Biblio
“Association Between Plasma Biomarkers of Amyloid, Tau, and Neurodegeneration with Cerebral Microbleeds.”, J Alzheimers Dis, vol. 87, no. 4, pp. 1537-1547, 2022.
, “Characterizing White Matter Tract Degeneration in Syndromic Variants of Alzheimer's Disease: A Diffusion Tensor Imaging Study.”, J Alzheimers Dis, vol. 49, no. 3, pp. 633-43, 2016.
, “A Comparison of Partial Volume Correction Techniques for Measuring Change in Serial Amyloid PET SUVR.”, J Alzheimers Dis, vol. 67, no. 1, pp. 181-195, 2019.
, “Early Postmenopausal Transdermal 17β-Estradiol Therapy and Amyloid-β Deposition.”, J Alzheimers Dis, vol. 53, no. 2, pp. 547-56, 2016.
, “FDG-PET and Neuropsychiatric Symptoms among Cognitively Normal Elderly Persons: The Mayo Clinic Study of Aging.”, J Alzheimers Dis, vol. 53, no. 4, pp. 1609-16, 2016.
, “Longitudinally Increasing Elevated Asymmetric Flortaucipir Binding in a Cognitively Unimpaired Amyloid-Negative Older Individual.”, J Alzheimers Dis, vol. 85, no. 1, pp. 59-64, 2021.
, “Medial Temporal Atrophy in Posterior Cortical Atrophy and Its Relationship to the Cingulate Island Sign.”, J Alzheimers Dis, vol. 86, no. 1, pp. 491-498, 2022.
, “Mediterranean Diet, Its Components, and Amyloid Imaging Biomarkers.”, J Alzheimers Dis, vol. 64, no. 1, pp. 281-290, 2018.
, “Patterns of Neuropsychological Dysfunction and Cortical Volume Changes in Logopenic Aphasia.”, J Alzheimers Dis, vol. 66, no. 3, pp. 1015-1025, 2018.
, “Polygenic Scores of Alzheimer's Disease Risk Genes Add Only Modestly to APOE in Explaining Variation in Amyloid PET Burden.”, J Alzheimers Dis, vol. 88, no. 4, pp. 1615-1625, 2022.
, “Regional Distribution, Asymmetry, and Clinical Correlates of Tau Uptake on [18F]AV-1451 PET in Atypical Alzheimer's Disease.”, J Alzheimers Dis, vol. 62, no. 4, pp. 1713-1724, 2018.
, “Statins and Brain Health: Alzheimer's Disease and Cerebrovascular Disease Biomarkers in Older Adults.”, J Alzheimers Dis, vol. 65, no. 4, pp. 1345-1352, 2018.
, “Varying Degrees of Temporoparietal Hypometabolism on FDG-PET Reveal Amyloid-Positive Logopenic Primary Progressive Aphasia is not a Homogeneous Clinical Entity.”, J Alzheimers Dis, vol. 55, no. 3, pp. 1019-1029, 2017.
,