Biblio
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“Morroniside-Induced PP2A Activation Antagonizes Tau Hyperphosphorylation in a Cellular Model of Neurodegeneration.”, J Alzheimers Dis, vol. 51, no. 1, pp. 33-44, 2016.
, “Morroniside-Induced PP2A Activation Antagonizes Tau Hyperphosphorylation in a Cellular Model of Neurodegeneration.”, J Alzheimers Dis, vol. 51, no. 1, pp. 33-44, 2016.
, “Shared Genetic Risk Factors for Late-Life Depression and Alzheimer's Disease.”, J Alzheimers Dis, vol. 52, no. 1, pp. 1-15, 2016.
, “Anti-Inflammatory Gene Therapy Improves Spatial Memory Performance in a Mouse Model of Alzheimer's Disease.”, J Alzheimers Dis, vol. 85, no. 3, pp. 1001-1008, 2022.
, “Predictive factors for disease progression in patients with early-onset Alzheimer's disease.”, J Alzheimers Dis, vol. 49, no. 1, pp. 85-91, 2016.
, “Tobacco Smoke-Induced Brain White Matter Myelin Dysfunction: Potential Co-Factor Role of Smoking in Neurodegeneration.”, J Alzheimers Dis, vol. 50, no. 1, pp. 133-48, 2016.
, “Tobacco Smoke-Induced Brain White Matter Myelin Dysfunction: Potential Co-Factor Role of Smoking in Neurodegeneration.”, J Alzheimers Dis, vol. 50, no. 1, pp. 133-48, 2016.
, “Tobacco Smoke-Induced Brain White Matter Myelin Dysfunction: Potential Co-Factor Role of Smoking in Neurodegeneration.”, J Alzheimers Dis, vol. 50, no. 1, pp. 133-48, 2016.
, “Alzheimer's Disease: Recent Concepts on the Relation of Mitochondrial Disturbances, Excitotoxicity, Neuroinflammation, and Kynurenines.”, J Alzheimers Dis, vol. 62, no. 2, pp. 523-547, 2018.
, “Serum C-Peptide, Visfatin, Resistin, and Ghrelin are Altered in Sporadic and GRN-Associated Frontotemporal Lobar Degeneration.”, J Alzheimers Dis, vol. 61, no. 3, pp. 1053-1060, 2018.
, “GDF11 Rejuvenates Cerebrovascular Structure and Function in an Animal Model of Alzheimer's Disease.”, J Alzheimers Dis, vol. 62, no. 2, pp. 807-819, 2018.
, “Integrated systems approach identifies genetic nodes and networks in late-onset Alzheimer's disease.”, Cell, vol. 153, no. 3, pp. 707-20, 2013.
, “Subjective Memory Complaints in APOEɛ4 Carriers are Associated with High Amyloid-β Burden.”, J Alzheimers Dis, vol. 49, no. 4, pp. 1115-22, 2016.
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