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“A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β.”, Sci Transl Med, vol. 4, no. 147, p. 147ra111, 2012.
, “A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β.”, Sci Transl Med, vol. 4, no. 147, p. 147ra111, 2012.
, “Emotional Dysregulation in Mild Behavioral Impairment Is Associated with Reduced Cortical Thickness in the Right Supramarginal Gyrus.”, J Alzheimers Dis, vol. 93, no. 2, pp. 521-532, 2023.
, “Modifiable Barriers for Recruitment and Retention of Older Adults Participants from Underrepresented Minorities in Alzheimer's Disease Research.”, J Alzheimers Dis, vol. 80, no. 3, pp. 927-940, 2021.
, “Regional differences in glucose metabolic decline and tau deposition in the Alzheimer's continuum brain.”, J Alzheimers Dis, vol. 102, no. 1, pp. 228-236, 2024.
, “Dilated Perivascular Spaces in the Centrum Semiovale Begin to Develop in Middle Age.”, J Alzheimers Dis, vol. 61, no. 4, pp. 1619-1626, 2018.
, “Dilated Perivascular Spaces in the Centrum Semiovale Begin to Develop in Middle Age.”, J Alzheimers Dis, vol. 61, no. 4, pp. 1619-1626, 2018.
, “Dilated Perivascular Spaces in the Centrum Semiovale Begin to Develop in Middle Age.”, J Alzheimers Dis, vol. 61, no. 4, pp. 1619-1626, 2018.
, “Mild Behavioral Impairment and Subjective Cognitive Decline Predict Cognitive and Functional Decline.”, J Alzheimers Dis, vol. 80, no. 1, pp. 459-469, 2021.
, “The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features.”, J Alzheimers Dis, vol. 61, no. 1, pp. 17-28, 2018.
, “The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features.”, J Alzheimers Dis, vol. 61, no. 1, pp. 17-28, 2018.
, “Role of Suppressor of Cytokine Signaling 3 (SOCS3) in Altering Activated Microglia Phenotype in APPswe/PS1dE9 Mice.”, J Alzheimers Dis, vol. 55, no. 3, pp. 1235-1247, 2017.
, “An operational approach to National Institute on Aging-Alzheimer's Association criteria for preclinical Alzheimer disease.”, Ann Neurol, vol. 71, no. 6, pp. 765-75, 2012.
, “Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers.”, Lancet Neurol, vol. 12, no. 2, pp. 207-16, 2013.
, “Psychotropic Drug Prescription in Patients with Dementia: Nursing Home Residents Versus Patients Living at Home.”, J Alzheimers Dis, vol. 49, no. 3, pp. 671-80, 2016.
, “Psychotropic Drug Prescription in Patients with Dementia: Nursing Home Residents Versus Patients Living at Home.”, J Alzheimers Dis, vol. 49, no. 3, pp. 671-80, 2016.
, “Medial Temporal Lobe Atrophy in Predementia Alzheimer's Disease: A Longitudinal Multi-Site Study Comparing Staging and A/T/N in a Clinical Research Cohort.”, J Alzheimers Dis, vol. 94, no. 1, pp. 259-279, 2023.
, “The Vanderbilt Memory & Aging Project: Study Design and Baseline Cohort Overview.”, J Alzheimers Dis, vol. 52, no. 2, pp. 539-59, 2016.
, “The Vanderbilt Memory & Aging Project: Study Design and Baseline Cohort Overview.”, J Alzheimers Dis, vol. 52, no. 2, pp. 539-59, 2016.
, “The Vanderbilt Memory & Aging Project: Study Design and Baseline Cohort Overview.”, J Alzheimers Dis, vol. 52, no. 2, pp. 539-59, 2016.
, “Cognitive Function Associated with Gut Microbial Abundance in Sucrose and S-Adenosyl-L-Methionine (SAMe) Metabolic Pathways.”, J Alzheimers Dis, vol. 87, no. 3, pp. 1115-1130, 2022.
, “Cognitive Function Associated with Gut Microbial Abundance in Sucrose and S-Adenosyl-L-Methionine (SAMe) Metabolic Pathways.”, J Alzheimers Dis, vol. 87, no. 3, pp. 1115-1130, 2022.
, “Memory-Related Frontal Brainwaves Predict Transition to Mild Cognitive Impairment in Healthy Older Individuals Five Years Before Diagnosis.”, J Alzheimers Dis, vol. 79, no. 2, pp. 531-541, 2021.
, “Memory-Related Frontal Brainwaves Predict Transition to Mild Cognitive Impairment in Healthy Older Individuals Five Years Before Diagnosis.”, J Alzheimers Dis, vol. 79, no. 2, pp. 531-541, 2021.
, “Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.”, Proc Natl Acad Sci U S A, vol. 108, no. 14, pp. 5819-24, 2011.
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