Yakeel T. Quiroz, United States of America

Harvard Medical School and Massachusetts General Hospital (MGH) Departments of Psychiatry and Neurology
Dr. Quiroz is Associate Professor in the Departments of Psychiatry and Neurology at Harvard Medical School and Massachusetts General Hospital (MGH) in Boston, MA. She is the Director of the MGH Familial Dementia Neuroimaging Lab and the Multicultural Alzheimer’s Prevention Program-MAPP. She earned her master’s degree in cognitive neuroscience and PhD in clinical psychology from Boston University. She completed a postdoctoral fellowship in neuropsychology and brain imaging of Alzheimer’s disease (AD) at MGH. Her research interests include brain imaging, genomics, early detection and preclinical biomarkers of Alzheimer’s disease and other dementias. She is the principal investigator of the Colombia-Boston (COLBOS) longitudinal biomarker study on autosomal-dominant Alzheimer’s disease, which follows individuals from the world’s largest extended family with a single, AD-causing mutation (E280A in Presenilin1). Dr. Quiroz’s research has focused on characterizing biological and physiological changes that may predispose individuals to develop memory loss or dementia later in life. Her work has already provided evidence of brain abnormalities in cognitively-intact individuals at high risk for AD, decades before their clinical onset. Her findings have helped the field to re-conceptualize Alzheimer as a sequence of changes that begins decades before cognitive decline, and which may be targeted by promising disease-slowing treatments at a time in which they might have their most profound effect. Her research work has resulted in several publications that have generated considerable discussion in the field and has achieved recognition by colleagues at the national and international level. Dr. Quiroz’s work has been recognized with several awards, including an NIH Director’s Early Independence Award, the FABBS Foundation Early Career Impact Award, the MGH Research Scholar Award and the Alzheimer’s Association Inge Grundke-Iqbal Award for Alzheimer’s Research.

Author Of 1 Presentation

AGE-RELATED TRAJECTORY OF TAU PATHOLOGY IN PRECLINICAL AUTOSOMAL DOMINANT ALZHEIMER'S DISEASE

Session Type
SYMPOSIUM
Date
14.03.2021, Sunday
Session Time
08:00 - 09:45
Room
On Demand Symposia D
Lecture Time
08:00 - 08:15
Session Icon
On-Demand

Abstract

Abstract Body

Aims

Examine baseline and longitudinal brain pathology (amyloid and tau) and memory decline in cognitively-unimpaired carriers of autosomal dominant Alzheimer's disease.


Methods

Members of the Colombian kindred with the PSEN1 E280A ADAD were enrolled in our ongoing study (40 nondemented carriers and 40 age-matched non-carriers; age 36 +/- 6 years old). Participants underwent a comprehensive neuropsychological evaluation, and Positron Emission Tomography (PET) scanning to measure cortical amyloid and regional tau burden (i.e., inferior temporal tau and entorhinal tau). Mann-Whitney tests and Spearman correlations were conducted to examine group differences and relationships among cognitive performance and AD pathology.


Results

Carriers performed significantly worse on MMSE (p=.001) and CERAD Word List Learning (p=.003), and had greater cortical amyloid (p<.001) and entorhinal tau burden (p=.025), compared to non-carriers. Memory scores negatively correlated with markers of AD pathology (p<.001).


Conclusions

Our results suggest that verbal memory decline relates to markers of AD pathology in cognitively-unimpaired individuals with PSEN1 E280A ADAD. Future research is needed to examine whether memory measures such as the CERAD Word List Learning may be useful in detecting subtle cognitive changes in those at risk for AD, prior to clinical onset.

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Presenter of 2 Presentations

AGE-RELATED TRAJECTORY OF TAU PATHOLOGY IN PRECLINICAL AUTOSOMAL DOMINANT ALZHEIMER'S DISEASE

Session Type
SYMPOSIUM
Date
14.03.2021, Sunday
Session Time
08:00 - 09:45
Room
On Demand Symposia D
Lecture Time
08:00 - 08:15
Session Icon
On-Demand

Abstract

Abstract Body

Aims

Examine baseline and longitudinal brain pathology (amyloid and tau) and memory decline in cognitively-unimpaired carriers of autosomal dominant Alzheimer's disease.


Methods

Members of the Colombian kindred with the PSEN1 E280A ADAD were enrolled in our ongoing study (40 nondemented carriers and 40 age-matched non-carriers; age 36 +/- 6 years old). Participants underwent a comprehensive neuropsychological evaluation, and Positron Emission Tomography (PET) scanning to measure cortical amyloid and regional tau burden (i.e., inferior temporal tau and entorhinal tau). Mann-Whitney tests and Spearman correlations were conducted to examine group differences and relationships among cognitive performance and AD pathology.


Results

Carriers performed significantly worse on MMSE (p=.001) and CERAD Word List Learning (p=.003), and had greater cortical amyloid (p<.001) and entorhinal tau burden (p=.025), compared to non-carriers. Memory scores negatively correlated with markers of AD pathology (p<.001).


Conclusions

Our results suggest that verbal memory decline relates to markers of AD pathology in cognitively-unimpaired individuals with PSEN1 E280A ADAD. Future research is needed to examine whether memory measures such as the CERAD Word List Learning may be useful in detecting subtle cognitive changes in those at risk for AD, prior to clinical onset.

Hide