Dr. Zahed is a board-certified, fellowship-trained neurologist with the Stanford Medicine Movement Disorders Center. She is also a clinical assistant professor in the Department of Neurology and Neurological Sciences.

She diagnoses and treats a wide range of movement disorders including Parkinson’s disease, Huntington’s disease, essential tremor, dystonia, and ataxia. She creates a personalized treatment plan for each of her patients using a variety of treatment options, including pharmacological and non-pharmacological options, deep brain stimulation (DBS) treatment for Parkinson's disease and tremors, and botulinum toxin injections for movement disorders and spasticity.

Prior to joining Stanford University, Dr. Zahed completed a neurology residency and fellowship in movement disorders at University of California, San Francisco (UCSF), where she also earned her MD and PhD in biomedical sciences. Dr. Zahed’s research interests include understanding the genetic and electrophysiological underpinnings of movement disorders and investigating applications of wearable technologies to monitor symptoms and improve the quality of life in patients with movement disorders. She also participates in clinical trials of new therapeutics for Parkinson’s disease and other movement disorders.

Dr. Zahed has published in Movement Disorders, Molecular Genetics & Genomic Medicine, The Journal of Clinical Investigation, American Journal of Human Genetics, Cell, and other peer-reviewed journals. She has presented to her peers at international, national, and regional meetings. These meetings have included the International Congress of Parkinson’s Disease and Movement Disorders, the Hereditary Disease Foundation Symposium, the World Society for Stereotactic and Functional Neurosurgery, and the Society for Neuroscience.

Dr. Zahed is a member of the International Parkinson and Movement Disorders Society.

Clinical Focus

  • Neurology

Academic Appointments

Professional Education

  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2021)
  • Residency: UCSF Dept of Neurology (2021) CA
  • Medical Education: University of California at San Francisco School of Medicine (2016) CA

All Publications

  • The Neurophysiology of Sleep in Parkinson's Disease. Movement disorders : official journal of the Movement Disorder Society Zahed, H., Zuzuarregui, J. R., Gilron, R., Denison, T., Starr, P. A., Little, S. 2021; 36 (7): 1526-1542


    Sleep disturbances are among the most common nonmotor complications of Parkinson's disease (PD), can present in prodromal stages, and progress with advancing disease. In addition to being a symptom of neurodegeneration, sleep disturbances may also contribute to disease progression. Currently, limited options exist to modulate sleep disturbances in PD. Studying the neurophysiological changes that affect sleep in PD at the cortical and subcortical level may yield new insights into mechanisms for reversal of sleep disruption. In this article, we review cortical and subcortical recording studies of sleep in PD with a particular focus on dissecting reported electrophysiological changes. These studies show that slow-wave sleep and rapid eye movement sleep are both notably disrupted in PD. We further explore the impact of these electrophysiological changes and discuss the potential for targeting sleep via stimulation therapy to modify PD-related motor and nonmotor symptoms. © 2021 International Parkinson and Movement Disorder Society.

    View details for DOI 10.1002/mds.28562

    View details for PubMedID 33826171

  • Using exome sequencing to decipher family history in a healthy individual: Comparison of pathogenic and population MTM1 variants. Molecular genetics & genomic medicine Penon, M., Zahed, H., Berger, V., Su, I., Shieh, J. T. 2018; 6 (5): 722-727


    When a family encounters the loss of a child early in life, extensive genetic testing of the affected neonate is sometimes not performed or not possible. However, the increasing availability of genomic sequencing may allow for direct application to families in cases where there is a condition inherited from parental gene(s). When neonatal testing is not possible, it is feasible to perform family testing as long as there is optimal interpretation of the genomic information. Here, we present an example of a healthy adult woman with a history of recurrent male neonatal losses due to severe respiratory distress who presented to Medical Genetics for evaluation. A family history of additional male neonatal loss was present, suggesting a potential inherited genetic etiology.Although there was no DNA available from the neonates, by performing exome sequencing on the healthy adult woman, we found a missense variant in MTM1 as a potential candidate, which was deemed pathogenic based on multiple criteria including past report.By performing an analysis of all known MTM1-disease associated mutations and control population variation, we can also better infer the effects of missense variations on MTM1, as not all variants are truncating. MTM1-X-linked myotubular myopathy is a condition that leads to male perinatal respiratory failure and a high risk for early mortality.The application of genetic testing in the healthy population here highlights the broader utility of genomic sequencing in evaluating unexplained recurrent neonatal loss, especially when genetic testing is not available on the affected neonates.

    View details for DOI 10.1002/mgg3.405

    View details for PubMedID 30047259

    View details for PubMedCentralID PMC6160706

  • Potential Role of Genomic Sequencing in the Early Diagnosis of Treatable Genetic Conditions. The Journal of pediatrics Zahed, H., Sparks, T. N., Li, B., Alsadah, A., Shieh, J. T. 2017; 189: 222-226.e1


    We present cases of 3 children diagnosed with the same genetic condition, Gitelman syndrome, at different stages using various genetic methods: panel testing, targeted single gene sequencing, and exome sequencing. We discuss the advantages and disadvantages of each method and review the potential of genomic sequencing for early disease detection.

    View details for DOI 10.1016/j.jpeds.2017.06.040

    View details for PubMedID 28947054

    View details for PubMedCentralID PMC6037534

  • Antimalarial myopathy in a systemic lupus erythematosus patient with quadriparesis and seizures: a case-based review. Clinical rheumatology Jafri, K., Zahed, H., Wysham, K. D., Patterson, S., Nolan, A. L., Bucknor, M. D., Chaganti, R. K. 2017; 36 (6): 1437-1444


    Weakness, seizures, and encephalopathy have a broad differential diagnosis in patients with systemic lupus erythematosus (SLE). We present a case of a 26-year-old female with a recent diagnosis of SLE who experienced a clinical deterioration with quadriparesis, seizures, and encephalopathy. Her quadriparesis was found to be secondary to biopsy-proven hydroxychloroquine-induced myopathy with concomitant inflammatory myopathy. Her seizures and encephalopathy were suspected to be multifactorial in the setting of sepsis and critical illness with possible contributions from neuropsychiatric manifestations of SLE and macrophage activation syndrome. She experienced a dramatic clinical recovery with discontinuation of hydroxychloroquine, treatment of lupus disease activity with mycophenolate mofetil and prednisone, and antibiotic treatment for methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia. This case-based review provides a systematic approach to quadriparesis, seizures, and encephalopathy in patients with SLE and an evidence-based discussion of antimalarial myopathy, which is of critical importance given the widespread use of antimalarial medications for rheumatologic diseases.

    View details for DOI 10.1007/s10067-017-3579-8

    View details for PubMedID 28236156

  • Serine 421 regulates mutant huntingtin toxicity and clearance in mice JOURNAL OF CLINICAL INVESTIGATION Kratter, I. H., Zahed, H., Lau, A., Tsvetkov, A. S., Daub, A. C., Weiberth, K. F., Gu, X., Saudou, F., Humbert, S., Yang, X., Osmand, A., Steffan, J. S., Masliah, E., Finkbeiner, S. 2016; 126 (9): 3585–97


    Huntington's disease (HD) is a progressive, adult-onset neurodegenerative disease caused by a polyglutamine (polyQ) expansion in the N-terminal region of the protein huntingtin (HTT). There are no cures or disease-modifying therapies for HD. HTT has a highly conserved Akt phosphorylation site at serine 421, and prior work in HD models found that phosphorylation at S421 (S421-P) diminishes the toxicity of mutant HTT (mHTT) fragments in neuronal cultures. However, whether S421-P affects the toxicity of mHTT in vivo remains unknown. In this work, we used murine models to investigate the role of S421-P in HTT-induced neurodegeneration. Specifically, we mutated the human mHTT gene within a BAC to express either an aspartic acid or an alanine at position 421, mimicking tonic phosphorylation (mHTT-S421D mice) or preventing phosphorylation (mHTT-S421A mice), respectively. Mimicking HTT phosphorylation strongly ameliorated mHTT-induced behavioral dysfunction and striatal neurodegeneration, whereas neuronal dysfunction persisted when S421 phosphorylation was blocked. We found that S421 phosphorylation mitigates neurodegeneration by increasing proteasome-dependent turnover of mHTT and reducing the presence of a toxic mHTT conformer. These data indicate that S421 is a potent modifier of mHTT toxicity and offer in vivo validation for S421 as a therapeutic target in HD.

    View details for DOI 10.1172/JCI80339

    View details for Web of Science ID 000382513400036

    View details for PubMedID 27525439

    View details for PubMedCentralID PMC5004962

  • Sequence-Level Analysis of the Major European Huntington Disease Haplotype AMERICAN JOURNAL OF HUMAN GENETICS Lee, J., Kim, K., Shin, A., Chao, M. J., Abu Elneel, K., Gillis, T., Mysore, J., Kaye, J. A., Zahed, H., Kratter, I. H., Daub, A. C., Finkbeiner, S., Li, H., Roach, J. C., Goodman, N., Hood, L., Myers, R. H., MacDonald, M. E., Gusella, J. F. 2015; 97 (3): 435–44


    Huntington disease (HD) reflects the dominant consequences of a CAG-repeat expansion in HTT. Analysis of common SNP-based haplotypes has revealed that most European HD subjects have distinguishable HTT haplotypes on their normal and disease chromosomes and that ∼50% of the latter share the same major HD haplotype. We reasoned that sequence-level investigation of this founder haplotype could provide significant insights into the history of HD and valuable information for gene-targeting approaches. Consequently, we performed whole-genome sequencing of HD and control subjects from four independent families in whom the major European HD haplotype segregates with the disease. Analysis of the full-sequence-based HTT haplotype indicated that these four families share a common ancestor sufficiently distant to have permitted the accumulation of family-specific variants. Confirmation of new CAG-expansion mutations on this haplotype suggests that unlike most founders of human disease, the common ancestor of HD-affected families with the major haplotype most likely did not have HD. Further, availability of the full sequence data validated the use of SNP imputation to predict the optimal variants for capturing heterozygosity in personalized allele-specific gene-silencing approaches. As few as ten SNPs are capable of revealing heterozygosity in more than 97% of European HD subjects. Extension of allele-specific silencing strategies to the few remaining homozygous individuals is likely to be achievable through additional known SNPs and discovery of private variants by complete sequencing of HTT. These data suggest that the current development of gene-based targeting for HD could be extended to personalized allele-specific approaches in essentially all HD individuals of European ancestry.

    View details for DOI 10.1016/j.ajhg.2015.07.017

    View details for Web of Science ID 000361084700006

    View details for PubMedID 26320893

    View details for PubMedCentralID PMC4564985

  • Oligodendrocyte-encoded HIF function couples postnatal myelination and white matter angiogenesis. Cell Yuen, T. J., Silbereis, J. C., Griveau, A., Chang, S. M., Daneman, R., Fancy, S. P., Zahed, H., Maltepe, E., Rowitch, D. H. 2014; 158 (2): 383-396


    Myelin sheaths provide critical functional and trophic support for axons in white matter tracts of the brain. Oligodendrocyte precursor cells (OPCs) have extraordinary metabolic requirements during development as they differentiate to produce multiple myelin segments, implying that they must first secure adequate access to blood supply. However, mechanisms that coordinate myelination and angiogenesis are unclear. Here, we show that oxygen tension, mediated by OPC-encoded hypoxia-inducible factor (HIF) function, is an essential regulator of postnatal myelination. Constitutive HIF1/2α stabilization resulted in OPC maturation arrest through autocrine activation of canonical Wnt7a/7b. Surprisingly, such OPCs also show paracrine activity that induces excessive postnatal white matter angiogenesis in vivo and directly stimulates endothelial cell proliferation in vitro. Conversely, OPC-specific HIF1/2α loss of function leads to insufficient angiogenesis in corpus callosum and catastrophic axon loss. These findings indicate that OPC-intrinsic HIF signaling couples postnatal white matter angiogenesis, axon integrity, and the onset of myelination in mammalian forebrain.

    View details for DOI 10.1016/j.cell.2014.04.052

    View details for PubMedID 25018103

    View details for PubMedCentralID PMC4149873

  • Constitutive Gs activation using a single-construct tetracycline-inducible expression system in embryonic stem cells and mice. Stem cell research & therapy Hsiao, E. C., Nguyen, T. D., Ng, J. K., Scott, M. J., Chang, W. C., Zahed, H., Conklin, B. R. 2011; 2 (2): 11


    The controlled expression of many genes, including G-protein coupled receptors (GPCRs), is important for delineating gene functions in complex model systems. Binary systems for inducible regulation of transgene expression are widely used in mice. One system is the tTA/TRE expression system, composed of a tetracycline-dependent DNA binding factor and a separate tetracycline operon. However, the requirement for two separate transgenes (one for each tTA or TRE component) makes this system less amenable to models requiring directed cell targeting, increases the risk of multiple transgene integration sites, and requires extensive screening for appropriately-functioning clones.We developed a single, polycistronic tetracycline-inducible expression platform to control the expression of multiple cistrons in mammalian cells. This platform has three basic constructs: regulator, responder, and destination vectors. The modular platform is compatible with both the TetOff (tTA) and TetOn (rtTA) systems. The modular Gateway recombineering-compatible components facilitate rapidly generating vectors to genetically modify mammalian cells. We apply this system to use the elongation factor 1α (EF1α) promoter to drive doxycycline-regulated expression of both the fluorescent marker mCherry and an engineered Gs-coupled GPCR "Rs1" separated by a 2A ribosomal skip site.We show that our combined expression construct drives expression of both the mCherry and Rs1 transgenes in a doxycycline-dependent manner. We successfully target the expression construct into the Rosa26 locus of mouse embryonic stem (ES) cells. Rs1 expression in mouse ES cells increases cAMP accumulation via both basal and ligand-induced Gs mechanisms and is associated with increased embryoid body size. Heterozygous mice carrying the Rs1 expression construct showed normal growth and weight, and developed small increases in bone formation that could be observed in the calvaria.Our results demonstrate the feasibility of a single-vector strategy that combines both the tTA and TRE tetracycline-regulated components for use in cells and mouse models. Although the EF1α promoter is useful for driving expression in pluripotent cells, a single copy of the EF1α promoter did not drive high levels of mCherry and Rs1 expression in the differentiated tissues of adult mice. These findings indicate that promoter selection is an important factor when developing transgene expression models.

    View details for DOI 10.1186/scrt52

    View details for PubMedID 21375737

    View details for PubMedCentralID PMC3226282

  • Specific ATM-mediated phosphorylation dependent on radiation quality. Radiation research Whalen, M. K., Gurai, S. K., Zahed-Kargaran, H., Pluth, J. M. 2008; 170 (3): 353-64


    To determine whether the physical differences between high- and low-LET radiation are reflected in the biological responses of exposed cells, we detailed phospho-protein profiles of three proteins functional in radiation repair and signal transduction. Detailing gamma-H2AX, pATF2 Ser490/498 and pSMC1 Ser957 kinetics after X-ray and iron-ion exposure also provides a window into understanding the underlying cellular responses. Phosphorylated forms of these proteins have been documented to co-localize at sites of double-strand breaks (DSBs) after low-LET radiation exposures, and two of these phosphorylations, pATF2 and pSMC1, are specifically dependent on ATM. Flow cytometry-based methods were used to quantify total levels of each phospho-protein at various times after irradiation. As expected, we observed a greater induction and persistence in gamma-H2AX after iron-ion (high-LET) exposure compared to X-ray (low-LET) exposure. In contrast, pATF2 and pSMC1 showed markedly lower induction levels after iron-ion exposure compared to equivalent doses of X rays. Quantification of pATF2 and pSMC1 foci revealed fewer cells containing foci and fewer foci per cell after iron-ion compared to X-ray exposure. These findings suggest that ATM responds to DSBs induced by high-LET radiation differently from DSBs induced by low-LET radiation.

    View details for DOI 10.1667/RR1354.1

    View details for PubMedID 18763865

  • Heregulin is sufficient for the promotion of tumorigenicity and metastasis of breast cancer cells in vivo. Molecular cancer research : MCR Atlas, E., Cardillo, M., Mehmi, I., Zahedkargaran, H., Tang, C., Lupu, R. 2003; 1 (3): 165-75


    Resistance of breast carcinomas to hormonal therapy is a clinical obstacle for the treatment of breast cancer. The molecular mechanisms and the factors involved in the progression of tumors from an estrogen (E2)-dependent to an E2-independent phenotype are not entirely understood. Heregulin (HRG) is a pleiotropic growth factor that binds to the erbB family of receptors, which are correlated with breast cancer progression and an aggressive phenotype in the breast carcinomas overexpressing the receptors. Previous studies in transgenic mice have shown that HRG is sufficient to induce mammary gland transformation and proliferation in the presence of hormonal stimulation. However, these studies did not address the important issue of the E2 independence that is part of the progression of breast cancer. In this study, we investigated the role of HRG in E2 independence. We were able to determine that HRG up-regulation was sufficient for the development of mammary tumors in the absence of E2 stimulation, a situation that mimics the progression of the human disease. We demonstrated that in ovariectomized nude mice, HRG induced E2 independence and antiestrogen resistance and promoted metastasis and preneoplastic transformation of the adjacent mouse mammary tissue. We show that one of the mechanisms by which HRG achieves the aggressive phenotype may be mediated via an increase in activated mitogen-activated protein kinase, an increase in a matrix-degrading enzyme, MMP-9, and the overexpression of vascular endothelial growth factors. The up-regulation of these genes occurred in the absence of any additional stimulation, in an autocrine manner. Our data provide new insights into the mechanisms of breast cancer progression in vivo, and reinforce the important role that HRG plays in this process.

    View details for PubMedID 12556556

  • Instrumental analysis in the organic lab: Microscale preparation and GC/MS analysis of deuterated butyl and ethyl acetates. Smith, L. R., Zahedkargaran, H. AMER CHEMICAL SOC. 2001: U121