A5088994386- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Immune cells in cancer
- Neuroscience and Neural Engineering
- Neurogenesis and neuroplasticity mechanisms
- Phosphorus compounds and reactions
- S100 Proteins and Annexins
- Barrier Structure and Function Studies
- Neural dynamics and brain function
- Photoreceptor and optogenetics research
- Crystal structures of chemical compounds
- Polymer Synthesis and Characterization
- COVID-19 Clinical Research Studies
- Long-Term Effects of COVID-19
- Birth, Development, and Health
- Synthesis and Reactivity of Sulfur-Containing Compounds
- Memory and Neural Mechanisms
- Extracellular vesicles in disease
- Diet and metabolism studies
- Synthesis of β-Lactam Compounds
- Neuroscience and Neuropharmacology Research
- interferon and immune responses
- MicroRNA in disease regulation
- Cholesterol and Lipid Metabolism
UK Dementia Research Institute
2024-2025
University College London
2024-2025
Broad Institute
2022-2023
DePaul University
2020-2022
Belden (United States)
2021
Northwestern University
2020
Abstract Microglia and complement can mediate neurodegeneration in Alzheimer’s disease (AD). By integrative multi-omics analysis, here we show that astrocytic microglial proteins are increased Tau P301S synapse fractions with age a C1q-dependent manner. In addition to microglia, identified astrocytes contribute substantially elimination hippocampi. Notably, found relatively more excitatory marker lysosomes, whereas lysosomes contained inhibitory material. C1q deletion reduced...
Complement overactivation mediates microglial synapse elimination in neurological diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but how complement activity is regulated the brain remains largely unknown. We identified that secreted neuronal pentraxin Nptx2 binds C1q thereby regulates its brain. Nptx2-deficient mice show increased activity, C1q-dependent engulfment, loss of excitatory synapses. In a neuroinflammation culture model aged TauP301S mice,...
Reduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer's disease (AD), but the underlying assumption that neurons are main source pathogenic Aβ is untested. Here, we challenge this prevailing belief by demonstrating oligodendrocytes an important human brain and play a key role promoting abnormal neuronal hyperactivity AD knock-in mouse model. We show selectively suppressing oligodendrocyte production improves pathology restores function model vivo. Our findings...
Alzheimer's disease (AD) is initiated by amyloid-beta (Aβ) accumulation in the neocortex; however, cortical layers and neuronal cell types first susceptible to Aβ remain unknown. Using vivo two-photon Ca2+ imaging visual cortex of AD mouse models, we found that layer 5 neurons displayed abnormally prolonged transients before substantial plaque formation. Neuropixels recordings revealed these abnormal were associated with reduced spiking impaired tuning parvalbumin (PV)-positive fast-spiking...
Ionic conductivity and membrane capacitance are two foundational parameters that govern neuron excitability. Conventional optogenetics has emerged as a powerful tool to temporarily manipulate ionic in intact biological systems. However, no analogous method exists for precisely manipulating cell enable long-lasting modulation of neuronal Genetically targetable chemical assembly conductive insulating polymers can modulate capacitance, but further development this technique been hindered by...
Reduction of amyloid beta (Aβ) has been shown to be effective in treating Alzheimer’s Disease (AD), but the underlying assumption that neurons are main source pathogenic Aβ is untested. Here we challenge this prevailing belief by demonstrating oligodendrocytes an important Aβ, and play a key role promoting abnormal neuronal hyperactivity AD. We show selectively suppressing oligodendrocyte production improves AD brain pathology restores function vivo . Our findings suggest targeting could...
A-Kinase Anchoring Protein 11 (AKAP11) is a shared genetic risk factor for schizophrenia and bipolar disorder, yet its role in the brain remains poorly understood. Through multi-omic analysis of Akap11 mutant mouse brains cultured astrocytes, we identified significant transcriptomic, proteomic, metabolomic alterations. Key findings include upregulation cholesterol fatty acid metabolic pathways, accumulation lipid species such as cholesteryl esters, triacylglycerols, ceramides,...
Novel trisubstituted ethylenes, alkoxy ring-substituted octyl phenylcyanoacrylates, RPhCH=C(CN)CO 2 CH (CH ) 6 3 (where R is 2-methoxy, 3-methoxy, 4-methoxy, 2-ethoxy, 3-ethoxy, 4-ethoxy, 4-propoxy, 4-butoxy, 4-hexyloxy) were prepared and copolymerized with styrene. The ethylenes synthesized by the piperidine catalyzed Knoevenagel condensation of benzaldehydes cyanoacetate, characterized CHN analysis, IR, 1 H 13 C NMR. All styrene in solution radical initiation (ABCN) at 70°C. compositions...
Novel alkoxy ring-substituted octyl phenylcyanoacrylates, RPhCH=C(CN)CO2CH2(CH2)6CH3 (where R is 2-methoxy, 3-methoxy, 4-methoxy, 2-ethoxy, 3-ethoxy, 4-ethoxy, 4-propoxy, 4-butoxy, 4-hexyloxy) were prepared and copolymerized with styrene. The acrylates synthesized by the piperidine catalyzed Knoevenagel condensation of benzaldehydes cyanoacetate, characterized CHN analysis, IR, 1H 13C NMR. All styrene in solution radical initiation (ABCN) at 70C. compositions copolymers calculated from...
Abstract Complement overactivation mediates microglial synapse elimination in neurological diseases like Alzheimer’s disease and frontotemporal dementia (FTD), but how complement activity is regulated the brain remains largely unknown. We identified that secreted neuronal pentraxin Nptx2 binds C1q thereby regulates its brain. Nptx2-deficient mice show increased C1q-dependent engulfment loss of excitatory synapses. In a neuroinflammation culture model aged TauP301S mice, AAV-mediated...