a higher diversity of infecting founder viruses is associated with markers of poorer clinical outcome.
An intracortical neural prosthetic system developed in animal studies is translated for clinical use in humans with paralysis. Neural control of computer cursor movements achieved with this system represent the highest performance reported to date.
Upregulation of the ATP-dependent ACF chromatin-remodeling complex in the NAc is a necessary and causal component for susceptibility to stress-induced depressive behaviors in mice, and this complex is also shown to be upregulated in the NAc of depressed humans.
Acetylation of tau at K174 is identified in Alzheimer's disease (AD) brain tissue and exacerbates tau-mediated neurodegeneration and memory impairments in mice. Pharmacological inhibition of tau acetylation ameliorates these phenotypes in a mouse model of AD.
The bromodomain and extraterminal (BET) inhibitor JQ1 synergizes with the histone deacetylase inhibitor SAHA to suppress tumor growth in mouse models of pancreatic cancer.
Minimal reduction of PU.1 in mice is sufficient to elicit a preleukemic state that, when combined with a DNA mismatch repair defect, results in progression to myelodysplastic syndrome and acute myeloid leukemia.
In NOTCH-induced T cell acute lymphoblastic leukemia, the resistance to anti-NOTCH therapy conferred by loss of the Pten tumor suppressor is linked to reversal of the effects of NOTCH inhibition on leukemic cell metabolism.
Two studies demonstrate that the methyltransferase KMT2D, which is recurrently mutated in several types of human B cell lymphoma, suppresses tumorigenesis by altering the epigenetic landscape of B cells; Kmt2d deletion in mice perturbs normal B cell development.
Two studies demonstrate that the methyltransferase KMT2D, which is recurrently mutated in several types of human B cell lymphoma, suppresses tumorigenesis by altering the epigenetic landscape of B cells; Kmt2d deletion in mice perturbs normal B cell development.
Although previous work indicated that the antitumor effects of anti-CD47 require macrophage phagocytosis of tumor cells, new work done in immunocompetent mice bearing syngeneic tumors reveals a key role for dendritic cell cross-priming of CD8+ T cells.
CD4+ T cell responses are classically induced by presentation of exogenous antigens by antigen-presenting cells. Miller et al. now report that endogenous presentation drives most CD4+ T cell responses in influenza-infected mice.
MALDI mass spectrometry shows distinct patterns of drug distribution in tuberculosis lesions in human lungs that provide insight into treatment efficacy.