Dr. Skylar-Scott is a board-certified, fellowship-trained cognitive and behavioral neurologist and clinical assistant professor at Stanford University. She is a Diplomate of the American Board of Psychiatry and Neurology as well as the United Council for Neurologic Subspecialties in Behavioral Neurology and Neuropsychiatry.

Her clinical interests include the treatment of cognitive and behavioral impairment due to Alzheimer’s disease, Parkinson’s disease, Lewy body dementia, posterior cortical atrophy, primary progressive aphasia, frontotemporal dementia, vascular dementia, primary age-related tauopathy, and limbic-predominant age-associated TDP-43 encephalopathy, among other disorders of cognition and behavior.

Her research interests include clinical trials for Alzheimer’s disease and how social and intellectual engagement can affect cognition. She has also investigated impaired consciousness in epilepsy and biomarkers for assessing Duchenne muscular dystrophy. Prior to joining Stanford, Dr. Skylar-Scott was a fellow in the Center for Alzheimer’s Research and Treatment (CART) in the Department of Neurology at Harvard Medical School/Brigham and Women’s Hospital. She also completed her undergraduate degree at MIT, her MD at Yale, and her residency at Harvard.

Dr. Skylar-Scott’s work has appeared in Neurology, Alzheimer's Research and Therapy, Pediatric Neurology, the Journal of Ultrasound in Medicine, Muscle & Nerve, and Epilepsia. She also has also been invited to write book chapters on Alzheimer’s disease, normal pressure hydrocephalus, Parkinson’s disease dementia and Lewy body dementia, and the cognitive and psychiatric consequences of neuroimmunological disorders published by Elsevier and McGraw-Hill.

Presentations by Dr. Skylar-Scott have focused on prevention of cognitive decline in at-risk elderly people, cognitive and neuropsychiatric manifestations of Parkinson’s disease, human prion diseases, and other topics. She has presented at meetings held by the American Academy of Neurology (AAN), the American Neurological Association (ANA), and the American Academy of Neuromuscular and Electrodiagnostic Medicine (AANEM).

For her research and scholarship, Dr. Skylar-Scott has earned honors from the American Academy of Neurology (AAN) and the Howard Hughes Medical Institute (HHMI). She was honored to receive the Golseth Young Investigator Award from the American Association of Neuromuscular & Electrodiagnostic Medicine. In addition, she won the Action Duchenne International Conference First Prize Poster for her research in Duchenne muscular dystrophy.

Dr. Skylar-Scott is a member of the American Neurological Association and American Academy of Neurology. Every year, she walks to raise money for Alzheimer's disease and Lewy body dementia.

Clinical Focus

  • Neurology

Academic Appointments

Professional Education

  • Board Certification: United Council for Neurologic Subspecialties, Behavioral Neurology and Neuropsychiatry (2022)
  • Board Certification, United Council for Neurologic Subspecialties, Behavioral Neurology and Neuropsychiatry (2022)
  • Medical Education: Yale School Of Medicine (2014) CT
  • Fellowship: Brigham and Women's Hospital Neurology Fellowship (2020) MA
  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2018)
  • Residency: Beth Israel Deaconess Medical Center Neurology Residency (2018) MA
  • Internship: Yale New Haven Medical Center Transitional Year (2015) CT

Clinical Trials

  • Safety, PK and Biodistribution of 18F-OP-801 in Patients With ALS, AD, MS, PD and Healthy Volunteers Recruiting

    This is a Phase 1/2 study to evaluate the safety and tolerability of 18F-OP-801 in subjects with ALS, AD, MS, PD and age-matched HVs. 18F-OP-801 is intended as a biomarker for PET imaging of activated microglia and macrophages in regions of neuroinflammation.

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All Publications

  • Alzheimer's disease and epilepsy: shared neuropathology guides current and future treatment strategies. Frontiers in neurology Lu, O., Kouser, T., Skylar-Scott, I. A. 2023; 14: 1241339


    Epilepsy is a cause of profound disability in patients with Alzheimer's disease (AD). The risk of being diagnosed with AD increases the risk for epilepsy, and in parallel, a history of epilepsy increases the likelihood of the development of AD. This bi-directional relationship may be due to underlying shared pathophysiologic hallmarks, including decreased cerebrospinal fluid amyloid beta 42 (Aβ42), increased hyperphosphorylated tau protein, and hippocampal hyperexcitability. Additionally, there are practical treatment considerations in patients with co-morbid AD and epilepsy-namely, there is a higher risk of seizures associated with medications commonly prescribed for Alzheimer's disease patients, including antidepressants and antipsychotics such as trazodone, serotonin norepinephrine reuptake inhibitors (SNRIs), and first-generation neuroleptics. Anti-amyloid antibodies like aducanumab and lecanemab present new and unique considerations in patients with co-morbid AD and epilepsy given the risk of seizures associated with amyloid-related imaging abnormalities (ARIA) seen with this drug class. Finally, we identify and detail five active studies, including two clinical trials of levetiracetam in the respective treatment of cognition and neuropsychiatric features of AD, a study characterizing the prevalence of epilepsy in AD via prolonged EEG monitoring, a study characterizing AD biomarkers in late-onset epilepsy, and a study evaluating hyperexcitability in AD. These ongoing trials may guide future clinical decision-making and the development of novel therapeutics.

    View details for DOI 10.3389/fneur.2023.1241339

    View details for PubMedID 37936917

    View details for PubMedCentralID PMC10626492

  • Lewy Body Dementia: An Overview of Promising Therapeutics. Current neurology and neuroscience reports Skylar-Scott, I. A., Sha, S. J. 2023


    Lewy body dementia (LBD) encompasses dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD). This article will emphasize potential disease-modifying therapies as well as investigative symptomatic treatments for non-motor symptoms including cognitive impairment and psychosis that can present a tremendous burden to patients with LBD and their caregivers.We review 11 prospective disease-modifying therapies (DMT) including four with phase 2 data (neflamapimod, nilotinib, bosutinib, and E2027); four with some limited data in symptomatic populations including phase 1, open-label, registry, or cohort data (vodabatinib, ambroxol, clenbuterol, and terazosin); and three with phase 1 data in healthy populations (Anle138b, fosgonimeton, and CT1812). We also appraise four symptomatic therapies for cognitive impairment, but due to safety and efficacy concerns, only NYX-458 remains under active investigation. Of symptomatic therapies for psychosis recently investigated, pimavanserin shows promise in LBD, but studies of nelotanserin have been suspended. Although the discovery of novel symptomatic and disease-modifying therapeutics remains a significant challenge, recently published and upcoming trials signify promising strides toward that aim.

    View details for DOI 10.1007/s11910-023-01292-0

    View details for PubMedID 37572228

    View details for PubMedCentralID 5496518

  • Performance of a fully-automated Lumipulse plasma phospho-tau181 assay for Alzheimer's disease. Alzheimer's research & therapy Wilson, E. N., Young, C. B., Ramos Benitez, J., Swarovski, M. S., Feinstein, I., Vandijck, M., Le Guen, Y., Kasireddy, N. M., Shahid, M., Corso, N. K., Wang, Q., Kennedy, G., Trelle, A. N., Lind, B., Channappa, D., Belnap, M., Ramirez, V., Skylar-Scott, I., Younes, K., Yutsis, M. V., Le Bastard, N., Quinn, J. F., van Dyck, C. H., Nairn, A., Fredericks, C. A., Tian, L., Kerchner, G. A., Montine, T. J., Sha, S. J., Davidzon, G., Henderson, V. W., Longo, F. M., Greicius, M. D., Wagner, A. D., Wyss-Coray, T., Poston, K. L., Mormino, E. C., Andreasson, K. I. 2022; 14 (1): 172


    BACKGROUND: The recent promise of disease-modifying therapies for Alzheimer's disease (AD) has reinforced the need for accurate biomarkers for early disease detection, diagnosis and treatment monitoring. Advances in the development of novel blood-based biomarkers for AD have revealed that plasma levels of tau phosphorylated at various residues are specific and sensitive to AD dementia. However, the currently available tests have shortcomings in access, throughput, and scalability that limit widespread implementation.METHODS: We evaluated the diagnostic and prognostic performance of a high-throughput and fully-automated Lumipulse plasma p-tau181 assay for the detection of AD. Plasma from older clinically unimpaired individuals (CU, n = 463) and patients with mild cognitive impairment (MCI, n = 107) or AD dementia (n = 78) were obtained from the longitudinal Stanford University Alzheimer's Disease Research Center (ADRC) and the Stanford Aging and Memory Study (SAMS) cohorts. We evaluated the discriminative accuracy of plasma p-tau181 for clinical AD diagnosis, association with amyloid beta peptides and p-tau181 concentrations in CSF, association with amyloid positron emission tomography (PET), and ability to predict longitudinal cognitive and functional change.RESULTS: The assay showed robust performance in differentiating AD from control participants (AUC 0.959, CI: 0.912 to 0.990), and was strongly associated with CSF p-tau181, CSF Abeta42/Abeta40 ratio, and amyloid-PET global SUVRs. Associations between plasma p-tau181 with CSF biomarkers were significant when examined separately in Abeta+ and Abeta- groups. Plasma p-tau181 significantly increased over time in CU and AD diagnostic groups. After controlling for clinical diagnosis, age, sex, and education, baseline plasma p-tau181 predicted change in MoCA overall and change in CDR Sum of Boxes in the AD group over follow-up of up to 5 years.CONCLUSIONS: This fully-automated and available blood-based biomarker assay therefore may be useful for early detection, diagnosis, prognosis, and treatment monitoring of AD.

    View details for DOI 10.1186/s13195-022-01116-2

    View details for PubMedID 36371232