Biblio
“Patterns of Brain Iron Accumulation in Vascular Dementia and Alzheimer's Dementia Using Quantitative Susceptibility Mapping Imaging.”, J Alzheimers Dis, vol. 51, no. 3, pp. 737-45, 2016.
, “Evaluation of Cerebrospinal Fluid Assay Variability in Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 2, pp. 463-70, 2016.
, “Tau Accumulation in Primary Motor Cortex of Variant Alzheimer's Disease with Spastic Paraparesis.”, J Alzheimers Dis, vol. 51, no. 3, pp. 671-5, 2016.
, “Fluoxetine Treatment Induces Seizure Behavior and Premature Death in APPswe/PS1dE9 Mice.”, J Alzheimers Dis, vol. 51, no. 3, pp. 677-82, 2016.
, “Do Microglia Default on Network Maintenance in Alzheimer's Disease?”, J Alzheimers Dis, vol. 51, no. 3, pp. 657-69, 2016.
, “Differential Diagnosis of Dementia with High Levels of Cerebrospinal Fluid Tau Protein.”, J Alzheimers Dis, vol. 51, no. 3, pp. 905-13, 2016.
, “Intranasal TAT-haFGF Improves Cognition and Amyloid-β Pathology in an AβPP/PS1 Mouse Model of Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 4, pp. 985-90, 2016.
, “Genetic Counseling and Testing for Alzheimer's Disease and Frontotemporal Lobar Degeneration: An Italian Consensus Protocol.”, J Alzheimers Dis, vol. 51, no. 1, pp. 277-91, 2016.
, “Apolipoprotein E Related Co-Morbidities and Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 4, pp. 935-48, 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.
, “Region-Specific Vulnerability to Oxidative Stress, Neuroinflammation, and Tau Hyperphosphorylation in Experimental Diabetes Mellitus Mice.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1209-24, 2016.
, “What are the Most Frequently Impaired Markers of Neurodegeneration in ADNI Subjects?”, J Alzheimers Dis, vol. 51, no. 3, pp. 793-800, 2016.
, “Enalapril Alone or Co-Administered with Losartan Rescues Cerebrovascular Dysfunction, but not Mnemonic Deficits or Amyloidosis in a Mouse Model of Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1183-95, 2016.
, “Drivers: A Biologically Contextualized, Cross-Inferential View of the Epidemiology of Neurodegenerative Disorders.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1003-22, 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.
, “Apolipoprotein ɛ4 is Associated with Dementia and Cognitive Impairment Predominantly Due to Alzheimer's Disease and Not with Vascular Cognitive Impairment: A Singapore-Based Cohort.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1111-8, 2016.
, “Metabolic Syndrome and Mild Cognitive Impairment: A Case-Control Study among Elderly in a Shanghai Suburb.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1175-82, 2016.
, “Brain-Specific Basal and Novelty-Induced Alternations in PI3K-Akt and MAPK/ERK Signaling in a Middle-Aged AβPP/PS1 Mouse Model of Alzheimer's Disease.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1157-73, 2016.
, “Functional Connectivity of Ventral and Dorsal Visual Streams in Posterior Cortical Atrophy.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1119-30, 2016.
, “Differential Mass Spectrometry Profiles of Tau Protein in the Cerebrospinal Fluid of Patients with Alzheimer's Disease, Progressive Supranuclear Palsy, and Dementia with Lewy Bodies.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1033-43, 2016.
, “Inhibition of Cholesterol Biosynthesis Reduces γ-Secretase Activity and Amyloid-β Generation.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1057-68, 2016.
, “Metallothioneins in Prion- and Amyloid-Related Diseases.”, J Alzheimers Dis, vol. 51, no. 3, pp. 637-56, 2016.
, “Prediction of Progressive Mild Cognitive Impairment by Multi-Modal Neuroimaging Biomarkers.”, J Alzheimers Dis, vol. 51, no. 4, pp. 1045-56, 2016.
, “Comparison of Prefrontal Atrophy and Episodic Memory Performance in Dysexecutive Alzheimer's Disease and Behavioral-Variant Frontotemporal Dementia.”, J Alzheimers Dis, vol. 51, no. 3, pp. 889-903, 2016.
, “Patients that have Undergone Hemodialysis Exhibit Lower Amyloid Deposition in the Brain: Evidence Supporting a Therapeutic Strategy for Alzheimer's Disease by Removal of Blood Amyloid.”, J Alzheimers Dis, vol. 51, no. 4, pp. 997-1002, 2016.
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