publication . Article . Other literature type . 2016

Amyloid-β and hyperphosphorylated tau synergy drives metabolic decline in preclinical Alzheimer's disease

Pascoal, T A; Mathotaarachchi, S; Mohades, S; Benedet, A L; Chung, C-O; Shin, M; Wang, S; Beaudry, T; Kang, M S; Soucy, J-P; ...
Open Access English
  • Published: 29 Mar 2016 Journal: Molecular Psychiatry, volume 22, issue 2, pages 306-311 (issn: 1359-4184, eissn: 1476-5578, Copyright policy)
  • Publisher: Nature Publishing Group
Abstract
This study was designed to test the interaction between amyloid-β and tau proteins as a determinant of metabolic decline in preclinical Alzheimer's disease (AD). We assessed 120 cognitively normal individuals with [18F]florbetapir positron emission tomography (PET) and cerebrospinal fluid (CSF) measurements at baseline, as well as [18F]fluorodeoxyglucose ([18F]FDG) PET at baseline and at 24 months. A voxel-based interaction model was built to test the associations between continuous measurements of CSF biomarkers, [18F]florbetapir and [18F]FDG standardized uptake value ratios (SUVR). We found that the synergistic interaction between [18F]florbetapir SUVR and CSF...
Subjects
free text keywords: Original Article
Funded by
NIH| Alzheimers Disease Neuroimaging Initiative
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1U01AG024904-01
  • Funding stream: NATIONAL INSTITUTE ON AGING
,
CIHR
Project
  • Funder: Canadian Institutes of Health Research (CIHR)
46 references, page 1 of 4

Jack CR Jr, Knopman DS, Jagust WJ, Petersen RC, Weiner MW, Aisen PS et al. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol 2013; 12: 207–216.23332364 [OpenAIRE] [PubMed]

Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 2002; 297: 353–356.12130773 [OpenAIRE] [PubMed]

Jack CR Jr., Wiste HJ, Knopman DS, Vemuri P, Mielke MM, Weigand SD et al. Rates of beta-amyloid accumulation are independent of hippocampal neurodegeneration. Neurology 2014; 82: 1605–1612.24706010 [OpenAIRE] [PubMed]

Knopman DS, Jack CR Jr., Wiste HJ, Weigand SD, Vemuri P, Lowe VJ et al. Selective worsening of brain injury biomarker abnormalities in cognitively normal elderly persons with beta-amyloidosis. JAMA Neurol 2013; 70: 1030–1038.23797806 [OpenAIRE] [PubMed]

Mormino EC, Betensky RA, Hedden T, Schultz AP, Amariglio RE, Rentz DM et al. Synergistic effect of beta-amyloid and neurodegeneration on cognitive decline in clinically normal individuals. JAMA Neurol 2014; 71: 1379–1385.25222039 [OpenAIRE] [PubMed]

Vos SJ, Xiong C, Visser PJ, Jasielec MS, Hassenstab J, Grant EA et al. Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. Lancet Neurol 2013; 12: 957–965.24012374 [OpenAIRE] [PubMed]

Knopman DS, Jack CR Jr., Wiste HJ, Weigand SD, Vemuri P, Lowe V et al. Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease. Neurology 2012; 78: 1576–1582.22551733 [OpenAIRE] [PubMed]

Roe CM, Fagan AM, Grant EA, Hassenstab J, Moulder KL, Maue Dreyfus D et al. Amyloid imaging and CSF biomarkers in predicting c ognitive impairment up to 7.5 years later. Neurology 2013; 80: 1784–1791.23576620 [OpenAIRE] [PubMed]

Duyckaerts C. Tau pathology in children and young adults: can you still be unconditionally baptist? Acta Neuropathol 2011; 121: 145–147.21225273 [OpenAIRE] [PubMed]

Trojanowski JQ. Tauists, Baptists, Syners, Apostates, and new data. Ann Neurol 2002; 52: 263–265.12205637 [OpenAIRE] [PubMed]

Fortea J, Vilaplana E, Alcolea D, Carmona-Iragui M, Sanchez-Saudinos MB, Sala I et al. Cerebrospinal fluid beta-amyloid and phospho-tau biomarker interactions affecting brain structure in preclinical Alzheimer disease. Ann Neurol 2014; 76: 223–230.24852682 [PubMed]

Desikan RS, McEvoy LK, Thompson WK, Holland D, Roddey JC, Blennow K et al. Amyloid-beta associated volume loss occurs only in the presence of phospho-tau. Ann Neurol 2011; 70: 657–661.22002658 [OpenAIRE] [PubMed]

Desikan RS, McEvoy LK, Thompson WK, Holland D, Brewer JB, Aisen PS et al. Amyloid-beta—associated clinical decline occurs only in the presence of elevated P-tau. Arch Neurol 2012; 69: 709–713.22529247 [OpenAIRE] [PubMed]

Ittner LM, Gotz J. Amyloid-beta and tau—a toxic pas de deux in Alzheimer's disease. Nat Rev Neurosci 2011; 12: 65–72.

Chabrier MA, Cheng D, Castello NA, Green KN, LaFerla FM. Synergistic effects of amyloid-beta and wild-type human tau on dendritic spine loss in a floxed double transgenic model of Alzheimer's disease. Neurobiol Dis 2014; 64: 107–117.24440055 [OpenAIRE] [PubMed]

46 references, page 1 of 4
Abstract
This study was designed to test the interaction between amyloid-β and tau proteins as a determinant of metabolic decline in preclinical Alzheimer's disease (AD). We assessed 120 cognitively normal individuals with [18F]florbetapir positron emission tomography (PET) and cerebrospinal fluid (CSF) measurements at baseline, as well as [18F]fluorodeoxyglucose ([18F]FDG) PET at baseline and at 24 months. A voxel-based interaction model was built to test the associations between continuous measurements of CSF biomarkers, [18F]florbetapir and [18F]FDG standardized uptake value ratios (SUVR). We found that the synergistic interaction between [18F]florbetapir SUVR and CSF...
Subjects
free text keywords: Original Article
Funded by
NIH| Alzheimers Disease Neuroimaging Initiative
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 1U01AG024904-01
  • Funding stream: NATIONAL INSTITUTE ON AGING
,
CIHR
Project
  • Funder: Canadian Institutes of Health Research (CIHR)
46 references, page 1 of 4

Jack CR Jr, Knopman DS, Jagust WJ, Petersen RC, Weiner MW, Aisen PS et al. Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol 2013; 12: 207–216.23332364 [OpenAIRE] [PubMed]

Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 2002; 297: 353–356.12130773 [OpenAIRE] [PubMed]

Jack CR Jr., Wiste HJ, Knopman DS, Vemuri P, Mielke MM, Weigand SD et al. Rates of beta-amyloid accumulation are independent of hippocampal neurodegeneration. Neurology 2014; 82: 1605–1612.24706010 [OpenAIRE] [PubMed]

Knopman DS, Jack CR Jr., Wiste HJ, Weigand SD, Vemuri P, Lowe VJ et al. Selective worsening of brain injury biomarker abnormalities in cognitively normal elderly persons with beta-amyloidosis. JAMA Neurol 2013; 70: 1030–1038.23797806 [OpenAIRE] [PubMed]

Mormino EC, Betensky RA, Hedden T, Schultz AP, Amariglio RE, Rentz DM et al. Synergistic effect of beta-amyloid and neurodegeneration on cognitive decline in clinically normal individuals. JAMA Neurol 2014; 71: 1379–1385.25222039 [OpenAIRE] [PubMed]

Vos SJ, Xiong C, Visser PJ, Jasielec MS, Hassenstab J, Grant EA et al. Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study. Lancet Neurol 2013; 12: 957–965.24012374 [OpenAIRE] [PubMed]

Knopman DS, Jack CR Jr., Wiste HJ, Weigand SD, Vemuri P, Lowe V et al. Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease. Neurology 2012; 78: 1576–1582.22551733 [OpenAIRE] [PubMed]

Roe CM, Fagan AM, Grant EA, Hassenstab J, Moulder KL, Maue Dreyfus D et al. Amyloid imaging and CSF biomarkers in predicting c ognitive impairment up to 7.5 years later. Neurology 2013; 80: 1784–1791.23576620 [OpenAIRE] [PubMed]

Duyckaerts C. Tau pathology in children and young adults: can you still be unconditionally baptist? Acta Neuropathol 2011; 121: 145–147.21225273 [OpenAIRE] [PubMed]

Trojanowski JQ. Tauists, Baptists, Syners, Apostates, and new data. Ann Neurol 2002; 52: 263–265.12205637 [OpenAIRE] [PubMed]

Fortea J, Vilaplana E, Alcolea D, Carmona-Iragui M, Sanchez-Saudinos MB, Sala I et al. Cerebrospinal fluid beta-amyloid and phospho-tau biomarker interactions affecting brain structure in preclinical Alzheimer disease. Ann Neurol 2014; 76: 223–230.24852682 [PubMed]

Desikan RS, McEvoy LK, Thompson WK, Holland D, Roddey JC, Blennow K et al. Amyloid-beta associated volume loss occurs only in the presence of phospho-tau. Ann Neurol 2011; 70: 657–661.22002658 [OpenAIRE] [PubMed]

Desikan RS, McEvoy LK, Thompson WK, Holland D, Brewer JB, Aisen PS et al. Amyloid-beta—associated clinical decline occurs only in the presence of elevated P-tau. Arch Neurol 2012; 69: 709–713.22529247 [OpenAIRE] [PubMed]

Ittner LM, Gotz J. Amyloid-beta and tau—a toxic pas de deux in Alzheimer's disease. Nat Rev Neurosci 2011; 12: 65–72.

Chabrier MA, Cheng D, Castello NA, Green KN, LaFerla FM. Synergistic effects of amyloid-beta and wild-type human tau on dendritic spine loss in a floxed double transgenic model of Alzheimer's disease. Neurobiol Dis 2014; 64: 107–117.24440055 [OpenAIRE] [PubMed]

46 references, page 1 of 4
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