Florbetapir PET analysis of amyloid-β deposition in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional study
Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinic...
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| Published in | Lancet neurology Vol. 11; no. 12; pp. 1057 - 1065 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.12.2012
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease.
Between Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18–60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition.
We enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3–33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively. 18F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3–40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions.
These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease.
Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona. |
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| AbstractList | Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease.
Between Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18–60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition.
We enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3–33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively. 18F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3–40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions.
These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease.
Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona. Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease.BACKGROUNDFibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease.Between Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18-60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition.METHODSBetween Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18-60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition.We enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3-33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively. (18)F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3-40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions.FINDINGSWe enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3-33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively. (18)F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3-40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions.These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease.INTERPRETATIONThese findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease.Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona.FUNDINGAvid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona. Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease. Between Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18-60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition. We enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3-33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively. (18)F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3-40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions. These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease. Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona. Summary Background Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease. Methods Between Aug 1 and Dec 6, 2011, members of the familial Alzheimer's disease Colombian kindred aged 18–60 years were recruited from the Alzheimer's Prevention Initiative's registry at the University of Antioquia, Medellín, Colombia. Cross-sectional assessment using florbetapir PET was done in symptomatic mutation carriers with mild cognitive impairment or mild dementia, asymptomatic carriers, and asymptomatic non-carriers. These assessments were done at the Banner Alzheimer's Institute in Phoenix, AZ, USA. A cortical grey matter mask consisting of six predefined regions.was used to measure mean cortical florbetapir PET binding. Cortical-to-pontine standard-uptake value ratios were used to characterise the cross-sectional accumulation of fibrillar Aβ deposition in carriers and non-carriers with regression analysis and to estimate the trajectories of fibrillar Aβ deposition. Findings We enrolled a cohort of 11 symptomatic individuals, 19 presymptomatic mutation carriers, and 20 asymptomatic non-carriers, ranging in age from 20 to 56 years. There was greater florbetapir binding in asymptomatic PSEN1 E280A mutation carriers than in age matched non-carriers. Fibrillar Aβ began to accumulate in PSEN 1E280A mutation carriers at a mean age of 28·2 years (95% CI 27·3–33·4), about 16 years and 21 years before the predicted median ages at mild cognitive impairment and dementia onset, respectively.18 F florbetapir binding rose steeply over the next 9·4 years and plateaued at a mean age of 37·6 years (95% CI 35·3–40·2), about 6 and 11 years before the expected respective median ages at mild cognitive impairment and dementia onset. Prominent florbetapir binding was seen in the anterior and posterior cingulate, precuneus, and parietotemporal and frontal grey matter, as well as in the basal ganglia. Binding in the basal ganglia was not seen earlier or more prominently than in other regions. Interpretation These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease. Funding Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona. |
| Author | Langbaum, Jessica BS Quiroz, Yakeel T Lopera, Francisco Lopez, Liliana Ayutyanont, Napatkamon Reiman, Eric M Thiyyagura, Pradeep Kosik, Kenneth S Fleisher, Adam S Reiman, Rebecca A Chen, Kewei Huentelman, Matthew J Giraldo, Margarita Mo, Hua Roontiva, Auttawut Garcia, Gloria Tariot, Pierre N Langois, Carolyn M Acosta-Baena, Natalia Jakimovich, Laura J Gomez, Madelyn Gutierrez Moreno, Sonia Lee, Wendy |
| Author_xml | – sequence: 1 givenname: Adam S surname: Fleisher fullname: Fleisher, Adam S email: adam.fleisher@bannerhealth.com organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 2 givenname: Kewei surname: Chen fullname: Chen, Kewei organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 3 givenname: Yakeel T surname: Quiroz fullname: Quiroz, Yakeel T organization: Center for Memory and Brain, Psychology Department, Boston University, Boston, MA, USA – sequence: 4 givenname: Laura J surname: Jakimovich fullname: Jakimovich, Laura J organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 5 givenname: Madelyn Gutierrez surname: Gomez fullname: Gomez, Madelyn Gutierrez organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 6 givenname: Carolyn M surname: Langois fullname: Langois, Carolyn M organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 7 givenname: Jessica BS surname: Langbaum fullname: Langbaum, Jessica BS organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 8 givenname: Napatkamon surname: Ayutyanont fullname: Ayutyanont, Napatkamon organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 9 givenname: Auttawut surname: Roontiva fullname: Roontiva, Auttawut organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 10 givenname: Pradeep surname: Thiyyagura fullname: Thiyyagura, Pradeep organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 11 givenname: Wendy surname: Lee fullname: Lee, Wendy organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 12 givenname: Hua surname: Mo fullname: Mo, Hua organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 13 givenname: Liliana surname: Lopez fullname: Lopez, Liliana organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 14 givenname: Sonia surname: Moreno fullname: Moreno, Sonia organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 15 givenname: Natalia surname: Acosta-Baena fullname: Acosta-Baena, Natalia organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 16 givenname: Margarita surname: Giraldo fullname: Giraldo, Margarita organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 17 givenname: Gloria surname: Garcia fullname: Garcia, Gloria organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 18 givenname: Rebecca A surname: Reiman fullname: Reiman, Rebecca A organization: Division of Neurogenomics, Translational Genomics Research Institute, Phoenix, AZ, USA – sequence: 19 givenname: Matthew J surname: Huentelman fullname: Huentelman, Matthew J organization: Division of Neurogenomics, Translational Genomics Research Institute, Phoenix, AZ, USA – sequence: 20 givenname: Kenneth S surname: Kosik fullname: Kosik, Kenneth S organization: Neuroscience Research Institute, Department of Molecular Cellular Developmental Biology, University of California, Santa Barbara, CA, USA – sequence: 21 givenname: Pierre N surname: Tariot fullname: Tariot, Pierre N organization: Banner Alzheimer's Institute, Phoenix, AZ, USA – sequence: 22 givenname: Francisco surname: Lopera fullname: Lopera, Francisco organization: Neurosciences Group, University of Antioquia, Medellín, Columbia – sequence: 23 givenname: Eric M surname: Reiman fullname: Reiman, Eric M organization: Banner Alzheimer's Institute, Phoenix, AZ, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23137949$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1007/BF00294646 10.1001/archneurol.2009.285 10.1038/sj.jcbfm.9600146 10.2967/jnumed.109.065284 10.1001/jama.1997.03540340027028 10.1001/jama.2010.2008 10.1016/j.neuroimage.2012.01.099 10.1001/archneurol.2011.150 10.1001/archneurol.2011.77 10.1016/S1474-4422(09)70299-6 10.1056/NEJM199603213341202 10.1016/j.jalz.2011.03.005 10.1523/JNEUROSCI.0730-07.2007 10.1385/JMN:17:2:101 10.1002/ana.20009 10.1073/pnas.0900345106 10.1016/S1474-4422(12)70228-4 10.1212/WNL.43.8.1467 10.1093/brain/awn107 10.1172/JCI24761 10.1093/brain/aws125 10.1212/WNL.58.12.1791 10.1016/j.cell.2005.02.008 10.1016/j.neurobiolaging.2010.04.007 10.1016/S1474-4422(10)70323-9 10.1017/S1041610297004973 10.1001/archneur.62.12.1881 10.1097/00005072-199005000-00003 10.1016/j.neuroimage.2004.05.007 10.1016/j.neurobiolaging.2009.08.016 10.1111/j.1365-2990.1997.tb01302.x 10.1001/archneur.65.4.540 10.1016/j.jalz.2011.03.008 10.1056/NEJMoa1202753 10.2217/bmm.09.91 |
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| References | Jack, Knopman, Jagust (bib7) 2010; 9 Albert, DeKosky, Dickson (bib20) 2011; 7 Reiman, Caselli, Yun (bib9) 1996; 334 Villain, Chetelat, Grassiot (bib26) 2012; 135 Morris, Price (bib3) 2001; 17 Acosta-Baena, Sepulveda-Falla, Lopera-Gomez (bib12) 2011; 10 Remes, Laru, Tuominen (bib33) 2008; 65 McKhann, Knopman, Chertkow (bib19) 2011; 7 Klunk, Price, Mathis (bib13) 2007; 27 Braak, Braak (bib34) 1990; 49 Lopera, Ardilla, Martinez (bib17) 1997; 277 Brilliant, Elble, Ghobrial, Struble (bib36) 1997; 23 Clark, Schneider, Bedell (bib24) 2011; 305 Sheikh, Yesavage (bib22) 1986 Thal, Rub, Orantes, Braak (bib37) 2002; 58 Fleisher, Houston, Eyler (bib10) 2005; 62 Bateman, Xiong, Benzinger (bib2) 2012; 367 Villemagne, Ataka, Mizuno (bib28) 2009; 66 Saunders, Strittmatter, Schmechel (bib21) 1993; 43 Meltzer, Cantwell, Greer (bib30) 2000; 41 Rowe, Ellis, Rimajova (bib4) 2010; 31 Reiman, Chen, Liu (bib11) 2009; 106 Edison, Hinz, Ramlackhansingh (bib27) 2012; 60 Sojkova, Zhou, An (bib29) 2011; 68 Duque-Castano, Roldan, Arango-Viana, Arcos-Burgos, Cubillo, Lopera (bib6) 1999; 29 Reiman, Quiroz, Fleisher (bib18) 2012 Reisberg (bib23) 1988; 24 Reiman, Langbaum, Tariot (bib8) 2010; 4 Bertram, Tanzi (bib15) 2005; 115 Tohka, Zijdenbos, Evans (bib31) 2004; 23 Koivunen, Verkkoniemi, Aalto (bib32) 2008; 131 Suenaga, Hirano, Llena, Yen, Dickson (bib35) 1990; 80 Fleisher, Chen, Liu (bib25) 2012 Braak, Braak (bib1) 1997; 9 Tanzi, Bertram (bib16) 2005; 120 Fleisher, Chen, Liu (bib5) 2011; 68 Klunk, Engler, Nordberg (bib38) 2004; 55 Price, Klunk, Lopresti (bib39) 2005; 25 Scholl, Almkvist, Axelman (bib14) 2011; 32 Choi, Golding, Zhuang (bib40) 2009; 50 Brilliant (10.1016/S1474-4422(12)70227-2_bib36) 1997; 23 Koivunen (10.1016/S1474-4422(12)70227-2_bib32) 2008; 131 Duque-Castano (10.1016/S1474-4422(12)70227-2_bib6) 1999; 29 Albert (10.1016/S1474-4422(12)70227-2_bib20) 2011; 7 Rowe (10.1016/S1474-4422(12)70227-2_bib4) 2010; 31 Thal (10.1016/S1474-4422(12)70227-2_bib37) 2002; 58 Morris (10.1016/S1474-4422(12)70227-2_bib3) 2001; 17 Braak (10.1016/S1474-4422(12)70227-2_bib34) 1990; 49 Fleisher (10.1016/S1474-4422(12)70227-2_bib25) 2012 Braak (10.1016/S1474-4422(12)70227-2_bib1) 1997; 9 Acosta-Baena (10.1016/S1474-4422(12)70227-2_bib12) 2011; 10 Fleisher (10.1016/S1474-4422(12)70227-2_bib10) 2005; 62 Reiman (10.1016/S1474-4422(12)70227-2_bib11) 2009; 106 Meltzer (10.1016/S1474-4422(12)70227-2_bib30) 2000; 41 Tanzi (10.1016/S1474-4422(12)70227-2_bib16) 2005; 120 McKhann (10.1016/S1474-4422(12)70227-2_bib19) 2011; 7 Saunders (10.1016/S1474-4422(12)70227-2_bib21) 1993; 43 Villain (10.1016/S1474-4422(12)70227-2_bib26) 2012; 135 Villemagne (10.1016/S1474-4422(12)70227-2_bib28) 2009; 66 Jack (10.1016/S1474-4422(12)70227-2_bib7) 2010; 9 Sheikh (10.1016/S1474-4422(12)70227-2_bib22) 1986 Bertram (10.1016/S1474-4422(12)70227-2_bib15) 2005; 115 Sojkova (10.1016/S1474-4422(12)70227-2_bib29) 2011; 68 Reiman (10.1016/S1474-4422(12)70227-2_bib18) 2012 Suenaga (10.1016/S1474-4422(12)70227-2_bib35) 1990; 80 Reiman (10.1016/S1474-4422(12)70227-2_bib8) 2010; 4 Tohka (10.1016/S1474-4422(12)70227-2_bib31) 2004; 23 Bateman (10.1016/S1474-4422(12)70227-2_bib2) 2012; 367 Klunk (10.1016/S1474-4422(12)70227-2_bib38) 2004; 55 Reisberg (10.1016/S1474-4422(12)70227-2_bib23) 1988; 24 Price (10.1016/S1474-4422(12)70227-2_bib39) 2005; 25 Klunk (10.1016/S1474-4422(12)70227-2_bib13) 2007; 27 Clark (10.1016/S1474-4422(12)70227-2_bib24) 2011; 305 Choi (10.1016/S1474-4422(12)70227-2_bib40) 2009; 50 Fleisher (10.1016/S1474-4422(12)70227-2_bib5) 2011; 68 Remes (10.1016/S1474-4422(12)70227-2_bib33) 2008; 65 Reiman (10.1016/S1474-4422(12)70227-2_bib9) 1996; 334 Scholl (10.1016/S1474-4422(12)70227-2_bib14) 2011; 32 Lopera (10.1016/S1474-4422(12)70227-2_bib17) 1997; 277 Edison (10.1016/S1474-4422(12)70227-2_bib27) 2012; 60 9447446 - Int Psychogeriatr. 1997;9 Suppl 1:257-61; discussion 269-72 20383319 - Biomark Med. 2010 Feb;4(1):3-14 14991808 - Ann Neurol. 2004 Mar;55(3):306-19 22306804 - Neuroimage. 2012 Apr 15;60(3):1716-23 12084879 - Neurology. 2002 Jun 25;58(12):1791-800 10528300 - Rev Neurol. 1999 Jul 1-15;29(1):1-6 8350998 - Neurology. 1993 Aug;43(8):1467-72 15931380 - J Clin Invest. 2005 Jun;115(6):1449-57 19796846 - Neurobiol Aging. 2011 Aug;32(8):1388-99 21747008 - Arch Neurol. 2011 Nov;68(11):1404-11 21296022 - Lancet Neurol. 2011 Mar;10(3):213-20 20083042 - Lancet Neurol. 2010 Jan;9(1):119-28 9292871 - Neuropathol Appl Neurobiol. 1997 Aug;23(4):322-5 23137948 - Lancet Neurol. 2012 Dec;11(12):1048-56 19837759 - J Nucl Med. 2009 Nov;50(11):1887-94 21514250 - Alzheimers Dement. 2011 May;7(3):263-9 22784036 - N Engl J Med. 2012 Aug 30;367(9):795-804 15325355 - Neuroimage. 2004 Sep;23(1):84-97 21514249 - Alzheimers Dement. 2011 May;7(3):270-9 22633529 - Neurobiol Aging. 2013 Jan;34(1):1-12 11816784 - J Mol Neurosci. 2001 Oct;17(2):101-18 21555640 - Arch Neurol. 2011 May;68(5):644-9 1692337 - J Neuropathol Exp Neurol. 1990 May;49(3):215-24 17553989 - J Neurosci. 2007 Jun 6;27(23):6174-84 15944649 - J Cereb Blood Flow Metab. 2005 Nov;25(11):1528-47 20008660 - Arch Neurol. 2009 Dec;66(12):1537-44 19346482 - Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6820-5 18413480 - Arch Neurol. 2008 Apr;65(4):540-4 15734686 - Cell. 2005 Feb 25;120(4):545-55 23165336 - Nat Rev Neurol. 2013 Jan;9(1):4 16344346 - Arch Neurol. 2005 Dec;62(12):1881-8 8592548 - N Engl J Med. 1996 Mar 21;334(12):752-8 20472326 - Neurobiol Aging. 2010 Aug;31(8):1275-83 3249767 - Psychopharmacol Bull. 1988;24(4):653-9 18583368 - Brain. 2008 Jul;131(Pt 7):1845-53 1698005 - Acta Neuropathol. 1990;80(3):280-6 9052708 - JAMA. 1997 Mar 12;277(10):793-9 21245183 - JAMA. 2011 Jan 19;305(3):275-83 11079492 - J Nucl Med. 2000 Nov;41(11):1842-8 22628162 - Brain. 2012 Jul;135(Pt 7):2126-39 23137951 - Lancet Neurol. 2012 Dec;11(12):1018-20 |
| References_xml | – volume: 106 start-page: 6820 year: 2009 end-page: 6825 ident: bib11 article-title: Fibrillar amyloid-beta burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease publication-title: Proc Natl Acad Sci USA – volume: 334 start-page: 752 year: 1996 end-page: 758 ident: bib9 article-title: Preclinical evidence of Alzheimer's disease in persons homozygous for the epsilon 4 allele for apolipoprotein E publication-title: N Engl J Med – volume: 29 start-page: 1 year: 1999 end-page: 6 ident: bib6 article-title: [Neuropathological findings in early-onset Alzheimer's disease ( publication-title: Rev Neurol – year: 2012 ident: bib25 article-title: APOE4 and age effects on florbetapir PET in healthy aging and Alzheimer disease publication-title: Neurobiol Aging – volume: 23 start-page: 322 year: 1997 end-page: 325 ident: bib36 article-title: The distribution of amyloid beta protein deposition in the corpus striatum of patients with Alzheimer's disease publication-title: Neuropathol Appl Neurobiol – volume: 9 start-page: 119 year: 2010 end-page: 128 ident: bib7 article-title: Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade publication-title: Lancet Neurol – volume: 68 start-page: 644 year: 2011 end-page: 649 ident: bib29 article-title: Longitudinal patterns of beta-amyloid deposition in nondemented older adults publication-title: Arch Neurol – volume: 58 start-page: 1791 year: 2002 end-page: 1800 ident: bib37 article-title: Phases of A beta-deposition in the human brain and its relevance for the development of AD publication-title: Neurology – volume: 65 start-page: 540 year: 2008 end-page: 544 ident: bib33 article-title: Carbon 11-labeled pittsburgh compound B positron emission tomographic amyloid imaging in patients with APP locus duplication publication-title: Arch Neurol – volume: 9 start-page: 257 year: 1997 end-page: 261 ident: bib1 article-title: Staging of Alzheimer-related cortical destruction publication-title: Int Psychogeriatr – volume: 80 start-page: 280 year: 1990 end-page: 286 ident: bib35 article-title: Modified Bielschowsky stain and immunohistochemical studies on striatal plaques in Alzheimer's disease publication-title: Acta Neuropathol – volume: 4 start-page: 3 year: 2010 end-page: 14 ident: bib8 article-title: Alzheimer's prevention initiative: a proposal to evaluate presymptomatic treatments as quickly as possible publication-title: Biomark Med – volume: 120 start-page: 545 year: 2005 end-page: 555 ident: bib16 article-title: Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective publication-title: Cell – volume: 27 start-page: 6174 year: 2007 end-page: 6184 ident: bib13 article-title: Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees publication-title: J Neurosci – year: 2012 ident: bib18 article-title: Brain imaging and fluid biomarker analysis in young adults at genetic risk for autosomal dominant Alzheimer's disease in the presenilin 1 E280A kindred: a case-control study publication-title: Lancet Neurol – volume: 50 start-page: 1887 year: 2009 end-page: 1894 ident: bib40 article-title: Preclinical properties of publication-title: J Nucl Med – volume: 115 start-page: 1449 year: 2005 end-page: 1457 ident: bib15 article-title: The genetic epidemiology of neurodegenerative disease publication-title: J Clin Invest – volume: 135 start-page: 2126 year: 2012 end-page: 2139 ident: bib26 article-title: Regional dynamics of amyloid-beta deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study publication-title: Brain – volume: 10 start-page: 213 year: 2011 end-page: 220 ident: bib12 article-title: Pre-dementia clinical stages in presenilin 1 E280A familial early-onset Alzheimer's disease: a retrospective cohort study publication-title: Lancet Neurol – volume: 32 start-page: 1388 year: 2011 end-page: 1399 ident: bib14 article-title: Glucose metabolism and PIB binding in carriers of a His163Tyr presenilin 1 mutation publication-title: Neurobiol Aging – volume: 23 start-page: 84 year: 2004 end-page: 97 ident: bib31 article-title: Fast and robust parameter estimation for statistical partial volume models in brain MRI publication-title: Neuroimage – volume: 31 start-page: 1275 year: 2010 end-page: 1283 ident: bib4 article-title: Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging publication-title: Neurobiol Aging – volume: 25 start-page: 1528 year: 2005 end-page: 1547 ident: bib39 article-title: Kinetic modeling of amyloid binding in humans using PET imaging and Pittsburgh compound-B publication-title: J Cereb Blood Flow Metab – volume: 41 start-page: 1842 year: 2000 end-page: 1848 ident: bib30 article-title: Does cerebral blood flow decline in healthy aging? A PET study with partial-volume correction publication-title: J Nucl Med – volume: 49 start-page: 215 year: 1990 end-page: 224 ident: bib34 article-title: Alzheimer's disease: striatal amyloid deposits and neurofibrillary changes publication-title: J Neuropathol Exp Neurol – volume: 367 start-page: 795 year: 2012 end-page: 804 ident: bib2 article-title: Clinical and biomarker changes in dominantly inherited Alzheimer's disease publication-title: N Engl J Med – start-page: 165 year: 1986 end-page: 173 ident: bib22 article-title: Geriatric depression scale (GDS): recent evidence and development of a shorter version publication-title: Clinical gerontology: a guide to assessment and intervention – volume: 62 start-page: 1881 year: 2005 end-page: 1888 ident: bib10 article-title: Identification of Alzheimer disease risk by functional magnetic resonance imaging publication-title: Arch Neurol – volume: 7 start-page: 270 year: 2011 end-page: 279 ident: bib20 article-title: The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging–Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease publication-title: Alzheimers Dement – volume: 43 start-page: 1467 year: 1993 end-page: 1472 ident: bib21 article-title: Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease publication-title: Neurology – volume: 7 start-page: 263 year: 2011 end-page: 269 ident: bib19 article-title: The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging–Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease publication-title: Alzheimers Dement – volume: 305 start-page: 275 year: 2011 end-page: 283 ident: bib24 article-title: Use of florbetapir-PET for imaging beta-amyloid pathology publication-title: JAMA – volume: 68 start-page: 1404 year: 2011 end-page: 1411 ident: bib5 article-title: Using positron emission tomography and florbetapir F18 to image cortical amyloid in patients with mild cognitive impairment or dementia due to Alzheimer disease publication-title: Arch Neurol – volume: 60 start-page: 1716 year: 2012 end-page: 1723 ident: bib27 article-title: Can target-to-pons ratio be used as a reliable method for the analysis of [11C]PiB brain scans? publication-title: Neuroimage – volume: 24 start-page: 653 year: 1988 end-page: 659 ident: bib23 article-title: Functional assessment staging (FAST) publication-title: Psychopharmacol Bull – volume: 55 start-page: 306 year: 2004 end-page: 319 ident: bib38 article-title: Imaging brain amyloid in Alzheimer's disease with Pittsburgh compound-B publication-title: Ann Neurol – volume: 277 start-page: 793 year: 1997 end-page: 799 ident: bib17 article-title: Clinical features of early-onset Alzheimer disease in a large kindred with an publication-title: JAMA – volume: 131 start-page: 1845 year: 2008 end-page: 1853 ident: bib32 article-title: PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease publication-title: Brain – volume: 17 start-page: 101 year: 2001 end-page: 118 ident: bib3 article-title: Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage Alzheimer's disease publication-title: J Mol Neurosci – volume: 66 start-page: 1537 year: 2009 end-page: 1544 ident: bib28 article-title: High striatal amyloid beta-peptide deposition across different autosomal Alzheimer disease mutation types publication-title: Arch Neurol – volume: 80 start-page: 280 year: 1990 ident: 10.1016/S1474-4422(12)70227-2_bib35 article-title: Modified Bielschowsky stain and immunohistochemical studies on striatal plaques in Alzheimer's disease publication-title: Acta Neuropathol doi: 10.1007/BF00294646 – volume: 66 start-page: 1537 year: 2009 ident: 10.1016/S1474-4422(12)70227-2_bib28 article-title: High striatal amyloid beta-peptide deposition across different autosomal Alzheimer disease mutation types publication-title: Arch Neurol doi: 10.1001/archneurol.2009.285 – volume: 25 start-page: 1528 year: 2005 ident: 10.1016/S1474-4422(12)70227-2_bib39 article-title: Kinetic modeling of amyloid binding in humans using PET imaging and Pittsburgh compound-B publication-title: J Cereb Blood Flow Metab doi: 10.1038/sj.jcbfm.9600146 – volume: 50 start-page: 1887 year: 2009 ident: 10.1016/S1474-4422(12)70227-2_bib40 article-title: Preclinical properties of 48F-AV-45: a PET agent for Abeta plaques in the brain publication-title: J Nucl Med doi: 10.2967/jnumed.109.065284 – volume: 277 start-page: 793 year: 1997 ident: 10.1016/S1474-4422(12)70227-2_bib17 article-title: Clinical features of early-onset Alzheimer disease in a large kindred with an E280A presenilin-1 mutation publication-title: JAMA doi: 10.1001/jama.1997.03540340027028 – volume: 305 start-page: 275 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib24 article-title: Use of florbetapir-PET for imaging beta-amyloid pathology publication-title: JAMA doi: 10.1001/jama.2010.2008 – volume: 60 start-page: 1716 year: 2012 ident: 10.1016/S1474-4422(12)70227-2_bib27 article-title: Can target-to-pons ratio be used as a reliable method for the analysis of [11C]PiB brain scans? publication-title: Neuroimage doi: 10.1016/j.neuroimage.2012.01.099 – volume: 68 start-page: 1404 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib5 article-title: Using positron emission tomography and florbetapir F18 to image cortical amyloid in patients with mild cognitive impairment or dementia due to Alzheimer disease publication-title: Arch Neurol doi: 10.1001/archneurol.2011.150 – volume: 68 start-page: 644 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib29 article-title: Longitudinal patterns of beta-amyloid deposition in nondemented older adults publication-title: Arch Neurol doi: 10.1001/archneurol.2011.77 – volume: 9 start-page: 119 year: 2010 ident: 10.1016/S1474-4422(12)70227-2_bib7 article-title: Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade publication-title: Lancet Neurol doi: 10.1016/S1474-4422(09)70299-6 – volume: 334 start-page: 752 year: 1996 ident: 10.1016/S1474-4422(12)70227-2_bib9 article-title: Preclinical evidence of Alzheimer's disease in persons homozygous for the epsilon 4 allele for apolipoprotein E publication-title: N Engl J Med doi: 10.1056/NEJM199603213341202 – volume: 7 start-page: 263 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib19 article-title: The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging–Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease publication-title: Alzheimers Dement doi: 10.1016/j.jalz.2011.03.005 – volume: 27 start-page: 6174 year: 2007 ident: 10.1016/S1474-4422(12)70227-2_bib13 article-title: Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees publication-title: J Neurosci doi: 10.1523/JNEUROSCI.0730-07.2007 – start-page: 165 year: 1986 ident: 10.1016/S1474-4422(12)70227-2_bib22 article-title: Geriatric depression scale (GDS): recent evidence and development of a shorter version – volume: 17 start-page: 101 year: 2001 ident: 10.1016/S1474-4422(12)70227-2_bib3 article-title: Pathologic correlates of nondemented aging, mild cognitive impairment, and early-stage Alzheimer's disease publication-title: J Mol Neurosci doi: 10.1385/JMN:17:2:101 – volume: 29 start-page: 1 year: 1999 ident: 10.1016/S1474-4422(12)70227-2_bib6 article-title: [Neuropathological findings in early-onset Alzheimer's disease (E280a-PS1 mutation)] publication-title: Rev Neurol – volume: 55 start-page: 306 year: 2004 ident: 10.1016/S1474-4422(12)70227-2_bib38 article-title: Imaging brain amyloid in Alzheimer's disease with Pittsburgh compound-B publication-title: Ann Neurol doi: 10.1002/ana.20009 – volume: 106 start-page: 6820 year: 2009 ident: 10.1016/S1474-4422(12)70227-2_bib11 article-title: Fibrillar amyloid-beta burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0900345106 – year: 2012 ident: 10.1016/S1474-4422(12)70227-2_bib18 article-title: Brain imaging and fluid biomarker analysis in young adults at genetic risk for autosomal dominant Alzheimer's disease in the presenilin 1 E280A kindred: a case-control study publication-title: Lancet Neurol doi: 10.1016/S1474-4422(12)70228-4 – volume: 43 start-page: 1467 year: 1993 ident: 10.1016/S1474-4422(12)70227-2_bib21 article-title: Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer's disease publication-title: Neurology doi: 10.1212/WNL.43.8.1467 – volume: 131 start-page: 1845 year: 2008 ident: 10.1016/S1474-4422(12)70227-2_bib32 article-title: PET amyloid ligand [11C]PIB uptake shows predominantly striatal increase in variant Alzheimer's disease publication-title: Brain doi: 10.1093/brain/awn107 – year: 2012 ident: 10.1016/S1474-4422(12)70227-2_bib25 article-title: APOE4 and age effects on florbetapir PET in healthy aging and Alzheimer disease publication-title: Neurobiol Aging – volume: 115 start-page: 1449 year: 2005 ident: 10.1016/S1474-4422(12)70227-2_bib15 article-title: The genetic epidemiology of neurodegenerative disease publication-title: J Clin Invest doi: 10.1172/JCI24761 – volume: 135 start-page: 2126 year: 2012 ident: 10.1016/S1474-4422(12)70227-2_bib26 article-title: Regional dynamics of amyloid-beta deposition in healthy elderly, mild cognitive impairment and Alzheimer's disease: a voxelwise PiB-PET longitudinal study publication-title: Brain doi: 10.1093/brain/aws125 – volume: 58 start-page: 1791 year: 2002 ident: 10.1016/S1474-4422(12)70227-2_bib37 article-title: Phases of A beta-deposition in the human brain and its relevance for the development of AD publication-title: Neurology doi: 10.1212/WNL.58.12.1791 – volume: 120 start-page: 545 year: 2005 ident: 10.1016/S1474-4422(12)70227-2_bib16 article-title: Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective publication-title: Cell doi: 10.1016/j.cell.2005.02.008 – volume: 31 start-page: 1275 year: 2010 ident: 10.1016/S1474-4422(12)70227-2_bib4 article-title: Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging publication-title: Neurobiol Aging doi: 10.1016/j.neurobiolaging.2010.04.007 – volume: 24 start-page: 653 year: 1988 ident: 10.1016/S1474-4422(12)70227-2_bib23 article-title: Functional assessment staging (FAST) publication-title: Psychopharmacol Bull – volume: 10 start-page: 213 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib12 article-title: Pre-dementia clinical stages in presenilin 1 E280A familial early-onset Alzheimer's disease: a retrospective cohort study publication-title: Lancet Neurol doi: 10.1016/S1474-4422(10)70323-9 – volume: 41 start-page: 1842 year: 2000 ident: 10.1016/S1474-4422(12)70227-2_bib30 article-title: Does cerebral blood flow decline in healthy aging? A PET study with partial-volume correction publication-title: J Nucl Med – volume: 9 start-page: 257 issue: suppl 1 year: 1997 ident: 10.1016/S1474-4422(12)70227-2_bib1 article-title: Staging of Alzheimer-related cortical destruction publication-title: Int Psychogeriatr doi: 10.1017/S1041610297004973 – volume: 62 start-page: 1881 year: 2005 ident: 10.1016/S1474-4422(12)70227-2_bib10 article-title: Identification of Alzheimer disease risk by functional magnetic resonance imaging publication-title: Arch Neurol doi: 10.1001/archneur.62.12.1881 – volume: 49 start-page: 215 year: 1990 ident: 10.1016/S1474-4422(12)70227-2_bib34 article-title: Alzheimer's disease: striatal amyloid deposits and neurofibrillary changes publication-title: J Neuropathol Exp Neurol doi: 10.1097/00005072-199005000-00003 – volume: 23 start-page: 84 year: 2004 ident: 10.1016/S1474-4422(12)70227-2_bib31 article-title: Fast and robust parameter estimation for statistical partial volume models in brain MRI publication-title: Neuroimage doi: 10.1016/j.neuroimage.2004.05.007 – volume: 32 start-page: 1388 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib14 article-title: Glucose metabolism and PIB binding in carriers of a His163Tyr presenilin 1 mutation publication-title: Neurobiol Aging doi: 10.1016/j.neurobiolaging.2009.08.016 – volume: 23 start-page: 322 year: 1997 ident: 10.1016/S1474-4422(12)70227-2_bib36 article-title: The distribution of amyloid beta protein deposition in the corpus striatum of patients with Alzheimer's disease publication-title: Neuropathol Appl Neurobiol doi: 10.1111/j.1365-2990.1997.tb01302.x – volume: 65 start-page: 540 year: 2008 ident: 10.1016/S1474-4422(12)70227-2_bib33 article-title: Carbon 11-labeled pittsburgh compound B positron emission tomographic amyloid imaging in patients with APP locus duplication publication-title: Arch Neurol doi: 10.1001/archneur.65.4.540 – volume: 7 start-page: 270 year: 2011 ident: 10.1016/S1474-4422(12)70227-2_bib20 article-title: The diagnosis of mild cognitive impairment due to Alzheimer's disease: recommendations from the National Institute on Aging–Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease publication-title: Alzheimers Dement doi: 10.1016/j.jalz.2011.03.008 – volume: 367 start-page: 795 year: 2012 ident: 10.1016/S1474-4422(12)70227-2_bib2 article-title: Clinical and biomarker changes in dominantly inherited Alzheimer's disease publication-title: N Engl J Med doi: 10.1056/NEJMoa1202753 – volume: 4 start-page: 3 year: 2010 ident: 10.1016/S1474-4422(12)70227-2_bib8 article-title: Alzheimer's prevention initiative: a proposal to evaluate presymptomatic treatments as quickly as possible publication-title: Biomark Med doi: 10.2217/bmm.09.91 – reference: 11079492 - J Nucl Med. 2000 Nov;41(11):1842-8 – reference: 19796846 - Neurobiol Aging. 2011 Aug;32(8):1388-99 – reference: 15734686 - Cell. 2005 Feb 25;120(4):545-55 – reference: 22784036 - N Engl J Med. 2012 Aug 30;367(9):795-804 – reference: 1698005 - Acta Neuropathol. 1990;80(3):280-6 – reference: 17553989 - J Neurosci. 2007 Jun 6;27(23):6174-84 – reference: 22306804 - Neuroimage. 2012 Apr 15;60(3):1716-23 – reference: 18413480 - Arch Neurol. 2008 Apr;65(4):540-4 – reference: 20083042 - Lancet Neurol. 2010 Jan;9(1):119-28 – reference: 23137948 - Lancet Neurol. 2012 Dec;11(12):1048-56 – reference: 22633529 - Neurobiol Aging. 2013 Jan;34(1):1-12 – reference: 22628162 - Brain. 2012 Jul;135(Pt 7):2126-39 – reference: 21245183 - JAMA. 2011 Jan 19;305(3):275-83 – reference: 15325355 - Neuroimage. 2004 Sep;23(1):84-97 – reference: 15944649 - J Cereb Blood Flow Metab. 2005 Nov;25(11):1528-47 – reference: 19837759 - J Nucl Med. 2009 Nov;50(11):1887-94 – reference: 9052708 - JAMA. 1997 Mar 12;277(10):793-9 – reference: 21747008 - Arch Neurol. 2011 Nov;68(11):1404-11 – reference: 20383319 - Biomark Med. 2010 Feb;4(1):3-14 – reference: 21555640 - Arch Neurol. 2011 May;68(5):644-9 – reference: 21514249 - Alzheimers Dement. 2011 May;7(3):270-9 – reference: 8350998 - Neurology. 1993 Aug;43(8):1467-72 – reference: 15931380 - J Clin Invest. 2005 Jun;115(6):1449-57 – reference: 11816784 - J Mol Neurosci. 2001 Oct;17(2):101-18 – reference: 14991808 - Ann Neurol. 2004 Mar;55(3):306-19 – reference: 9447446 - Int Psychogeriatr. 1997;9 Suppl 1:257-61; discussion 269-72 – reference: 19346482 - Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6820-5 – reference: 16344346 - Arch Neurol. 2005 Dec;62(12):1881-8 – reference: 20472326 - Neurobiol Aging. 2010 Aug;31(8):1275-83 – reference: 9292871 - Neuropathol Appl Neurobiol. 1997 Aug;23(4):322-5 – reference: 21514250 - Alzheimers Dement. 2011 May;7(3):263-9 – reference: 18583368 - Brain. 2008 Jul;131(Pt 7):1845-53 – reference: 12084879 - Neurology. 2002 Jun 25;58(12):1791-800 – reference: 10528300 - Rev Neurol. 1999 Jul 1-15;29(1):1-6 – reference: 3249767 - Psychopharmacol Bull. 1988;24(4):653-9 – reference: 8592548 - N Engl J Med. 1996 Mar 21;334(12):752-8 – reference: 23165336 - Nat Rev Neurol. 2013 Jan;9(1):4 – reference: 23137951 - Lancet Neurol. 2012 Dec;11(12):1018-20 – reference: 21296022 - Lancet Neurol. 2011 Mar;10(3):213-20 – reference: 1692337 - J Neuropathol Exp Neurol. 1990 May;49(3):215-24 – reference: 20008660 - Arch Neurol. 2009 Dec;66(12):1537-44 |
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| Snippet | Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease.... Summary Background Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with... |
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| SubjectTerms | Adult Alzheimer Disease - diagnosis Alzheimer Disease - diagnostic imaging Alzheimer Disease - genetics Amyloid beta-Peptides - metabolism Aniline Compounds - metabolism Cohort Studies Cross-Sectional Studies Ethylene Glycols - metabolism Female Fluorine Radioisotopes - metabolism Humans Male Middle Aged Neurology Positron-Emission Tomography - methods Presenilin-1 - genetics Registries Young Adult |
| Title | Florbetapir PET analysis of amyloid-β deposition in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional study |
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