About

Victor W. Henderson, MD, MS, is a professor of Epidemiology and Population Health, Neurology, and Neurological Sciences at Stanford University. His research interests focus on neuroepidemiology and brain–behavior relations in aging and dementia. He investigates risk factors for cognitive aging and neurodegenerative dementia, as well as interventions to help prevent and treat these disorders. Henderson directs the NIH Stanford Alzheimer's Disease Research Center and co-directs the master’s degree program in Epidemiology & Clinical Research. His work includes studying the effects of α-synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging, as well as examining the risk of cancer in patients with first-time seizures. He has contributed to understanding the clinical and biological aspects of cognitive decline, dementia, and related neurological conditions, and has held various academic and administrative roles at Stanford and previously at the University of Southern California. Henderson is recognized for his expertise in behavioral neurology, neuropsychiatry, and epidemiology, and has received numerous honors and awards for his contributions to the field.

Research topics

• Medicine
• Biology
• Bioinformatics
• Neuroscience
• Genetics
• Gerontology
• Internal medicine
• Audiology
• Physiology
• Cognitive psychology
• Pathology
• Speech recognition
• Psychology

Selected publications

• A framework of digital biomarkers for neurodegenerative diseases

  Nature Reviews Bioengineering · 2026-04-23

  article
  PublisherDOI

• Risk of Cancer in Patients With First-Time Seizure

  JAMA Neurology · 2026-04-27

  articleOpen access

  Importance: Seizures are a known complication of cancer, but whether they may be the first sign of undiagnosed neurological and nonneurological cancer remains unclear. Objective: To examine neurological and nonneurological cancer risk in patients with first-time seizures vs the general population. Design, Setting, and Participants: This population-based cohort study was conducted using nationwide Danish medical registries from January 1996 through December 2022. Follow-up extended until cancer diagnosis (excluding nonmelanoma skin cancer), emigration, death, or December 31, 2022. Analyses were performed from January 2025 through December 2025. All persons aged 18 years or older with a first-time hospital diagnosis of seizure and no preceding cancer were included. Exposure: First-time seizure diagnosis. Main Outcomes and Measures: The primary outcomes were absolute risks (ARs) of cancer and standardized incidence ratios (SIRs) relative to the general Danish population with 95% confidence intervals, which were computed for all cancers, neurological and nonneurological cancers, and site-specific cancer within 1 year, from 1 to less than 5 years, and from 5 to 20 years after the first seizure. Results: Among 49 894 adults with first-time seizure (median [IQR] age at seizure diagnosis, 51.5 [35.6-67.8] years; 20 648 [41.4%] women), a total of 1172 neurological and 850 nonneurological cancers were observed within the first year of follow-up; 87 neurological and 1226 nonneurological cancers were observed during the period from 1 to less than 5 years; and 112 neurological and 2120 nonneurological cancers were observed during the period from 5 to 20 years. In these time periods, the ARs for any cancer were 4.1%, 3.5%, and 13.4%, with SIRs of 5.30 (95% CI, 5.07-5.54), 1.18 (95% CI, 1.12-1.25), and 1.34 (95% CI, 1.28-1.40). ARs for neurological cancers were 2.4%, 0.2%, and 0.7%, with SIRs of 76.1 (95% CI, 71.8-80.6), 1.85 (95% CI, 1.48-2.28), and 1.46 (95% CI, 1.20-1.75). ARs for nonneurological cancers were 1.7%, 3.3%, and 12.8%, with SIRs of 2.32 (95% CI, 2.17-2.48), 1.15 (95% CI, 1.09-1.22), and 1.33 (95% CI, 1.28-1.39). Conclusions and Relevance: Per the results of this cohort study, first-time seizures were associated with clearly elevated short-term relative risk of cancer and slightly elevated long-term risk, indicating they may be an early clinical sign of both neurological and nonneurological occult cancers. These findings highlight the importance of considering broader diagnostic assessments after first-time seizures in select patients.

  PublisherOA PDFDOI

• Ultra-high Resolution in vivo 7T MRI Detects Hippocampal Subfield Iron in Mild Cognitive Impairment and Alzheimer’s Disease

  Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition · 2025-09-16

  article

  Motivation: Iron dysregulation and deposition may play a role in neurodegeneration in Alzheimer's disease (AD), but limited studies have pushed the boundaries of MRI resolution to accurately quantify iron, particularly in the hippocampus. Goal(s): Utilize ultra-high resolution MRI and QSM for quantitative analysis of hippocampal subfield iron deposition to investigate the role of brain iron in AD. Approach: We acquired 7T multi-echo gradient echo MRI on 19 living human subjects (healthy, mild cognitive impairment, AD) to detect hippocampal source-separated QSM/R2* abnormalities and quantify iron concentrations within hippocampal subfields. Results: Increased R2* and QSM-χ+ was detected in the subiculum-CA1 hippocampal subfields with worsening disease status. Impact: This study successfully performed in vivo ultra-high resolution MRI to quantify iron deposition in hippocampi of MCI and AD patients, contributing to the development of iron as a neuroimaging biomarker for AD.

  PublisherDOI

• Plasma phosphorylated tau 217 detects amyloid-β in Neuronal Synuclein Disease

  npj Parkinson s Disease · 2025-09-09

  preprintOpen access

  Abstract Background Multiple proteinopathies commonly coexist in neurodegenerative diseases, therefore it is critical to understand plasma biomarker performance to detect proteinopathies in these complex diseases. While plasma biomarkers can accurately detect amyloid-β in individuals with Alzheimer’s disease, their performance accuracy is unknown in individuals with Neuronal Synuclein Disease (NSD). Objective To determine the accuracy of plasma pTau217, pTau181, Aβ42/40, GFAP, and NfL to detect amyloid-β in NSD. Additionally, to establish and validate cut-points for the most promising amyloid-β plasma biomarker in NSD. Methods This cross-sectional cohort study analyzed data from two observational cohorts from Stanford University and Sant Pau Hospital. The discovery cohort participants were biologically-defined by NSD and Aβ status among clinical Lewy body disease (LBD), Alzheimer’s disease (AD), or cognitively unimpaired (CU) individuals. The two validation cohorts consisted of clinically-defined LBD participants. Data were analyzed from 2/2024-3/2025. Plasma pTau217, pTau181, Aβ42/40, GFAP, and NfL were analyzed as potential biomarkers for amyloid-β in NSD, using cerebrospinal fluid Aβ42/40 and Aβ positron emission tomography as reference gold-standards. Diagnostic accuracy was determined using Receiver Operating Characteristic (ROC) analysis. Results We included 253 participants (mean[SD] age=71[9.9] years), 180 from the discovery cohort and 73 from the clinical validation cohorts. In the discovery cohort, plasma pTau217, pTau181, Aβ42/40, and GFAP levels significantly differed between Aβ+ and Aβ-participants, regardless of NSD status. Plasma NfL levels were significantly higher in the NSD+/Aβ+ group compared to all other groups. Plasma pTau217 showed the largest median fold-change between Aβ+ and Aβ-participants and demonstrated the highest diagnostic performance in detecting amyloid-β in NSD (Area Under the Curve=0.92, 95% CI=0.81-0.98). Applying one-or two-reference cut points for plasma pTau217 in the validation cohorts could reduce the need for additional amyloid-β testing in 41-56% of clinically-defined LBD participants. Conclusions Plasma pTau217 accurately detects amyloid-β in NSD individuals, with reproducible cut points in clinical LBD cohorts. Our findings demonstrate plasma pTau217 is a cost-effective and minimally-invasive tool for determining amyloid-β in mixed-etiology neurodegenerative diseases of aging.

  PublisherOA PDFDOI

• Agraphia

  Elsevier eBooks · 2025-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Amyloid PET predicts longitudinal functional and cognitive trajectories in a heterogeneous cohort

  Alzheimer s & Dementia · 2025-03-01 · 11 citations

  articleOpen access

  INTRODUCTION: Amyloid positron emission tomography (PET) is increasingly available for diagnosis of Alzheimer`s disease (AD); however, its practical implications in heterogenous cohorts are debated. METHODS: Amyloid PET from 890 National Alzheimer`s Coordinating Center participants with up to 10 years post-PET follow up was analyzed. Cox proportional hazards and linear mixed models were used to investigate amyloid burden prediction of etiology and prospective functional status and cognitive decline. RESULTS: Amyloid positivity was associated with progression from unimpaired to mild cognitive impairment and dementia. Amyloid burden in the unimpaired group was associated with lower initial memory levels and faster decline in memory, language, and global cognition. In the Impaired group, amyloid was associated with lower initial levels and faster decline for memory, language, executive function, and global cognition. DISCUSSION: Amyloid burden is an important prognostic marker in a clinically heterogeneous cohort. Future work is needed to establish the proportion of decline driven by AD versus non-AD processes in the context of mixed pathology. HIGHLIGHTS: Our findings highlight the importance of amyloid positron emission tomography (PET) in heterogenous cohorts, including diverse demographics, clinical syndromes, and underlying etiologies. The results also provide evidence that higher amyloid levels were linked to functional progression from unimpaired cognition to mild cognitive impairment (MCI) and from MCI to dementia. In cognitively unimpaired individuals, higher amyloid burden was associated with poorer memory at baseline and subsequent declines in memory, language, and global cognition. Among individuals with cognitive impairment, amyloid burden was associated with worse initial memory, language, executive function, and global cognition, and faster declines over time.

  PublisherOA PDFDOI

• Early glycemic control and subsequent risk of incident dementia among new metformin users

  The American Journal of Medicine · 2025-11-05

  articleOpen access
  PublisherOA PDFDOI

• Effects of α-synuclein pathology in normal aging and Alzheimer’s disease

  medRxiv · 2025-08-08

  preprintOpen access

  Abstract Objective α-synuclein is the hallmark pathology of Parkinson’s disease and dementia with Lewy bodies, described together as Lewy body disease (LBD). α-synuclein is also commonly observed in the context of Alzheimer’s disease (AD). Here we investigate the frequency of α-synuclein biomarker positivity in clinically unimpaired (CU) individuals and an AD research cohort, as well as associations with demographics, AD biomarkers, cognitive performance, and clinical outcomes. Methods We assessed α-synuclein status (α-syn+/-) in 270 CU and 56 clinically diagnosed AD participants (29 mild cognitive impairment and 27 dementia) using a cerebrospinal fluid seed amplification assay (α-syn SAA). Eighty-five LBD spectrum participants were included for comparison. AD biomarker levels were measured with cerebrospinal fluid β-amyloid42/40 and p-tau181. Participants received cognitive testing, the Neuropsychiatric Inventory Questionnaire and the Movement Disorders Society Unified Parkinson’s Disease Rating Scale. Results α-syn was detected in 9% of CU, 14% of AD mild cognitive impairment, and 19% of AD dementia participants, whereas 81% of individuals with LBD spectrum clinical diagnoses were α-syn+. α-syn+ CU were older, performed worse on tests of executive function and working memory, and reported more LBD-related non-motor symptoms relative to α-syn-CU. α-syn status in CU was not significantly associated with β-amyloid or tau, memory performance, motor symptoms, or neuropsychiatric symptoms. Conclusions Using the CSF SAA biomarker, α-syn positivity independently predicts subtle cognitive changes and early clinical symptoms in aging. These cross-sectional findings represent an important addition to the limited but growing literature characterizing the frequency and effects of α-syn positivity in clinically healthy older adults and individuals with AD.

  PublisherOA PDFDOI

• Parkinson’s disease is characterized by vitamin B6-dependent inflammatory kynurenine pathway dysfunction

  npj Parkinson s Disease · 2025-04-26 · 13 citations

  articleOpen access

  Abstract Recent studies demonstrate that Parkinson’s disease (PD) is associated with dysregulated metabolic flux through the kynurenine pathway (KP), in which tryptophan is converted to kynurenine (KYN), and KYN is subsequently metabolized to neuroactive compounds quinolinic acid (QA) and kynurenic acid (KA). Here, we used mass-spectrometry to compare blood and cerebral spinal fluid (CSF) KP metabolites between 158 unimpaired older adults and 177 participants with PD. We found increased neuroexcitatory QA/KA ratio in both plasma and CSF of PD participants associated with peripheral and cerebral inflammation and vitamin B 6 deficiency. Furthermore, increased QA tracked with CSF tau, CSF soluble TREM2 (sTREM2) and severity of both motor and non-motor PD clinical symptoms. Finally, PD patient subgroups with distinct KP profiles displayed distinct PD clinical features. These data validate the KP as a site of brain and periphery crosstalk, integrating B-vitamin status, inflammation and metabolism to ultimately influence PD clinical manifestation.

  PublisherOA PDFDOI

• Alexia

  Elsevier eBooks · 2025-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

Recent grants

• Biomarker Core

  NIH · $42.6M · 2020–2030

• Core E: Outreach, Recruitment and Education Core

  NIH · $15.2M · 2020

• NIH Grant R01AG034639

  NIH · $824k · 2014

• NIH Grant R01AG023038

  NIH · $1.1M · 2011

• NIH Grant P50AG005142

  NIH · $107.0M · 2021

Frequent coauthors

• Henrik Toft Sørensen

  Aarhus University Hospital

  243 shared

• Erzsébet Horváth‐Puhó

  Aarhus University Hospital

  141 shared

• Kasper Adelborg

  Aarhus University Hospital

  94 shared

• Nils Skajaa

  Aarhus University Hospital

  90 shared

• Kenneth J. Rothman

  88 shared

• JoAnn E. Manson

  Brigham and Women's Hospital

  77 shared

• Lau Caspar Thygesen

  76 shared

• Stephen R. Rapp

  University of California, San Diego

  71 shared

Labs

• Stanford Alzheimer's Disease Research CenterPI

Education

• M.D.

  University of Southern California

• M.S.

  University of Southern California

• B.S.

  University of California, Los Angeles

Awards & honors

• Christopher M. Filley Lectureship in Behavioral Neurology, U…
• Honorary Skou Professor, Aarhus University, Denmark (2019–)
• Distinguished Service Award, International Menopause Society…
• Top Doctors (Neurology), Castle Connolly book series (3rd-14…
• Lawrence C. McHenry Award, American Academy of Neurology (20…