Biblio
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Author Title Type Year Filters: First Letter Of Last Name is B [Clear All Filters]
“Comparison of Steady-State Pharmacokinetics of Donepezil Transdermal Delivery System with Oral Donepezil.”, J Alzheimers Dis, vol. 90, no. 1, pp. 161-172, 2022.
, “Cleveland Clinic Cognitive Battery (C3B): Normative, Reliability, and Validation Studies of a Self-Administered Computerized Tool for Screening Cognitive Dysfunction in Primary Care.”, J Alzheimers Dis, vol. 92, no. 3, pp. 1051-1066, 2023.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Human apoE isoforms differentially regulate brain amyloid-β peptide clearance.”, Sci Transl Med, vol. 3, no. 89, p. 89ra57, 2011.
, “Human apoE isoforms differentially regulate brain amyloid-β peptide clearance.”, Sci Transl Med, vol. 3, no. 89, p. 89ra57, 2011.
, “Predictive Value of Cerebrospinal Fluid Visinin-Like Protein-1 Levels for Alzheimer's Disease Early Detection and Differential Diagnosis in Patients with Mild Cognitive Impairment.”, J Alzheimers Dis, vol. 50, no. 3, pp. 765-78, 2016.
, “Anti-amyloid β autoantibodies in cerebral amyloid angiopathy-related inflammation: implications for amyloid-modifying therapies.”, Ann Neurol, vol. 73, no. 4, pp. 449-58, 2013.
, “Anti-amyloid β autoantibodies in cerebral amyloid angiopathy-related inflammation: implications for amyloid-modifying therapies.”, Ann Neurol, vol. 73, no. 4, pp. 449-58, 2013.
, “Clinical Impact of a Second FDG-PET in Atypical/Unclear Dementia Syndromes.”, J Alzheimers Dis, vol. 49, no. 3, pp. 695-705, 2016.
, “Clinical Impact of a Second FDG-PET in Atypical/Unclear Dementia Syndromes.”, J Alzheimers Dis, vol. 49, no. 3, pp. 695-705, 2016.
, “Clinical Impact of a Second FDG-PET in Atypical/Unclear Dementia Syndromes.”, J Alzheimers Dis, vol. 49, no. 3, pp. 695-705, 2016.
, “Characterizing Aging, Mild Cognitive Impairment, and Dementia with Blood-Based Biomarkers and Neuropsychology.”, J Alzheimers Dis, vol. 50, no. 1, pp. 111-26, 2016.
, “Reduction of Amyloid-β Plasma Levels by Hemodialysis: An Anti-Amyloid Treatment Strategy?”, J Alzheimers Dis, vol. 50, no. 3, pp. 791-6, 2016.
, “Looking for Neuroimaging Markers in Frontotemporal Lobar Degeneration Clinical Trials: A Multi-Voxel Pattern Analysis Study in Granulin Disease.”, J Alzheimers Dis, vol. 51, no. 1, pp. 249-62, 2016.
, “Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study.”, J Alzheimers Dis, vol. 50, no. 3, pp. 887-94, 2016.
, “Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study.”, J Alzheimers Dis, vol. 50, no. 3, pp. 887-94, 2016.
, “Plasma Phospholipid and Sphingolipid Alterations in Presenilin1 Mutation Carriers: A Pilot Study.”, J Alzheimers Dis, vol. 50, no. 3, pp. 887-94, 2016.
, “Association of Serum Vitamin D with the Risk of Incident Dementia and Subclinical Indices of Brain Aging: The Framingham Heart Study.”, J Alzheimers Dis, vol. 51, no. 2, pp. 451-61, 2016.
, “Association of Serum Vitamin D with the Risk of Incident Dementia and Subclinical Indices of Brain Aging: The Framingham Heart Study.”, J Alzheimers Dis, vol. 51, no. 2, pp. 451-61, 2016.
, “Preliminary Study of Plasma Exosomal Tau as a Potential Biomarker for Chronic Traumatic Encephalopathy.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1099-109, 2016.
, “Differential Diagnosis of Dementia with High Levels of Cerebrospinal Fluid Tau Protein.”, J Alzheimers Dis, vol. 51, no. 3, pp. 905-13, 2016.
, “Differential Diagnosis of Dementia with High Levels of Cerebrospinal Fluid Tau Protein.”, J Alzheimers Dis, vol. 51, no. 3, pp. 905-13, 2016.
, “The Cognitive Change Index as a Measure of Self and Informant Perception of Cognitive Decline: Relation to Neuropsychological Tests.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1145-55, 2016.
, “White Matter Abnormalities Track Disease Progression in PSEN1 Autosomal Dominant Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 3, pp. 827-35, 2016.
, “White Matter Abnormalities Track Disease Progression in PSEN1 Autosomal Dominant Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 3, pp. 827-35, 2016.
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