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A <i>Drosophila</i> computational brain model reveals sensorimotor processing
Differences in misinformation sharing can lead to politically asymmetric sanctions
Flickering gamma-ray flashes, the missing link between gamma glows and TGFs
Rapid homologue juxtaposition during meiotic chromosome pairing
Neuronal wiring diagram of an adult brain
Network statistics of the whole-brain connectome of <i>Drosophila</i>
Bulk high-temperature superconductivity in pressurized tetragonal La<sub>2</sub>PrNi<sub>2</sub>O<sub>7</sub>
The fly connectome reveals a path to the effectome
Neurotechnology race ramps up, but fundamental questions remain
The global imbalance of neurological conditions
High-performers and specialists in neuroscience research
Hundreds of methane super-sources pinpointed in satellite data
How a potent immune therapy loses its punch against a blood cancer
‘Milestone’ study suggests microbiome-boosting foods can treat severe malnutrition
If approach holds up, it could “result in health benefits to millions of malnourished children worldwide,” experts say
Mild brain injuries don’t predispose kids to criminal behavior, Danish study suggests
But scientists say in some settings concussions may still contribute to risk of later criminal justice involvement
New advisory body needed to guide U.S. biomedical research policy, panel says
National Academy of Medicine report cites failure to address health inequities, life expectancy
Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by amyloid plaques and cognitive decline, the latter of which is thought to be driven by soluble oligomeric amyloid-β (oAβ). The dysregulation of G protein-gated inwardly rectifying K^(+) (GIRK; also known as Kir3) channels has been implicated in rodent models of AD. Here, seeking mechanistic insights, we uncovered a sex-dependent facet of GIRK-dependent signaling in AD-related amyloid pathophysiology. Synthetic...
Alzheimer's disease-linked risk alleles elevate microglial cGAS-associated senescence and neurodegeneration in a tauopathy model
The strongest risk factors for late-onset sporadic Alzheimer's disease (AD) include the ε4 allele of apolipoprotein E (APOE), the R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2), and female sex. Here, we combine APOE4 and TREM2^(R47H) (R47H) in female P301S tauopathy mice to identify the pathways activated when AD risk is the strongest, thereby highlighting detrimental disease mechanisms. We find that R47H induces neurodegeneration in 9- to 10-month-old female APOE4...
A tau dephosphorylation-targeting chimeraselectively recruits protein phosphatase-1 to ameliorate Alzheimer's disease and tauopathies
Abnormal accumulation of hyperphosphorylated tau (pTau) is a major cause of neurodegeneration in Alzheimer's disease (AD) and related tauopathies. Therefore, reducing pTau holds therapeutic promise for these diseases. Here, we developed a chimeric peptide, named D20, for selective facilitation of tau dephosphorylation by recruiting protein phosphatase 1 (PP1) to tau. PP1 is one of the active phosphatases that dephosphorylates tau. In both cultured primary hippocampal neurons and mouse models for...
Nuclear envelope budding inhibition slows down progerin-induced aging process
Progerin causes Hutchinson-Gilford progeria syndrome (HGPS), but how progerin accelerates aging is still an interesting question. Here, we provide evidence linking nuclear envelope (NE) budding and accelerated aging. Mechanistically, progerin disrupts nuclear lamina to induce NE budding in concert with lamin A/C, resulting in transport of chromatin into the cytoplasm where it is removed via autophagy, whereas emerin antagonizes this process. Primary cells from both HGPS patients and mouse models...