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“Report of the task force on designing clinical trials in early (predementia) AD.”, Neurology, vol. 76, no. 3, pp. 280-6, 2011.
, “Report of the task force on designing clinical trials in early (predementia) AD.”, Neurology, vol. 76, no. 3, pp. 280-6, 2011.
, “Report of the task force on designing clinical trials in early (predementia) AD.”, Neurology, vol. 76, no. 3, pp. 280-6, 2011.
, “Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.”, Proc Natl Acad Sci U S A, vol. 108, no. 14, pp. 5819-24, 2011.
, “Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.”, Proc Natl Acad Sci U S A, vol. 108, no. 14, pp. 5819-24, 2011.
, “Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.”, Proc Natl Acad Sci U S A, vol. 108, no. 14, pp. 5819-24, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease.”, Alzheimers Dement, vol. 7, no. 3, pp. 280-92, 2011.
, “Vascular risk factors promote conversion from mild cognitive impairment to Alzheimer disease.”, Neurology, vol. 76, no. 17, pp. 1485-91, 2011.
, “Vascular risk factors promote conversion from mild cognitive impairment to Alzheimer disease.”, Neurology, vol. 76, no. 17, pp. 1485-91, 2011.
, “Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia.”, Arch Gen Psychiatry, vol. 69, no. 1, pp. 98-106, 2012.
, “Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia.”, Arch Gen Psychiatry, vol. 69, no. 1, pp. 98-106, 2012.
, “Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia.”, Arch Gen Psychiatry, vol. 69, no. 1, pp. 98-106, 2012.
, “Cognitive reserve in ageing and Alzheimer's disease.”, Lancet Neurol, vol. 11, no. 11, pp. 1006-12, 2012.
, “Cognitive reserve in ageing and Alzheimer's disease.”, Lancet Neurol, vol. 11, no. 11, pp. 1006-12, 2012.
, “Cognitive reserve in ageing and Alzheimer's disease.”, Lancet Neurol, vol. 11, no. 11, pp. 1006-12, 2012.
, “Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline.”, J Clin Invest, vol. 122, no. 4, pp. 1316-38, 2012.
, “Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline.”, J Clin Invest, vol. 122, no. 4, pp. 1316-38, 2012.
, “Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline.”, J Clin Invest, vol. 122, no. 4, pp. 1316-38, 2012.
, “Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline.”, J Clin Invest, vol. 122, no. 4, pp. 1316-38, 2012.
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