Dr. Sami Jihad Barmada MD, PHD
Neurologist | Neurology
505 Parnassus Ave Box 0114 San Francisco CA, 94143About
Dr. Sami Barmada is a distinguished Neurologist in San Francisco, CA. Dr. Barmada 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. Barmada employs advanced techniques and personalized treatment plans to improve patient outcomes. As a neurologist, Dr. Barmada is committed to staying abreast of the latest developments in neurological research and therapies.
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Expert Publications
Data provided by the National Library of Medicine- Genetic defects in acetylcholine signalling promote protein degradation in muscle cells of Caenorhabditis elegans.
- Visualization of prion infection in transgenic mice expressing green fluorescent protein-tagged prion protein.
- Opposed growth factor signals control protein degradation in muscles of Caenorhabditis elegans.
- Prion protein with an octapeptide insertion has impaired neuroprotective activity in transgenic mice.
- GFP-tagged mutant prion protein forms intra-axonal aggregates in transgenic mice.
- Prion protein with an insertional mutation accumulates on axonal and dendritic plasmalemma and is associated with distinctive ultrastructural changes.
- Cytoplasmic mislocalization of TDP-43 is toxic to neurons and enhanced by a mutation associated with familial amyotrophic lateral sclerosis.
- Pathogenic TARDBP mutations in amyotrophic lateral sclerosis and frontotemporal dementia: disease-associated pathways.
- Progranulin deficiency promotes neuroinflammation and neuron loss following toxin-induced injury.
- Inhibition of RNA lariat debranching enzyme suppresses TDP-43 toxicity in ALS disease models.
- Astrocyte pathology and the absence of non-cell autonomy in an induced pluripotent stem cell model of TDP-43 proteinopathy.
- Autophagy induction enhances TDP43 turnover and survival in neuronal ALS models.
- Linking RNA Dysfunction and Neurodegeneration in Amyotrophic Lateral Sclerosis.
- Amelioration of toxicity in neuronal models of amyotrophic lateral sclerosis by hUPF1.
- Distinct C9orf72-Associated Dipeptide Repeat Structures Correlate with Neuronal Toxicity.
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