Biblio
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“Pupillary Responses as a Biomarker of Early Risk for Alzheimer's Disease.”, J Alzheimers Dis, vol. 56, no. 4, pp. 1419-1428, 2017.
, “Reduced Cardiovascular Functions in Patients with Alzheimer's Disease.”, J Alzheimers Dis, vol. 58, no. 3, pp. 919-925, 2017.
, “Reduced Cerebrospinal Fluid Concentration of Apolipoprotein A-I in Patients with Alzheimer's Disease.”, J Alzheimers Dis, vol. 59, no. 3, pp. 1017-1026, 2017.
, “Reduced Cerebrospinal Fluid Concentration of Apolipoprotein A-I in Patients with Alzheimer's Disease.”, J Alzheimers Dis, vol. 59, no. 3, pp. 1017-1026, 2017.
, “Relation of Odor Identification with Alzheimer's Disease Markers in Cerebrospinal Fluid and Cognition.”, J Alzheimers Dis, vol. 60, no. 3, pp. 1025-1034, 2017.
, “Risk Factors for Mild Cognitive Impairment in German Primary Care Practices.”, J Alzheimers Dis, vol. 56, no. 1, pp. 379-384, 2017.
, “Sample Size Estimation for Alzheimer's Disease Trials from Japanese ADNI Serial Magnetic Resonance Imaging.”, J Alzheimers Dis, vol. 56, no. 1, pp. 75-88, 2017.
, “Sample Size Estimation for Alzheimer's Disease Trials from Japanese ADNI Serial Magnetic Resonance Imaging.”, J Alzheimers Dis, vol. 56, no. 1, pp. 75-88, 2017.
, “Screening for Alzheimer's Disease: Cognitive Impairment in Self-Referred and Memory Clinic-Referred Patients.”, J Alzheimers Dis, vol. 60, no. 4, pp. 1621-1631, 2017.
, “Sex Difference in Aerobic Exercise Efficacy to Improve Cognition in Older Adults with Vascular Cognitive Impairment: Secondary Analysis of a Randomized Controlled Trial.”, J Alzheimers Dis, vol. 60, no. 4, pp. 1397-1410, 2017.
, “Sleep Deprivation Induced Plasma Amyloid-β Transport Disturbance in Healthy Young Adults.”, J Alzheimers Dis, vol. 57, no. 3, pp. 899-906, 2017.
, “Sporadic Cases with Novel Mutations and Pedigree in Hereditary Leukoencephalopathy with Axonal Spheroids.”, J Alzheimers Dis, vol. 56, no. 3, pp. 893-898, 2017.
, “Stress-Induced Synaptic Dysfunction and Neurotransmitter Release in Alzheimer's Disease: Can Neurotransmitters and Neuromodulators be Potential Therapeutic Targets?”, J Alzheimers Dis, vol. 57, no. 4, pp. 1017-1039, 2017.
, “Stress-Induced Synaptic Dysfunction and Neurotransmitter Release in Alzheimer's Disease: Can Neurotransmitters and Neuromodulators be Potential Therapeutic Targets?”, J Alzheimers Dis, vol. 57, no. 4, pp. 1017-1039, 2017.
, “Tai Chi Chuan and Baduanjin Increase Grey Matter Volume in Older Adults: A Brain Imaging Study.”, J Alzheimers Dis, vol. 60, no. 2, pp. 389-400, 2017.
, “Tau Pathology Promotes the Reorganization of the Extracellular Matrix and Inhibits the Formation of Perineuronal Nets by Regulating the Expression and the Distribution of Hyaluronic Acid Synthases.”, J Alzheimers Dis, vol. 57, no. 2, pp. 395-409, 2017.
, “Temporal Order of Alzheimer's Disease-Related Cognitive Marker Changes in BLSA and WRAP Longitudinal Studies.”, J Alzheimers Dis, vol. 59, no. 4, pp. 1335-1347, 2017.
, “Temporal Order of Alzheimer's Disease-Related Cognitive Marker Changes in BLSA and WRAP Longitudinal Studies.”, J Alzheimers Dis, vol. 59, no. 4, pp. 1335-1347, 2017.
, “TMEM230 Accumulation in Granulovacuolar Degeneration Bodies and Dystrophic Neurites of Alzheimer's Disease.”, J Alzheimers Dis, vol. 58, no. 4, pp. 1027-1033, 2017.
, “Trajectories of Multidimensional Caregiver Burden in Chinese Informal Caregivers for Dementia: Evidence from Exploratory and Confirmatory Factor Analysis of the Zarit Burden Interview.”, J Alzheimers Dis, vol. 59, no. 4, pp. 1317-1325, 2017.
, “Two Novel Mutations in the First Transmembrane Domain of Presenilin1 Cause Young-Onset Alzheimer's Disease.”, J Alzheimers Dis, vol. 58, no. 4, pp. 1035-1041, 2017.
, “Two Novel Mutations in the First Transmembrane Domain of Presenilin1 Cause Young-Onset Alzheimer's Disease.”, J Alzheimers Dis, vol. 58, no. 4, pp. 1035-1041, 2017.
, “Urine Formaldehyde Predicts Cognitive Impairment in Post-Stroke Dementia and Alzheimer's Disease.”, J Alzheimers Dis, vol. 55, no. 3, pp. 1031-1038, 2017.
, “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.
, “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.
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