Kenneth J. Colodner

ORCID: 0000-0003-1830-3483
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neurobiology and Insect Physiology Research
  • Nerve injury and regeneration
  • Cellular transport and secretion
  • RNA regulation and disease
  • Hippo pathway signaling and YAP/TAZ
  • Neurofibromatosis and Schwannoma Cases
  • Cholinesterase and Neurodegenerative Diseases
  • interferon and immune responses
  • RNA Research and Splicing
  • Barrier Structure and Function Studies
  • Genetics, Aging, and Longevity in Model Organisms
  • MicroRNA in disease regulation
  • Complement system in diseases
  • Circadian rhythm and melatonin
  • Neuroscience and Neuropharmacology Research

Mount Holyoke College
2015-2023

Boston Children's Hospital
2015

Brigham and Women's Hospital
2005-2011

Harvard University
2005-2011

The complement system is part of the innate immune response responsible for removing pathogens and cellular debris, in addition to helping refine CNS neuronal connections via microglia-mediated pruning inappropriate synapses during brain development. However, less known about role normal aging. Here, we studied central component, C3, synaptic health We examined behavior as well electrophysiological, synaptic, changes brains C3 -deficient male mice ( KO) compared with age-, strain-,...

10.1523/jneurosci.1698-15.2015 article EN cc-by-nc-sa Journal of Neuroscience 2015-09-23

Although alterations in glial structure and function commonly accompany death of neurons neurodegenerative diseases, the role glia play modulating neuronal loss is poorly understood. We have created a model Alexander disease Drosophila by expressing disease-linked mutant versions fibrillary acidic protein (GFAP) fly glia. find aggregation human GFAP into inclusions bearing hallmarks authentic Rosenthal fibers. also observe significant toxicity to glia, which mediated oxidative stress. Both...

10.1523/jneurosci.3410-10.2011 article EN cc-by-nc-sa Journal of Neuroscience 2011-02-23

A subset of neurodegenerative tauopathies is characterized by abundant filamentous inclusions hyperphosphorylated tau in both neurons and glia. Although the contribution neuronal to behavioral changes loss diseases has been studied extensively, functional consequences deposition glial cells have less well characterized. To investigate role abnormal accumulation aggregation cells, we created a Drosophila model tauopathy expressing human wild-type adult fly cells. Glial expression resulted...

10.1523/jneurosci.2491-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-12-01

Although a number of studies have demonstrated proliferation nonneoplastic astrocytes in experimental animal models, the proliferative potential human has not been well defined. Using double-label immunohistochemistry, we identified proliferating cells with marker MIB-1 and glial fibrillary acidic protein staining biopsy autopsy tissue. labeling was monitored variety conditions containing significant numbers reactive astrocytes, including infections, arteriovenous malformations,...

10.1093/jnen/64.2.163 article EN Journal of Neuropathology & Experimental Neurology 2005-02-01

Abstract Neurofibromatosis type 1 is a chronic multisystemic genetic disorder that results from loss of function in the neurofibromin protein. Neurofibromin may regulate metabolism, though underlying mechanisms remain largely unknown. Here we show regulates metabolic homeostasis Drosophila via discrete neuronal circuit. Loss increases rate Ras GAP-related domain-dependent mechanism, feeding homeostatically, and alters lipid stores turnover kinetics. The increase independent locomotor...

10.1038/s41467-021-24505-x article EN cc-by Nature Communications 2021-07-13

Tauopathies are a class of neurodegenerative diseases characterized by the abnormal phosphorylation and accumulation microtubule-associated protein, Tau. These associated with degeneration dysfunction noradrenergic system, critical regulator memory, locomotion, fight or flight response. Though Tau pathology accumulates early in neurons, relationship between noradrenaline signaling tauopathy pathogenesis remains unclear. The fruit fly, Drosophila melanogaster, is valuable model organism...

10.1016/j.neulet.2021.135937 article EN cc-by Neuroscience Letters 2021-04-25

The blood-brain barrier (BBB) is a multicellular construct that regulates the diffusion and transport of metabolites, ions, toxins, inflammatory mediators into out central nervous system (CNS). Its integrity essential for proper brain physiology, its breakdown has been shown to contribute neurological dysfunction. BBB in vertebrates exists primarily through coordination between endothelial cells, pericytes, astrocytes, while invertebrates, which lack vascularized circulatory system,...

10.3390/ijms24031886 article EN International Journal of Molecular Sciences 2023-01-18

Tauopathies are a class of neurodegenerative diseases characterized by the abnormal phosphorylation and accumulation microtubule-associated protein, tau, in both neuronal glial cells. Though tau pathology cells is prominent feature many these disorders, pathological contribution lesions to tauopathy pathogenesis remains largely unknown. Moreover, while predominantly found central nervous system, role for peripheral system has been described, though not well characterized. To investigate...

10.1371/journal.pone.0226380 article EN cc-by PLoS ONE 2019-12-10

ABSTRACT Neurofibromatosis type 1 (NF1) is a genetic disorder predisposing patients to range of features, the most characteristic which include areas abnormal skin pigmentation and benign tumors associated with peripheral nerves, termed neurofibromas. Less common, but more serious symptoms also malignant nerve sheath tumors, other malignancies, learning disabilities. The NF1 gene encodes neurofibromin, large protein that functions as negative regulator Ras signaling mediates pleiotropic...

10.1101/834788 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-11-08
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