Professor, Anesthesiology, University of Maryland School of Medicine
Neurology
Dr. Alan I. Faden, MD
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Alan I. Faden, MD is an expert in the field of Neurology. He went to University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine is ranked 10 in research and 19 in primary care medicine He received awards:"Whos Who in Medicine and Healthcare". Alan Faden is a published doctor and has 101 publications published. The lastest was: 'Structure and expression of a rat kappa opioid receptor gene.'
Publications
- Cell cycle inhibition limits development and maintenance of neuropathic pain following spinal cord injury.
- Progressive inflammation-mediated neurodegeneration after traumatic brain or spinal cord injury.
- Microglial/macrophage polarization dynamics following traumatic brain injury.
- Ablation of the transcription factors E2F1-2 limits neuroinflammation and associated neurological deficits after contusive spinal cord injury.
- Function and mechanisms of autophagy in brain and spinal cord trauma.
- Acyl-2-aminobenzimidazoles: A novel class of neuroprotective agents targeting mGluR5.
- Voluntary exercise preconditioning activates multiple anti-apoptotic mechanisms and improves neurological recovery after experimental traumatic brain injury.
- Chronic Neurodegeneration After Traumatic Brain Injury: Alzheimer Disease, Chronic Traumatic Encephalopathy, or Persistent Neuroinflammation?
- Novel mGluR5 Positive Allosteric Modulator Improves Functional Recovery, Attenuates Neurodegeneration, and Alters Microglial Polarization after Experimental Traumatic ...
- Selective CDK inhibitors: promising candidates for future clinical traumatic brain injury trials.
- Chronic decrease in wakefulness and disruption of sleep-wake behavior after experimental traumatic brain injury.
- Isolated spinal cord contusion in rats induces chronic brain neuroinflammation, neurodegeneration, and cognitive impairment.
- Isolated spinal cord contusion in rats induces chronic brain neuroinflammation, neurodegeneration, and cognitive impairment: Involvement of cell cycle activation.
- Repeated mild traumatic brain injury causes chronic neuroinflammation, changes in hippocampal synaptic plasticity, and associated cognitive deficits.
- Inhibition of amyloid precursor protein secretases reduces recovery after spinal cord injury.
- Boc-protected 1-(3-oxocycloalkyl)ureas via a one-step Curtius rearrangement: mechanism and scope.
- Progressive neurodegeneration after experimental brain trauma: association with chronic microglial activation.
- PARP-1 Inhibition Attenuates Neuronal Loss, Microglia Activation and Neurological Deficits after Traumatic Brain Injury.
- CR8, a novel inhibitor of CDK, limits microglial activation, astrocytosis, neuronal loss, and neurologic dysfunction after experimental traumatic brain injury.
- Neurotherapeutics: Concept, Translation, Transition.
- Positive Allosteric Modulators (PAMs) of Metabotropic Glutamate Receptor 5 (mGluR5) Attenuate Microglial Activation.
- Neuroprotective effects of geranylgeranylacetone in experimental traumatic brain injury.
- Cell cycle activation contributes to increased neuronal activity in the posterior thalamic nucleus and associated chronic hyperesthesia after rat spinal cord contusion.
- TrkB.T1 Contributes to Neuropathic Pain after Spinal Cord Injury through Regulation of Cell Cycle Pathways.
- Estimation of Ligand Efficacies of Metabotropic Glutamate Receptors from Conformational Forces Obtained from Molecular Dynamics Simulations.
- Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states.
- Late exercise reduces neuroinflammation and cognitive dysfunction after traumatic brain injury.
- Activation of mGluR5 and Inhibition of NADPH Oxidase Improves Functional Recovery after Traumatic Brain Injury.
- CR8, a Selective and Potent CDK Inhibitor, Provides Neuroprotection in Experimental Traumatic Brain Injury.
- Delayed inflammatory mRNA and protein expression after spinal cord injury.
- Cyclin D1 Gene Ablation Confers Neuroprotection in Traumatic Brain Injury.
- Microglial activation and traumatic brain injury.
- Selective CDK inhibitor limits neuroinflammation and progressive neurodegeneration after brain trauma.
- Cell cycle activation and spinal cord injury.
- Modulation of ABCA1 by an LXR agonist reduces beta-amyloid levels and improves outcome after traumatic brain injury.
- Transitions and transformations.
- Neuropathological differences between rats and mice after spinal cord injury.
- Cell death mechanisms and modulation in traumatic brain injury.
- Cell cycle activation and CNS injury.
- Activation of metabotropic glutamate receptor 5 improves recovery after spinal cord injury in rodents.
- Activation of metabotropic glutamate receptor 5 modulates microglial reactivity and neurotoxicity by inhibiting NADPH oxidase.
- Metabotropic glutamate receptor 5 activation inhibits microglial associated inflammation and neurotoxicity.
- Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury.
- Multifunctional drug treatment in neurotrauma.
- Metabotropic glutamate receptors as targets for multipotential treatment of neurological disorders.
- Roscovitine reduces neuronal loss, glial activation, and neurologic deficits after brain trauma.
- Cortical injury increases cholesterol 24S hydroxylase (Cyp46) levels in the rat brain.
- Role of cell cycle proteins in CNS injury.
- Neuroprotection: challenges and opportunities.
- Changing the name of the journal.
- Expression of two temporally distinct microglia-related gene clusters after spinal cord injury.
- Neuroprotective effects of selective group II mGluR activation in brain trauma and traumatic neuronal injury.
- Metabotropic glutamate receptor subtype 5 antagonists MPEP and MTEP.
- Role of the cell cycle in the pathobiology of central nervous system trauma.
- Gene expression profiling of experimental traumatic spinal cord injury as a function of distance from impact site and injury severity.
- Novel neuroprotective tripeptides and dipeptides.
- Ceramide induces neuronal apoptosis through mitogen-activated protein kinases and causes release of multiple mitochondrial proteins.
- Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury.
- In vivo and in vitro characterization of novel neuronal plasticity factors identified following spinal cord injury.
- Neuronal plasticity after spinal cord injury: identification of a gene cluster driving neurite outgrowth.
- Caspase inhibitor z-DEVD-fmk attenuates calpain and necrotic cell death in vitro and after traumatic brain injury.
- The pathobiology of moderate diffuse traumatic brain injury as identified using a new experimental model of injury in rats.
- BOK and NOXA are essential mediators of p53-dependent apoptosis.
- The "dark side" of endocannabinoids: a neurotoxic role for anandamide.
- Mechanisms of neural cell death: implications for development of neuroprotective treatment strategies.
- Modulation of stretch-induced enhancement of neuronal NMDA receptor current by mGluR1 depends upon presence of glia.
- Gene expression profile changes are commonly modulated across models and species after traumatic brain injury.
- Gene profiling in spinal cord injury shows role of cell cycle in neuronal death.
- Ceramide-induced neuronal apoptosis is associated with dephosphorylation of Akt, BAD, FKHR, GSK-3beta, and induction of the mitochondrial-dependent intrinsic caspase p...
- Neuroprotective and nootropic actions of a novel cyclized dipeptide after controlled cortical impact injury in mice.
- Novel diketopiperazine enhances motor and cognitive recovery after traumatic brain injury in rats and shows neuroprotection in vitro and in vivo.
- Ceramide induces neuronal apoptosis through the caspase-9/caspase-3 pathway.
- Multiple caspases are activated after traumatic brain injury: evidence for involvement in functional outcome.
- Neuronal and glial mGluR5 modulation prevents stretch-induced enhancement of NMDA receptor current.
- Ceramide-induced cell death in primary neuronal cultures: upregulation of ceramide levels during neuronal apoptosis.
- Thyrotropin-releasing hormone improves neurologic recovery after spinal trauma in cats.
- Thyrotropin releasing hormone improves blood pressure and survival in endotoxic shock.
- Treatment of experimental stroke: comparison of naloxone and thyrotropin releasing hormone.
- Neuropeptides and spinal cord injury.
- Action of naloxone and TRH on the autonomic regulation of circulation.
- Spinal shock and injury: experimental therapeutic approaches.
- Progressive isolated segmental anhidrosis.
- Comparison of early and late naloxone treatment in experimental spinal injury.
- Naloxone reverses the pathophysiology of shock through an antagonism of endorphin systems.
- A role for endorphins in the pathophysiology of spinal cord injury.
- Dopamine partially mediates the cardiovascular effects of naloxone after spinal injury.
- Disclosure of information to patients in medical care.
- Disclosure standards and informed consent.
- Hypophysectomy alters cardiorespiratory variables: central effects of pituitary endorphins in shock.
- Naloxone treatment of endotoxin shock: stereospecificity of physiologic and pharmacologic effects in the rat.
- Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.
- Opiate antagonist improves neurologic recovery after spinal injury.
- Treatment with thyrotropin-releasing hormone (TRH) in patients with traumatic spinal cord injuries.
- Intrathecal dynorphin-A infusion in rat spinal cord causes energy depletion, edema and neurologic dysfunction.
- Sequential expression of c-fos protooncogene, TNF-alpha, and dynorphin genes in spinal cord following experimental traumatic injury.
- Effects of acute ethanol intoxication on experimental brain injury in the rat: neurobehavioral and phosphorus-31 nuclear magnetic resonance spectroscopy studies.
- Neuroprotective effects of 619C89, a use-dependent sodium channel blocker, in rat traumatic brain injury.
- N-methyl-D-aspartate receptors mediate post-traumatic increases of protein kinase C in rat brain.
- High- and low-affinity NMDA receptor-binding sites in rat spinal cord: effects of traumatic injury.
- Structure and expression of a rat kappa opioid receptor gene.
Schools
U Of Chgo Div Of Bio Sci Pritzker Sch Of Med
Doctors Specialties
- Neurology
Accepted Insurances
Awards
- Whos Who in Medicine and Healthcare
Education
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UCSF -
University of Pennsylvania -
University of Chicago Pritzker School of Medicine
Hospital
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University of Maryland Medical Center -
MedStar Georgetown University Hospital
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