Biblio
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“Dogs with Cognitive Dysfunction as a Spontaneous Model for Early Alzheimer's Disease: A Translational Study of Neuropathological and Inflammatory Markers.”, J Alzheimers Dis, vol. 52, no. 2, pp. 433-49, 2016.
, “Dogs with Cognitive Dysfunction as a Spontaneous Model for Early Alzheimer's Disease: A Translational Study of Neuropathological and Inflammatory Markers.”, J Alzheimers Dis, vol. 52, no. 2, pp. 433-49, 2016.
, “Effect of Continuous Propofol Infusion in Rat on Tau Phosphorylation with or without Temperature Control.”, J Alzheimers Dis, vol. 51, no. 1, pp. 213-26, 2016.
, “Effect of Tween-20 on Core Biomarkers Measured in Cerebrospinal Fluid from Patients with Alzheimer's Disease, Mild Cognitive Impairment, or Healthy Control Individuals.”, J Alzheimers Dis, vol. 49, no. 2, pp. 493-502, 2016.
, “Efficacy and Safety of ABT-126 in Subjects with Mild-to-Moderate Alzheimer's Disease on Stable Doses of Acetylcholinesterase Inhibitors: A Randomized, Double-Blind, Placebo-Controlled Study.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1237-47, 2016.
, “Efficacy and Safety of MMFS-01, a Synapse Density Enhancer, for Treating Cognitive Impairment in Older Adults: A Randomized, Double-Blind, Placebo-Controlled Trial.”, J Alzheimers Dis, vol. 49, no. 4, pp. 971-90, 2016.
, “Efficacy and Safety of Sustained Release Donepezil High Dose versus Immediate Release Donepezil Standard Dose in Japanese Patients with Severe Alzheimer's Disease: A Randomized, Double-Blind Trial.”, J Alzheimers Dis, vol. 52, no. 1, pp. 345-57, 2016.
, “Evaluation of Cerebrospinal Fluid Assay Variability in Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 2, pp. 463-70, 2016.
, “Exercise Plus Cognitive Performance Over and Above Exercise Alone in Subjects with Mild Cognitive Impairment.”, J Alzheimers Dis, vol. 50, no. 1, pp. 19-25, 2016.
, “Fibrillar Amyloid-β Accumulation Triggers an Inflammatory Mechanism Leading to Hyperphosphorylation of the Carboxyl-Terminal End of Tau Polypeptide in the Hippocampal Formation of the 3×Tg-AD Transgenic Mouse.”, J Alzheimers Dis, vol. 52, no. 1, pp. 243-69, 2016.
, “Gene Expression Profiling in the APP/PS1KI Mouse Model of Familial Alzheimer's Disease.”, J Alzheimers Dis, vol. 50, no. 2, pp. 397-409, 2016.
, “Greater specificity for cerebrospinal fluid P-tau231 over P-tau181 in the differentiation of healthy controls from Alzheimer's disease.”, J Alzheimers Dis, vol. 49, no. 1, pp. 93-100, 2016.
, “GSK-3β is Dephosphorylated by PP2A in a Leu309 Methylation-Independent Manner.”, J Alzheimers Dis, vol. 49, no. 2, pp. 365-75, 2016.
, “Hemisphere Asymmetry of Response to Pharmacologic Treatment in an Alzheimer's Disease Mouse Model.”, J Alzheimers Dis, vol. 51, no. 2, pp. 333-8, 2016.
, “Hierarchical Distribution of the Tau Cytoskeletal Pathology in the Thalamus of Alzheimer's Disease Patients.”, J Alzheimers Dis, vol. 49, no. 4, pp. 905-15, 2016.
, “Hierarchical Distribution of the Tau Cytoskeletal Pathology in the Thalamus of Alzheimer's Disease Patients.”, J Alzheimers Dis, vol. 49, no. 4, pp. 905-15, 2016.
, “Homotaurine Effects on Hippocampal Volume Loss and Episodic Memory in Amnestic Mild Cognitive Impairment.”, J Alzheimers Dis, vol. 50, no. 3, pp. 807-16, 2016.
, “Hyperactivity with Agitative-Like Behavior in a Mouse Tauopathy Model.”, J Alzheimers Dis, vol. 49, no. 3, pp. 783-95, 2016.
, “Hyperactivity with Agitative-Like Behavior in a Mouse Tauopathy Model.”, J Alzheimers Dis, vol. 49, no. 3, pp. 783-95, 2016.
, “Hyperactivity with Agitative-Like Behavior in a Mouse Tauopathy Model.”, J Alzheimers Dis, vol. 49, no. 3, pp. 783-95, 2016.
, “Impact of Omega-3 Fatty Acid Supplementation on Memory Functions in Healthy Older Adults.”, J Alzheimers Dis, vol. 51, no. 3, pp. 713-25, 2016.
, “Impaired Autophagy in APOE4 Astrocytes.”, J Alzheimers Dis, vol. 51, no. 3, pp. 915-27, 2016.
, “Increased Intrinsic Activity of Medial-Temporal Lobe Subregions is Associated with Decreased Cortical Thickness of Medial-Parietal Areas in Patients with Alzheimer's Disease Dementia.”, J Alzheimers Dis, vol. 51, no. 1, pp. 313-26, 2016.
, “Inhibition of Cholesterol Biosynthesis Reduces γ-Secretase Activity and Amyloid-β Generation.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1057-68, 2016.
, “Inhibition of Cholesterol Biosynthesis Reduces γ-Secretase Activity and Amyloid-β Generation.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1057-68, 2016.
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