A5084303709- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- MicroRNA in disease regulation
- Autophagy in Disease and Therapy
- Neurological Disease Mechanisms and Treatments
- Alzheimer's disease research and treatments
- Extracellular vesicles in disease
- Endoplasmic Reticulum Stress and Disease
- Cancer-related molecular mechanisms research
- RNA modifications and cancer
- Energy and Environment Impacts
- Immune Cell Function and Interaction
- Nerve injury and regeneration
- Neonatal and fetal brain pathology
- ATP Synthase and ATPases Research
- Connexins and lens biology
- Neuroscience and Neuropharmacology Research
- Sirtuins and Resveratrol in Medicine
- Kruppel-like factors research
- Machine Learning in Bioinformatics
- PI3K/AKT/mTOR signaling in cancer
Albert Einstein College of Medicine
2022-2025
Temple University
2018-2021
Temple University Hospital
2018-2021
Activation of microglia is a prominent pathological feature in tauopathies, including Alzheimer's disease. How activation contributes to tau toxicity remains largely unknown. Here we show that nuclear factor kappa-light-chain-enhancer activated B cells (NF-κB) signaling, by tau, drives microglial-mediated propagation and toxicity. Constitutive microglial NF-κB exacerbated, while inactivation diminished, seeding spreading young PS19 mice. Inhibition enhanced the retention reduced release...
Aging leads to progressive decline in organ and tissue integrity function, partly due loss of proteostasis autophagy malfunctioning. A decrease with age chaperone-mediated (CMA), a selective type lysosomal degradation, has been reported various organs cells from rodents humans. Disruption CMA recapitulates features aging, whereas activating mice protects against age-related diseases such as Alzheimer's, retinal degeneration and/or atherosclerosis. However, sex-specific cell-type-specific...
Chaperone-mediated autophagy (CMA) is a selective form of that contributes to the maintenance cellular homeostasis. CMA activity declines with age in most tissues and systems, including immune system, due reduction levels lysosome-associated membrane protein type 2A (LAMP2A), an essential component. In this study, we show overexpressing copy hLAMP2A within T cells since middle-age can prevent some their age-associated loss function. Our data support idea preserving LAMP2A expression through...
Oligodendrocyte precursor cells (OPCs) are essential for developmental myelination and oligodendrocyte regeneration after CNS injury. These progenitors express calcium-permeable AMPA receptors (AMPARs) form direct synapses with neurons throughout the CNS, but roles of this signaling unclear. To enable selective alteration properties AMPARs in oligodendroglia, we generate mice that allow cell-specific overexpression EGFP-GluA2 vivo. In healthy conditions, OPC-specific GluA2 significantly...
Abstract Autophagy is essential for protein quality control and regulation of the functional proteome. Failure autophagy pathways with age contributes to loss proteostasis in aged organisms accelerates progression age‐related diseases. In this work, we show that activity endosomal microautophagy (eMI), a selective type occurring late endosomes, declines identify sub‐proteome affected by function. Proteomics endosomes from old mice revealed an aberrant glycation signature Hsc70, chaperone...
Oligodendrocytes (OLs), the myelin-forming CNS glia, are highly vulnerable to cellular stresses, and a severe myelin loss underlies numerous disorders. Expedited OL regeneration may prevent further axonal damage facilitate functional repair. Although adult progenitors (OPCs) primary players for regeneration, targetable OPC-specific intracellular signaling mechanisms facilitated remain elusive. Here, we report that OPC-targeted PTEN inactivation in mouse, contrast OL-specific manipulations,...
Abstract Dysregulation of autophagy, the lysosomal degradation intracellular components, has been universally described in cancer. While activity macroautophagy changes a context-dependent manner cancers, upregulation chaperone-mediated autophagy (CMA) is well-described all solid tumors studied to date. Upregulated CMA directly contributes both tumor growth and protection against anti-oncogenic interventions cancers. Selective pro-apoptotic proteins, such as mutant p53 PUMA, misfolded...
Calcium influx through ionotropic glutamate receptors expressed on non-excitable glia may regulate important cell events via subcellular signaling mechanisms. Oligodendrocytes and OPCs, two glial populations supporting CNS myelination myelin repair, express AMPA (AMPARs), but the role of AMPAR-mediated calcium in these is unclear. Here, we developed a mouse genetic system enabling cell-specific overexpression GluA2, calcium-impermeable subunit, blocked AMPARs oligodendroglia. Surprisingly,...