A5021126931- Neuroscience and Neuropharmacology Research
- Mast cells and histamine
- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Neurological Disease Mechanisms and Treatments
- Asthma and respiratory diseases
- Immune Response and Inflammation
- Neural dynamics and brain function
- Mitochondrial Function and Pathology
- Monoclonal and Polyclonal Antibodies Research
- Retinal Development and Disorders
- Neuroscience and Neural Engineering
- Circadian rhythm and melatonin
- Inflammation biomarkers and pathways
- Memory and Neural Mechanisms
- Immune Cell Function and Interaction
- Photoreceptor and optogenetics research
- Anesthesia and Neurotoxicity Research
New York University
2020-2024
NYU Langone Health
2023
Instituto Politécnico Nacional
2016
Center for Research and Advanced Studies of the National Polytechnic Institute
2011-2012
Universidad Nacional Autónoma de México
2011
Mast cells (MCs) control allergic reactions and contribute to protective innate immune responses through TLR4 activation. The tyrosine kinase Lyn is important the high affinity IgE receptor (FcεRI) signal transduction system in MCs, but its role on signalling cascade still elusive. Here, we characterized several TLR4-triggered bone marrow-derived mast (BMMCs) from wild-type (WT) −/− mice. We found that MCs secreted lower amounts of TNF-α after LPS challenge when compared with WT cells. BMMCs...
Abstract Mast cells produce proinflammatory cytokines in response to TLR4 ligands, but the signaling pathways involved are not fully described. In this study, participation of Src family kinase Fyn production TNF after stimulation with LPS was evaluated using bone marrow–derived mast from wild-type and Fyn-deficient mice. Fyn−/− showed higher LPS-induced secretion preformed de novo–synthesized TNF. both cell types, colocalized vesicle-associated membrane protein (VAMP)3-positive...
Abstract INTRODUCTION Anesthesia often exacerbates memory recall difficulties in individuals with Alzheimer's disease (AD), but the underlying mechanisms remain unclear. METHODS We used vivo Ca 2+ imaging, viral‐based circuit tracing, and chemogenetic approaches to investigate anesthesia‐induced remote impairment mouse models of presymptomatic AD. RESULTS Our study identified pyramidal neuron hyperactivity anterior cingulate cortex (ACC) as a significant contributor impairment. This ACC...
Abstract The selective vulnerability of hippocampal area CA 1 to ischemia‐induced injury is a well‐known phenomenon. However, the cellular mechanisms that confer resistance 3 against ischemic damage remain elusive. Here, we show oxygen–glucose deprivation–reperfusion ( OGD ‐ RP ), an in vitro model mimic pathological conditions stroke, increases phosphorylation level tropomyosin receptor kinase B (TrkB) 3. Slices preincubated with brain‐derived neurotrophic factor BDNF ) or...
Abstract We previously reported altered neuronal Ca 2+ dynamics in the motor cortex of 12-month-old JNPL3 tauopathy mice during quiet wakefulness or forced running, with a tau antibody treatment significantly restoring activity profile and decreasing pathological these 1 . Whether functional deficits occur at an early stage if is effective younger needed further investigation. In addition, network firing patterns have not been well studied behaving models. this study, we first performed vivo...
Abstract Tau protein truncated at aspartate 421 (Asp421) is a characteristic feature of Alzheimer’s disease (AD) and other tauopathies. It likely to have role in their pathogenesis by promoting tau aggregation. Here, using two tauopathy mouse models, we show that monoclonal antibody against Asp421, 5G2, led a) 59-74% clearance insoluble the brains JNPL3 mice following thirteen-week treatment period, b) 46% decrease levels brain interstitial fluid immediately single dose 5G2 as examined...
Abstract INTRODUCTION It is unclear how early neuronal deficits occur in tauopathies, if these are associated with changes network activity, and they can be alleviated therapies. METHODS To address this, we performed vivo two‐photon Ca 2+ imaging tauopathy mice at 6 versus 12 months, compared to controls, treated the younger animals a tau antibody. RESULTS Neuronal function was impaired months but did not deteriorate further presumably because cortical burden comparable ages. At neurons were...
Abstract Background Microglia are the main innate immune cells capable of engulfing dead and cellular debris in brain. Trem2 receptor is expressed microglia plays an important role phagocytosis. This has been linked to Alzheimer’s disease involved uptake amyloid plaques by microglia. However, how engulf this process remain unclear. Method We used two‐photon microscopy image primary motor cortex Cx3cr1 gfp/+ mice, :Trem2 ‐/‐ R47H/+ Thy GCaMP6 mice. These mice were placed on a custom made,...
Abstract Background We crossed mouse models Thy‐1 GCaMP6 , Cx3cr1 CreER :tdTomato flox and GFP with PS19 P301S tauopathy mice to visualize neuronal calcium microglia structural dynamics in vivo during the progression of tau pathology after immunotherapy. Method By using two‐photon live imaging head‐restrained attached a custom‐made, free‐floating treadmill, we examined activity L2/3 pyramidal neurons motor cortex two intravenous antibody injections targeting truncated Asp421 epitope tau....