Aggregator
Evidence of the pair-instability gap from black-hole masses
Electric dipole moment drives the dynamics of the TNFR1 complex I signalosome
Moiré engineering of Cooper-pair density modulation states
A µ-opioid receptor superagonist analgesic with minimal adverse effects
Dopaminergic mechanisms of dynamical social specialization
Developmental organization of sensory and sympathetic ganglia
Gene regulatory landscape dissected by single-cell four-omics sequencing
The 1000 Chinese Pangenome empowers medical and population genetics
Entanglement and electronic coherence in attosecond molecular photoionization
DNA damage burden causes selective CUX2 neuron loss in neuroinflammation
These advanced solar cells have an antique source: old bullets
These scientists chased a jet to learn more about ‘lean-burn’ contrails
Structural modifications in strain-engineered bilayer nickelate thin films
100 years of synthetic fuels
Trippy tobacco? Plants engineered to make five psychedelics at once
Approach could enable production of new medications for depression, anxiety, and post-traumatic stress
Alzheimer's disease pathology degrades an NMDA receptor-dependent spontaneous activity pattern in cortico-hippocampal circuits
Memory-based cognition relies on the integrity of cortico-hippocampal circuits, which are compromised in Alzheimer's disease (AD) as β-amyloid (Aβ) and tau accumulate. However, the mechanisms linking this pathology to circuit dysfunction remain unclear. In mouse models, using in vivo two-photon and Neuropixels recordings, we show that Aβ-tau pathology promotes both region- and layer-specific impairments, involving reduced burst firing in superficial cortical layers and CA1 and reduced mean...
GLP-1 receptor agonist fails to halt Alzheimer's disease
No abstract
Large-scale CSF and plasma proteomics reveal immune, synaptic, and extracellular matrix disruptions across neurodegenerative diseases
Neurodegenerative diseases (NDs), including Alzheimer's disease (AD), Parkinson's disease (PD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD), share overlapping clinical and pathological features. We analyzed cerebrospinal fluid (CSF) and plasma proteomes from 2,705 and 3,009 samples, respectively, across these NDs, identifying disease-specific and shared molecular signatures. CSF showed more disease-associated proteins than plasma, with AD and DLB exhibiting the strongest...
Recapitulation of plaque formation, tau pathology, and neurodegeneration in a human 3D matrix model of Alzheimer's disease
This study aims at implementing a 3D cell culture model of Alzheimer's disease (AD). To that end we engineered human induced pluripotent stem cell (iPSC)-derived neural stem cells to conditionally overexpress FAD mutant APP and PSEN1 variants. After differentiation in 3D basement membrane matrices, cultures exhibited increased Aβ(42) and Aβ(40) levels and a highly pathogenic shift of the Aβ(42/40) ratio. Typical AD phenotypes such as amyloid deposition and tau pathology were observed alongside...
Characterizing spatiotemporal white matter hyperintensity pathophysiology in vivo to disentangle vascular and neurodegenerative contributions
White matter hyperintensities (WMHs) are neuroimaging markers widely interpreted as caused by cerebral small vessel disease, yet emerging evidence suggests that a subset may have a neurodegenerative etiology. Current imaging methods have lacked the specificity to disentangle biological processes underlying WMHs in vivo. Here, we used voxel-level normative modeling and seven microstructural MRI markers with complementary biophysical sensitivities to generate single-subject high-resolution WMH...