Dr. Erik D. Roberson M.D.
Neurologist | Neurology
400 Parnassus Ave # A840 San Francisco CA, 94143About
Dr. Erik Roberson is a distinguished Neurologist in San Francisco, CA. Dr. Roberson specializes in diagnosing, treating, and managing disorders of the brain and nervous system. With expertise in handling complex conditions like epilepsy, multiple sclerosis, and migraines, Dr. Roberson employs advanced techniques and personalized treatment plans to improve patient outcomes. As a neurologist, Dr. Roberson is committed to staying abreast of the latest developments in neurological research and therapies.
Board Certification
Psychiatry and NeurologyAmerican Board of Psychiatry and NeurologyABPN
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease.
- Frontotemporal dementia.
- 100 years and counting: prospects for defeating Alzheimer's disease.
- Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model.
- Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease.
- Loss of Hsp70 exacerbates pathogenesis but not levels of fibrillar aggregates in a mouse model of Huntington's disease.
- Beyond diagnosis: what biomarkers are teaching us about the "bio"logy of Alzheimer disease.
- Contemporary approaches to Alzheimer's disease and frontotemporal dementia.
- Step-by-step in situ hybridization method for localizing gene expression changes in the brain.
- Quantifying biomarkers of cognitive dysfunction and neuronal network hyperexcitability in mouse models of Alzheimer's disease: depletion of calcium-dependent proteins and inhibitory hippocampal remodeling.
- Mouse models of Alzheimer's disease.
- Frontotemporal degeneration, the next therapeutic frontier: molecules and animal models for frontotemporal degeneration drug development.
- Usp14 deficiency increases tau phosphorylation without altering tau degradation or causing tau-dependent deficits.
- Mouse models of frontotemporal dementia.
- Amyloid-β signals through tau to drive ectopic neuronal cell cycle re-entry in Alzheimer's disease.
Treatments
- Memory Disorders
Fellowships
- University of California Medical Center 2003
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