President, South Florida ENT Associates, P.A.
Otolaryngology (ENT)
Dr. Jonathan D. Cooper, MD
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Jonathan D. Cooper practices Otolaryngology (ENT). He graduated from New York Medical College. He received 2 awards: "CMS Meaningful Use Stage 1 Certification" and "Fellow (FAAO-HNS)". Jonathan Cooper has written publications. He has 36 publications published with PubMed. The lastest paper is: 'Nonclinical evaluation of CNS-administered TPP1 enzyme replacement in canine CLN2 neuronal ceroid lipofuscinosis.'
Publications
- An Anti-Neuroinflammatory That Targets Dysregulated Glia Enhances the Efficacy of CNS-Directed Gene Therapy in Murine Infantile Neuronal Ceroid Lipofuscinosis.
- Nonclinical evaluation of CNS-administered TPP1 enzyme replacement in canine CLN2 neuronal ceroid lipofuscinosis.
- Partial Correction of the CNS Lysosomal Storage Defect in a Mouse Model of Juvenile Neuronal Ceroid Lipofuscinosis by Neonatal CNS Administration of an Adeno-Associate...
- Pathogenesis and therapies for infantile neuronal ceroid lipofuscinosis (infantile CLN1 Disease).
- Contrasting Effects of Haloperidol and Lithium on Rodent Brain Structure: A Magnetic Resonance Imaging Study with Postmortem Confirmation.
- Early glial activation, synaptic changes and axonal pathology in the thalamocortical system of Niemann-Pick type C1 mice.
- Cln5-deficiency in mice leads to microglial activation, defective myelination and changes in lipid metabolism.
- Early Microglial Activation Precedes Neuronal Loss in the Brain of the Cstb-/- Mouse Model of Progressive Myoclonus Epilepsy, EPM1.
- Morphologic and Functional Correlates of Synaptic Pathology in the Cathepsin D Knockout Mouse Model of Congenital Neuronal Ceroid Lipofuscinosis.
- Galactolipid deficiency in the early pathogenesis of neuronal ceroid lipofuscinosis model Cln8(mnd) : implications to delayed myelination and oligodendrocyte maturation.
- Intravenous administration of AAV2/9 to the fetal and neonatal mouse leads to differential targeting of CNS cell types and extensive transduction of the nervous system.
- Loss of amyloid precursor protein in a mouse model of Niemann-Pick type C disease exacerbates its phenotype and disrupts tau homeostasis.
- Insulin receptor substrate 2 is a negative regulator of memory formation.
- Distinct neuropathologic phenotypes after disrupting the chloride transport proteins ClC-6 or ClC-7/Ostm1.
- DHHC5 interacts with PDZ domain 3 of post-synaptic density-95 (PSD-95) protein and plays a role in learning and memory.
- Neuroprotection of host cells by human central nervous system stem cells in a mouse model of infantile neuronal ceroid lipofuscinosis.
- Progressive thalamocortical neuron Loss in Cln5 deficient mice: Distinct effects in Finnish variant late infantile NCL.
- Cerebellar pathology and motor deficits in the palmitoyl protein thioesterase 1-deficient mouse.
- Location and connectivity determine GABAergic interneuron survival in the brains of South Hampshire sheep with CLN6 neuronal ceroid lipofuscinosis.
- Moving towards therapies for juvenile Batten Disease?
- Intraventricular enzyme replacement improves Disease phenotypes in a mouse model of late infantile neuronal ceroid lipofuscinosis.
- Synaptic changes in the thalamocortical system of cathepsin D-deficient mice: a model of human congenital neuronal ceroid-lipofuscinosis.
- IgG entry and deposition are components of the neuroimmune response in Batten Disease.
- Successive neuron Loss in the thalamus and cortex in a mouse model of infantile neuronal ceroid lipofuscinosis.
- Visual deficits in a mouse model of Batten disease are the result of optic nerve degeneration and Loss of dorsal lateral geniculate thalamic neurons.
- CNS-directed AAV2-mediated gene therapy ameliorates functional deficits in a murine model of infantile neuronal ceroid lipofuscinosis.
- High resolution 1H NMR-based metabolomics indicates a neurotransmitter cycling deficit in cerebral tissue from a mouse model of Batten Disease.
- Thalamocortical neuron Loss and localized astrocytosis in the Cln3Deltaex7/8 knock-in mouse model of Batten disease.
- Glial activation spreads from specific cerebral foci and precedes neurodegeneration in presymptomatic ovine neuronal ceroid lipofuscinosis (CLN6).
- FGFR3 regulates brain size by controlling progenitor cell proliferation and apoPtosis during embryonic development.
- Regional and cellular neuropathology in the palmitoyl protein thioesterase-1 null mutant mouse model of infantile neuronal ceroid lipofuscinosis.
- p38alpha stress-activated protein kinase phosphorylates neurofilaments and is associated with neurofilament pathology in amyotrophic lateral sclerosis.
- The neuronal adaptor protein X11alpha reduces Abeta levels in the brains of Alzheimer's APPswe Tg2576 transgenic mice.
- Identification of a novel, membrane-associated neuronal kinase, cyclin-dependent kinase 5/p35-regulated kinase.
- A murine model of variant late infantile ceroid lipofuscinosis recapitulates behavioral and pathological phenotypes of human Disease.
Schools
New York Medical College
Jackson Meml Hospital University Miami
Union College
Procedures Preformed
- Antrostomy and Antrotomy (Sinus Surgery)
- Balloon Sinuplasty
- Diagnostic Nasal and-or Sinus Endoscopy
- Ear Surgery
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Conditions Treated
- Acoustic Neuroma
- Acute Sinusitis
- Acute Tonsillitis
- Allergic Rhinitis
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Doctors Specialties
- Ear, Nose, and Throat
- Otolaryngology (ENT)
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
- Fellow (FAAO-HNS)
Education
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Jackson Memorial Hospital - Jackson Health System -
New York Medical College
Drug Facts
| NPI NUMBER | 1407856222 | |
| NPPES Provider LastName | COOPER | |
| NPPES Provider FirstName | JONATHAN | |
| NPPES Provider ZIPCode | 333262394 | |
| NPPES Provider State | FL | |
| Specialty Description | Otolaryngology | |
| Total Claim Count | 677.0 | |
| Distinct Opioid Count | 1.0 | |
| Opioid Claim Count | 16.0 | |
| Percent Opioid Claims | 2.36 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1407856222 |
| Last Name Of The Provider | COOPER |
| First Name Of The Provider | JONATHAN |
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