Biblio
] , “Synaptic Compensation as a Probable Cause of Prolonged Mild Cognitive Impairment in Alzheimer's Disease: Implications from a Transgenic Mouse Model of the Disease.”, J Alzheimers Dis, vol. 56, no. 4, pp. 1385-1401, 2017.
, “Rbfox3/NeuN Regulates Alternative Splicing of Tau Exon 10.”, J Alzheimers Dis, vol. 66, no. 4, pp. 1695-1704, 2018.
, “Rats Display Sexual Dimorphism in Phosphorylation of Brain Tau with Age.”, J Alzheimers Dis, vol. 82, no. 2, pp. 855-869, 2021.
, “Prevention of Amyloid-β and Tau Pathologies, Associated Neurodegeneration, and Cognitive Deficit by Early Treatment with a Neurotrophic Compound.”, J Alzheimers Dis, vol. 58, no. 1, pp. 215-230, 2017.
, “A Novel Therapeutic Approach to Treat Alzheimer's Disease by Neurotrophic Support During the Period of Synaptic Compensation.”, J Alzheimers Dis, vol. 62, no. 3, pp. 1211-1218, 2018.
, “Neurotrophic Treatment Initiated During Early Postnatal Development Prevents the Alzheimer-Like Behavior and Synaptic Dysfunction.”, J Alzheimers Dis, vol. 82, no. 2, pp. 631-646, 2021.
, “Mechanism of Tau Hyperphosphorylation Involving Lysosomal Enzyme Asparagine Endopeptidase in a Mouse Model of Brain Ischemia.”, J Alzheimers Dis, vol. 63, no. 2, pp. 821-833, 2018.
, “Involvement of Activation of Asparaginyl Endopeptidase in Tau Hyperphosphorylation in Repetitive Mild Traumatic Brain Injury.”, J Alzheimers Dis, vol. 64, no. 3, pp. 709-722, 2018.
, “GSK-3β is Dephosphorylated by PP2A in a Leu309 Methylation-Independent Manner.”, J Alzheimers Dis, vol. 49, no. 2, pp. 365-75, 2016.
, “COVID-19 and Neurodegenerative Diseases: Prion-Like Spread and Long-Term Consequences.”, J Alzheimers Dis, vol. 88, no. 2, pp. 399-416, 2022.
, “Calpain I Activation Causes GLUT3 Proteolysis and Downregulation of O-GlcNAcylation in Alzheimer's Disease Brain.”, J Alzheimers Dis, vol. 62, no. 4, pp. 1737-1746, 2018.
