About

Yakeel Quiroz is a Professor in the Department of Psychological & Brain Sciences at Boston University, where she also serves as the Director of the Multicultural Alzheimer’s Prevention & Protection (MAPP) Lab. She previously held the position of Associate Professor of Psychiatry at Harvard Medical School and directed innovative clinical and research initiatives at Massachusetts General Hospital (MGH) for over a decade. Dr. Quiroz earned her MA in cognitive neuroscience and PhD in clinical psychology from Boston University, and completed specialized postdoctoral training in neuropsychology and neuroimaging at MGH/Harvard Medical School. Her research focuses on identifying early cognitive and biological markers of Alzheimer’s disease and uncovering mechanisms that support cognitive resilience and delay dementia onset. She has studied Colombian families with early-onset autosomal dominant Alzheimer’s disease caused by mutations in the Presenilin-1 gene for over 20 years, providing insights into the biological trajectory of Alzheimer’s from preclinical to clinical stages and investigating protective mechanisms in individuals who remain cognitively resilient despite carrying the mutation. Dr. Quiroz leads multiple NIH-funded studies, including the Colombia-Boston biomarker study, the Boston Latino Aging Study, and the Healthy Aging and Resilient Brain Study, and is a Co-Investigator on the Harvard Aging Brain Study and the Alzheimer’s Clinical Trials Consortium. Her work has earned national and international recognition, including the NIH Director’s Pioneer Early Independence Award, the International Neuropsychological Society Early Career Award, and the Alzheimer’s Association’s Inge Grundke-Iqbal Award.

Research topics

• Medicine
• Internal medicine
• Pathology
• Psychology
• Biology
• Psychiatry
• Oncology
• Cardiology
• Genetics
• Neuroscience
• Gerontology
• Radiology
• Bioinformatics

Selected publications

• Global Cardiovascular Risk Profile and Cerebrovascular Abnormalities in Presymptomatic Individuals with CADASIL or Autosomal Dominant Alzheimer’s Disease

  Journal of Alzheimer s Disease · 2021 · 6 citations

  Senior authorCorresponding
  • Medicine
  • Internal medicine
  • Cardiology

  BACKGROUND: Cardiovascular risk factors increase the risk of developing dementia, including Alzheimer's disease and vascular dementia. OBJECTIVE: Studying individuals with autosomal dominant mutations leading to the early onset of dementia, this study examines the effect of the global cardiovascular risk profile on early cognitive and neuroimaging features of Alzheimer's disease and vascular dementia. METHODS: We studied 85 non-demented and stroke-free individuals, including 20 subjects with Presenilin1 (PSEN1) E280A mutation leading to the early onset of autosomal dominant Alzheimer's disease (ADAD), 20 subjects with NOTCH3 mutations leading to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and to the early onset of vascular dementia, and 45 non-affected family members (non-carriers). All subjects underwent clinical and neuropsychological evaluations and an MRI. The global cardiovascular risk profile was estimated using the office-based Framingham Cardiovascular Risk Profile (FCRP) score. RESULTS: In individuals with CADASIL, a higher FCRP score was associated with a reduced hippocampal volume (B = -0.06, p < 0.05) and an increased severity of cerebral microbleeds (B = 0.13, p < 0.001), lacunes (B = 0.30, p < 0.001), and perivascular space enlargement in the basal ganglia (B = 0.50, p < 0.05). There was no significant association between the FCRP score and neuroimaging measures in ADAD or non-carrier subjects. While the FCRP score was related to performance in executive function in non-carrier subjects (B = 0.06, p < 0.05), it was not significantly associated with cognitive performance in individuals with CADASIL or ADAD. CONCLUSION: Our results suggest that individuals with CADASIL and other forms of vascular cognitive impairment might particularly benefit from early interventions aimed at controlling cardiovascular risks.

  PublisherOA PDFDOI

• The INECO Frontal Screening for the Evaluation of Executive Dysfunction in Cerebral Small Vessel Disease: Evidence from Quantitative MRI in a CADASIL Cohort from Colombia

  Journal of the International Neuropsychological Society · 2020 · 9 citations

  Senior authorCorresponding
  • Medicine
  • Psychology
  • Pathology

  OBJECTIVES: Executive dysfunction is a predominant cognitive symptom in cerebral small vessel disease (SVD). The Institute of Cognitive Neurology Frontal Screening (IFS) is a well-validated screening tool allowing the rapid assessment of multiple components of executive function in Spanish-speaking individuals. In this study, we examined performance on the IFS in subjects with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), an inherited condition leading to the early onset of SVD. We further explored associations between performance on the IFS and magnetic resonance imaging (MRI) markers of SVD. METHODS: We recruited 24 asymptomatic CADASIL subjects and 23 noncarriers from Colombia. All subjects underwent a research MRI and a neuropsychological evaluation, including the IFS. Structural MRI markers of SVD were quantified in each subject, together with an SVD Sum Score representing the overall burden of cerebrovascular alterations. General linear model, correlation, and receiver operating characteristic curve analyses were used to explore group differences on the IFS and relationships with MRI markers of SVD. RESULTS: CADASIL subjects had a significantly reduced performance on the IFS Total Score. Performance on the IFS correlated with all quantified markers of SVD, except for brain atrophy and perivascular spaces enlargement. Finally, while the IFS Total Score was not able to accurately discriminate between carriers and noncarriers, it showed adequate sensitivity and specificity in detecting the presence of multiple MRI markers of SVD. CONCLUSIONS: These results suggest that the IFS may be a useful screening tool to assess executive function and disease severity in the context of SVD.

  PublisherDOI

• World‐Wide FINGERS Network: A global approach to risk reduction and prevention of dementia

  Alzheimer s & Dementia · 2020 · 507 citations

  • Gerontology
  • Medicine
  • Psychology

  Reducing the risk of dementia can halt the worldwide increase of affected people. The multifactorial and heterogeneous nature of late-onset dementia, including Alzheimer's disease (AD), indicates a potential impact of multidomain lifestyle interventions on risk reduction. The positive results of the landmark multidomain Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) support such an approach. The World-Wide FINGERS (WW-FINGERS), launched in 2017 and including over 25 countries, is the first global network of multidomain lifestyle intervention trials for dementia risk reduction and prevention. WW-FINGERS aims to adapt, test, and optimize the FINGER model to reduce risk across the spectrum of cognitive decline-from at-risk asymptomatic states to early symptomatic stages-in different geographical, cultural, and economic settings. WW-FINGERS aims to harmonize and adapt multidomain interventions across various countries and settings, to facilitate data sharing and analysis across studies, and to promote international joint initiatives to identify globally implementable and effective preventive strategies.

  DOI

• Genetic and nongenetic factors associated with CADASIL: A retrospective cohort study

  Journal of the Neurological Sciences · 2020 · 9 citations

  • Medicine
  • Internal medicine
  • Oncology
  PublisherOA PDFDOI

• Discriminative Accuracy of Plasma Phospho-tau217 for Alzheimer Disease vs Other Neurodegenerative Disorders

  JAMA · 2020 · 1479 citations

  • Medicine
  • Internal medicine
  • Oncology

  Importance: There are limitations in current diagnostic testing approaches for Alzheimer disease (AD). Objective: To examine plasma tau phosphorylated at threonine 217 (P-tau217) as a diagnostic biomarker for AD. Design, Setting, and Participants: Three cross-sectional cohorts: an Arizona-based neuropathology cohort (cohort 1), including 34 participants with AD and 47 without AD (dates of enrollment, May 2007-January 2019); the Swedish BioFINDER-2 cohort (cohort 2), including cognitively unimpaired participants (n = 301) and clinically diagnosed patients with mild cognitive impairment (MCI) (n = 178), AD dementia (n = 121), and other neurodegenerative diseases (n = 99) (April 2017-September 2019); and a Colombian autosomal-dominant AD kindred (cohort 3), including 365 PSEN1 E280A mutation carriers and 257 mutation noncarriers (December 2013-February 2017). Exposures: Plasma P-tau217. Main Outcomes and Measures: Primary outcome was the discriminative accuracy of plasma P-tau217 for AD (clinical or neuropathological diagnosis). Secondary outcome was the association with tau pathology (determined using neuropathology or positron emission tomography [PET]). Results: Mean age was 83.5 (SD, 8.5) years in cohort 1, 69.1 (SD, 10.3) years in cohort 2, and 35.8 (SD, 10.7) years in cohort 3; 38% were women in cohort 1, 51% in cohort 2, and 57% in cohort 3. In cohort 1, antemortem plasma P-tau217 differentiated neuropathologically defined AD from non-AD (area under the curve [AUC], 0.89 [95% CI, 0.81-0.97]) with significantly higher accuracy than plasma P-tau181 and neurofilament light chain (NfL) (AUC range, 0.50-0.72; P < .05). The discriminative accuracy of plasma P-tau217 in cohort 2 for clinical AD dementia vs other neurodegenerative diseases (AUC, 0.96 [95% CI, 0.93-0.98]) was significantly higher than plasma P-tau181, plasma NfL, and MRI measures (AUC range, 0.50-0.81; P < .001) but not significantly different compared with cerebrospinal fluid (CSF) P-tau217, CSF P-tau181, and tau-PET (AUC range, 0.90-0.99; P > .15). In cohort 3, plasma P-tau217 levels were significantly greater among PSEN1 mutation carriers, compared with noncarriers, from approximately 25 years and older, which is 20 years prior to estimated onset of MCI among mutation carriers. Plasma P-tau217 levels correlated with tau tangles in participants with (Spearman ρ = 0.64; P < .001), but not without (Spearman ρ = 0.15; P = .33), β-amyloid plaques in cohort 1. In cohort 2, plasma P-tau217 discriminated abnormal vs normal tau-PET scans (AUC, 0.93 [95% CI, 0.91-0.96]) with significantly higher accuracy than plasma P-tau181, plasma NfL, CSF P-tau181, CSF Aβ42:Aβ40 ratio, and MRI measures (AUC range, 0.67-0.90; P < .05), but its performance was not significantly different compared with CSF P-tau217 (AUC, 0.96; P = .22). Conclusions and Relevance: Among 1402 participants from 3 selected cohorts, plasma P-tau217 discriminated AD from other neurodegenerative diseases, with significantly higher accuracy than established plasma- and MRI-based biomarkers, and its performance was not significantly different from key CSF- or PET-based measures. Further research is needed to optimize the assay, validate the findings in unselected and diverse populations, and determine its potential role in clinical care.

  DOI

• Exceptionally low likelihood of Alzheimer’s dementia in APOE2 homozygotes from a 5,000-person neuropathological study

  Nature Communications · 2020 · 484 citations

  • Medicine
  • Neuroscience
  • Gerontology

  Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. We generated Alzheimer's dementia odds ratios and other findings in more than 5,000 clinically characterized and neuropathologically characterized Alzheimer's dementia cases and controls. APOE2/2 was associated with a low Alzheimer's dementia odds ratios compared to APOE2/3 and 3/3, and an exceptionally low odds ratio compared to APOE4/4, and the impact of APOE2 and APOE4 gene dose was significantly greater in the neuropathologically confirmed group than in more than 24,000 neuropathologically unconfirmed cases and controls. Finding and targeting the factors by which APOE and its variants influence Alzheimer's disease could have a major impact on the understanding, treatment and prevention of the disease.

  PublisherOA PDFDOI

Recent grants

• Nerve growth factor (NGF) metabolic dysfunction as a marker of cognitive decline in autosomal dominant Alzheimer's disease

  NIH · $2.0M · 2022–2025

• Resilience to Cognitive Decline and Resistance to Alzheimer's Disease and Related Neurodegenerative Diseases in Individuals from Colombia with Autosomal Dominant Dementias

  NIH · $3.8M · 2023–2026

• NIH Grant F31NS078786

  NIH · $27k · 2012

• Relationship between tau pathology and cognitive impairment in autosomal dominant Alzheimer's disease

  NIH · $3.8M · 2017–2023

• Memory network dysfunction as an early marker of preclinical Alzheimer's Disease

  NIH · $2.3M · 2014–2019

Frequent coauthors

• Reisa A. Sperling

  Harvard University

  708 shared

• Eric M. Reiman

  Arizona Alzheimer’s Consortium

  605 shared

• Francisco Lopera

  471 shared

• Clara Vila‐Castelar

  Harvard University

  431 shared

• Keith A. Johnson

  Massachusetts General Hospital

  410 shared

• Edmarie Guzmán‐Vélez

  Boston University

  353 shared

• Jennifer R. Gatchel

  337 shared

• Ana Baena

  Colciencias

  321 shared

Labs

• Developmental SciencePI

Education

• Ph.D., Clinical Psychology

  Boston University

• M.A., Cognitive Neuroscience

  Boston University

Awards & honors

• NIH Director’s Pioneer Early Independence Award
• International Neuropsychological Society (INS) Early Career…
• Alzheimer’s Association’s Inge Grundke-Iqbal Award for most…

Similar researchers at Boston University

• Alexa S. Beiserh-188
• David Boash-156
• Benjamin Sovacoolh-143
• Kathryn L. Lunettah-132
• Ranga Mynenih-130