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Review

Positron Emission Tomography in Alzheimer‘s Disease: Early Prediction and Differentiation

, , , , &
Pages 23-38 | Published online: 18 Dec 2008

Bibliography

  • Kung HC , HoyertDL, XuJ, MurphySL: Deaths: final data for 2005.Natl Vital Stat. Rep.56(10), 1–120 (2008).
  • McKhann G , DrachmanD, FolsteinM, KatzmanR, PriceD, StadlanEM: Clinical diagnosis of Alzheimer‘s disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer‘s Disease.Neurology34, 939–944 (1984).
  • Hebert LE , ScherrPA, BieniasJL, BennettDA, EvansDA: Alzheimer disease in the US population: prevalence estimates using the 2000 census.Arch. Neurol.60(80), 1119–1122 (2003).
  • Mirra SS , HeymanA, McKeelDet al.: The Consortium to Establish a Registry for Alzheimer‘s Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer‘s disease.Neurology41, 479–486 (1991).
  • Price JL , MorrisJC: Tangles and plaques in nondemented aging and ‘preclinical‘ Alzheimer‘s disease.Ann. Neurol.45, 358–368 (1999).
  • Braak H , BraakE: Development of Alzheimer-related neurofibrillary changes in the neocortex inversely recapitulates cortical myelogenesis.Acta Neuropathol.92, 197–201 (1996).
  • Delacourte A , DavidJP, SergeantNet al.: The biochemical pathway of neurofibrillary degeneration in aging and Alzheimer‘s disease.Neurology52, 1158–1165 (1999).
  • Morris JC , StorandtM, McKeelDWet al.: Cerebral amyloid deposition and diffuse plaques in ‘normal‘ aging: evidence for presymptomatic and very mild Alzheiemer‘s disease.Neurology46, 707–719 (1996).
  • Braak H , BraakE: Neuropathological stageing of Alzheimer-related changes.Acta Neuropathologica82, 239–259 (1991).
  • Morrison JH , HofPR: Life and death of neurons in the aging brain.Science278, 412–419 (1997).
  • Hyman BT , Van Hoesen GW, Damasio AR, Barnes CL: Alzheimer‘s disease: cell-specific pathology isolates the hippocampal formation. Science225, 1168–1170 (1984).
  • Etiene D , KraftJ, GanjuNet al.: Cerebrovascular pathology contributes to the heterogeneity of Alzheimer‘s disease.J. Alz. Dis.1(2), 119–134 (1998).
  • Snowdon DA , GreinerLH, MortimerJAet al.: Brain infarction and the clinical expression of Alzheimer‘s disease: the Nun study.JAMA277(10), 813–817(1997).
  • Arriagada PV , MarzloffK, HymanBT: Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer‘s disease.Neurology42, 1681–1688 (1992).
  • Giannakopoulos P , HofPR, MottierS, MichelJP, BourasC: Neuropathological changes in the cerebral cortex of 1258 cases from a geriatric hospital: retrospective clinicopathological evaluation of a 10-year autopsy population.Acta Neuropathol.87, 456–468 (1994).
  • Ulrich J : Alzheimer changes in nondemented patients younger than sixty-five: Possible early stages of Alzheimer‘s disease and senile dementia of Alzheimer type.Ann. Neurol.17, 273–277 (1985).
  • Selkoe DJ : Alzheimer‘s disease: genotypes, phenotype, and treatments.Science275, 630–631 (1997).
  • Lambert MP , BarlowAK, ChromyBAet al.: Diffusible, nonfibrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins.Proc. Natl Acad. Sci. USA95(11), 6448–6453 (1998).
  • Consensus Working Group: Consensus report of the Working Group on: ‘Molecular and Biochemical Markers of Alzheimer‘s Disease‘. The Ronald and Nancy Reagan Research Institute of the Alzheimer‘s Association and the National Institute on Aging. Neurobiol. Aging19, 109–116 (1998).
  • Nestor PJ , ScheltensP, HodgesJR: Advances in the early detection of Alzheimer‘s disease.Nat. Med.10, S34-S41 (2004).
  • de Leon MJ , McRaeT, TsaiJRet al.: Abnormal cortisol response in Alzheimer‘s disease linked to hippocampal atrophy.Lancet2, 391–392 (1988).
  • de Leon MJ , GeorgeAE, StylopoulosLA, SmithG, MillerDC: Early marker for Alzheimer‘s disease: the atrophic hippocampus.Lancet2, 672–673 (1989).
  • Jack CR , PetersenRC, XuY, O‘BrienPC, SmithGE, IvnikRJ: Rates of hippocampal atrophy correlate with change in clinical status in aging and AD.Neurology55, 484–489 (2000).
  • Rusinek H , De Santi S, Frid Det al.: Regional brain atrophy rate predicts future cognitive decline: 6-year longitudinal MR imaging study of normal aging. Radiology229, 691–696 (2003).
  • den Heijer T , GeerlingsMI, HoebeekFE, HofmanA, KoudstaalPJ, BretelerM: Use of hippocampal and amygdalar volumes on magnetic resonance imaging to predict dementia in cognitively intact elderly people.Arch. Gen. Psychiat.63, 57–62 (2006).
  • O‘Sullivan M , NgoE, ViswanathanAet al.: Hippocampal volume is an independent predictor of cognitive performance in CADASIL.Neurobiol. AgingDOI: 10.1016/j.neurobiolaging.2007.09.002 (2008) (Epub ahead of print).
  • Blennow K , de Leon MJ, Zetterberg H: Alzheimer‘s disease. Lancet Neurology368, 387–403 (2006).
  • Sokoloff L : Relation between physiological functions and energy metabolism in the central nervous system.J. Neurochem.29, 13–26 (1977).
  • Magistretti PJ , PellerinL, RothmanDL, ShulmanRG: Energy on demand.Science283, 496–497 (1999).
  • Attwell D , Iadecola C; The neural basis of functional brain imaging signals. Trends Neurosci.25, 621–625 (2002).
  • Malonek D , GrinvaldA: Interactions between electrical activity and cortical microcirculation revealed by imaging spectroscopy: implications for functional brain mapping.Science272, 551–554 (1996).
  • Rocher AB , ChaponF, BlaizotX, Baron J-C, Chavoix C: Resting-state brain glucose utilization as measured by PET is directly related to regional synaptophysin levels: a study in baboons. Neuroimage20, 1894–1898 (2004).
  • Magistretti PJ , PellerinL: The contribution of astrocytes to the 18F-2-deoxyglucose signal in PET activation studies.Mol. Psychiatry1, 445–452 (1996).
  • Pellerin L , MagistrettiPJ: Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization.Proc. Natl Acad. Sci. USA91(22), 10625–10629 (1994).
  • Mosconi L : Brain glucose metabolism in the early and specific diagnosis of Alzheimer‘s disease.Eur. J. Nucl. Med.32, 486–510 (2005).
  • Friedland RP , BudingerTF, GanzEet al.: Regional cerebral metabolic alterations in dementia of the Alzheimer type: Positron emission tomography with [18F] fluorodeoxyglucose.J. Comput. Assist. Tomogr.7, 590–598 (1983).
  • Frackowiak RSJ , PozzilliC, LeggNJet al.: A prospective study of regional cerebral blood flow and oxygen utilization in dementia using positron emission tomography and oxygen-15.J. Cereb. Blood Flow Metab.1, S453–S454 (1981).
  • Minoshima S , GiordaniB, BerentS, FreyKA, FosterNL, KuhlDE: Metabolic reduction in the posterior cingulate cortex in very early Alzheimer‘s disease.Ann. Neurol.42, 85–94 (1997).
  • Ferris SH , de Leon MJ, Wolf APet al.: Positron emission tomography in the study of aging and senile dementia. Neurobiol. Aging1, 127–131 (1980).
  • Kim EJ , ChoSS, JeongYet al.: Glucose metabolism in early onset versus late onset Alzheimer‘s disease: an SPM analysis of 120 patients.Brain128, 1790–1801 (2005).
  • Foster NL , ChaseTN, MansiLet al.: Cortical abnormalities in Alzheimer‘s disease.Ann. Neurol.66, 649–654 (1984).
  • Mazziotta JC , PhelpsME: Positron emission tomography studies of the brain. Positron Emission Tomography & Autoradiography. In: Principles & Applications for the Brain & Heart. PhelpsME, MazziottaJC, SchelbertH (Eds). Raven Press, NY, USA493–579 (1986).
  • Herholz K , SalmonE, PeraniDet al.: Discrimination between Alzheimer dementia and controls by automated analysis of multicenter FDG PET.Neuroimage17, 302–316 (2002).
  • Silverman DHS , SmallGW, ChangCYet al.: Positron emission tomography in evaluation of dementia: regional brain metabolism and long-term outcome.JAMA286, 2120–2127 (2001).
  • Szelies B , MielkeR, HerholzK, Heiss W-D: Quantitative topographical EEG compared with FDG PET for classification of vascular and degenerative dementia. Electroencephalogr. Clin. Neurophysiol.91(2), 131–139 (1994).
  • de Leon MJ , McRaeT, RusinekHet al.: Cortisol reduces hippocampal glucose metabolism in normal elderly but not in Alzheimer‘s disease.J. Clin. Endocrinol. Metab.82, 3251–3259 (1997).
  • Ouchi Y , NobezawaS, OkadaH, YoshikawaE, FutatsubashiM, KanekoM: Altered glucose metabolism in the hippocampal head in memory impairment.Neurology51, 136–142 (1998).
  • de Leon MJ , ConvitA, WolfOTet al.: Prediction of cognitive decline in normal elderly subjects with 2-[18F]fluoro-2-deoxy-D-glucose/positron-emission tomography (FDG/PET).Proc. Natl Acad. Sci. USA98, 10966–10971 (2001).
  • De Santi S , de Leon MJ, Rusinek Het al.: Hippocampal formation glucose metabolism and volume losses in MCI and AD. Neurobiol. Aging22, 529–539 (2001).
  • Nestor PJ , FryerTD, SmielewskiP, HodgesJR: Limbic hypometabolism in Alzheimer‘s disease and mild cognitive impairment.Ann. Neurol.54, 343–351 (2003).
  • Mosconi L , TsuiWH, De Santi S: Reduced hippocampal metabolism in mild cognitive impairment and Alzheimer‘s disease: automated FDG-PET image analysis. Neurology64, 1860–1867 (2005).
  • Mosconi L , De Santi S, Li Yet al.: Visual rating of medial temporal lobe metabolism in mild cognitive impairment and Alzheimer‘s disease using FDG-PET. Eur. J. Nucl. Med.33, 210–221 (2006).
  • Mosconi L , De Santi S, Li Jet al.: Hippocampal hypometabolism predicts cognitive decline from normal aging. Neurobiol. Aging29, 676–692 (2008).
  • Mosconi L , TsuiWH, RusinekHet al.: Quantitation, regional vulnerability and kinetic modeling of brain glucose metabolism in mild Alzheimer‘s disease.Eur. J. Nucl. Med. Mol. Imaging34, 1467–1479 (2007).
  • de Leon MJ , GeorgeAE, GolombJet al.: Frequency of hippocampal formation atrophy in normal aging and Alzheimer‘s disease.Neurobiol. Aging18, 1–11 (1997).
  • Chetelat G , DesgrangesB, LandeauBet al.: Direct voxel-based comparison between grey matter hypometabolism and atrophy in Alzheimer‘s disease.Brain131(1), 60–71 (2007).
  • Tanzi RE , BertramL: New frontiers in Alzheimer‘s disease genetics.Neuron32, 181–184 (2001).
  • Kennedy AM , NewmanSK, FrackowiakRSet al.: Chromosome 14 linked familial Alzheimer‘s disease. A clinico-pathological study of a single pedigree.Brain118, 185–205 (1995).
  • Kennedy AM , FrackowiakRSJ, NewmanSKet al.: Deficits in cerebral glucose metabolism demonstrated by positron emission tomography in individuals at risk of familial Alzheimer‘s disease.Neurosci. Lett.186, 17–20 (1995).
  • Mosconi L , SorbiS, de Leon MJet al.: Hypometabolism exceeds atrophy in presymptomatic early-onset familial Alzheimer‘s disease. J. Nucl. Med.47, 1778–1786 (2006).
  • Petersen RC , StevensJC, GanguliM, TangalosEG, CummingsJL, DeKoskyST: Practice parameter: Early detection of dementia: mild cognitive impiarment (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology.Neurology56, 1133–1142 (2001).
  • Gauthier S , ReisbergB, ZaudigMet al.: Mild cognitive impairment.Lancet367(9518), 1262–1270 (2006).
  • Herholz K , NordbergA, SalmonEet al.: Impairment of neocortical metabolism predicts progression in Alzheimer‘s disease.Dement. Geriatr. Cogn. Disord.10, 494–504 (1999).
  • Arnaiz E , JelicV, AlmkvistOet al.: Impaired cerebral glucose metabolism and cognitive functioning predict deterioration in mild cognitive impairment.NeuroReport12, 851–855 (2001).
  • Chetelat G , DesgrangesB, De La Sayette V, Viader F, Eustache F, Baron JC: Mild cognitive impairment: can FDG-PET predict who is to rapidly convert to Alzheimer‘s disease?. Neurology60, 1374–1377 (2003).
  • Drzezga A , LautenschlagerN, SiebnerHet al.: Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer‘s disease: a PET follow-up study.Eur. J. Nucl. Med. Mol. Imaging30, 1104–1113 (2003).
  • Drzezga A , GrimmerT, RiemenschneiderMet al.: Prediction of individual outcome in MCI by means of genetic assessment and 18F-FDG PET.J. Nucl. Med.46, 1625–1632 (2005).
  • Anchisi D , BorroniB, FranceschiMet al.: Heterogeneity of brain glucose metaboism in mild cognitive impairment and clinical progression to Alzheimer disease.Arch. Neurol.62, 1728–1733 (2005).
  • Haxby JV , GradyCL, KossEet al.: Longitudinal study of cerebral metabolic asymmetries and associated neuropsychological patterns in early dementia of the Alzheimer type.Arch. Neurol.47, 753–760 (1990).
  • Reed BR , JagustWJ, SeabJP, OberBA: Memory and regional cerebral blood flow in mildly symptomatic Alzheimer‘s disease.Neurol.39, 1537–1539 (1989).
  • Berent S , GiordaniB, FosterNet al.: Neuropsychological function and cerebral glucose utilization in isolated memory impairment and Alzheimer‘s disease.J. Psychiat. Res.33, 7–16 (1999).
  • Mosconi L , PeraniD, SorbiSet al.: MCI conversion to dementia and the APOE genotype: a prediction study with FDG-PET.Neurology63, 2332–2340 (2004).
  • Petersen RC , SmithGE, WaringSC, IvnikRJ, TangalosEG, KokmenE: Mild cognitive impairment: clinical characterization and outcome.Arch. Neurol.56, 303–308 (1999).
  • Jagust WJ , GitchoA, SunF, KuczynskiB, MungasD, HaanM: Brain imaging evidence of preclinical Alzheimer‘s disease in normal aging.Ann. Neurol.59, 673–681 (2006).
  • Skurk T , Alberti-HuberC, HerderC, HaunerH: Relationship between adipocyte size and adipokine expression and secretion.J. Clin. Endocrinol. Metab.92(3), 1023–1033 (2007).
  • Corder EH , SaundersAM, StrittmatterWJet al.: Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer‘s disease in late onset families.Science261, 921–923 (1993).
  • Farrer LA , CupplesLA, HainesJLet al.: Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease.JAMA278, 1349–1356 (1997).
  • Laws SM , HoneE, GandyS, MartinsRN: Expanding the association between the APOEgene and the risk of Alzheimer‘s disease: possible roles for APOE promoter polymorphisms and alterations in APOEtranscription.J. Neurochem.84, 1215–1236 (2003).
  • Small GW , MazziottaJC, CollinsMTet al.: Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease.JAMA273, 942–947 (1995).
  • Reiman EM , CaselliRJ, YunLSet al.: Preclinical evidence of Alzheimer‘s disease in persons homozygous for the E4 allele for apolipoprotein E.N. Engl. J. Med.334, 752–758 (1996).
  • Small GW , ErcoliLM, SilvermanDHSet al.: Cerebral metabolic and cognitive decline in persons at genetic risk for Alzheimer‘s disease.Proc. Natl Acad. Sci. USA97, 6037–6042 (2000).
  • Reiman EM , CaselliRJ, ChenK, AlexanderGE, BandyD, FrostJ: Declining brain activity in cognitively normal apolipoprotein E ε4 heterozygotes: a foundation for using positron emission tomography to efficiently test treatmentsto prevent Alzheimer‘s disease.Proc. Natl Acad. Sci. USA98, 3334–3339 (2001).
  • Reiman EM , ChenK, AlexanderGEet al.: Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer‘s dementia.Proc.Natl Acad. Sci. USA101, 284–289 (2004).
  • Reiman EM , UeckerA, CaselliRJet al.: Hippocampal volumes in cognitively normal persons at genetic risk for Alzheimer‘s disease.Ann. Neurol.44, 288–291 (1998).
  • Mosconi L , De Santi S, Brys Met al.: Hypometabolism and altered CSF markers in normal ApoE E4 carriers with subjective memory complaints. Biol. Psychiatry63, 609–618 (2008).
  • Geerlings MI , JonkerC, BouterLM, AderHJ, SchmandB: Associationbetween memory complaints and incident Alzheimer‘s disease in elderly people with normal baseline cognition.Am. J. Psychiat.156, 531–537 (1999).
  • Bobinski M , de Leon MJ, Convit Aet al.: MRI of entorhinal cortex in mild Alzheimer‘s disease. Lancet353, 38–40 (1999).
  • Cupples LA , FarrerLA, SadovnikAD, RelkinN, WhitehouseP, GreenP: Estimating risk curves for first-degree relatives of patients with Alzheimer‘s disease: The REVEAL study.Genet. Med.6, 192–196 (2004).
  • Green RC , CupplesLA, GoRet al.: Risk of dementia among white and African–American relatives of patients with Alzheimer disease.JAMA287, 329–336 (2002).
  • Silverman JM , CiresiG, SmithCJ, MarinDB, Schnaider-BeeriM: Variability of familial risk of Alzheimer disease across the late life span.Arch. Gen. Psychiat.62, 565–573 (2005).
  • Mosconi L , BrysM, SwitalskiRet al.: Maternal family history of Alzheimer‘s disease predisposes to reduced brain glucose metabolism.Proc. Natl Acad. Sci. USA104, 19067–19072 (2007).
  • Lin MT , BealMF: Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases.Nature443, 787–795 (2006).
  • Foster NL , HeidebrinkJL, ClarkCMet al.: FDG-PET improves accuracy in distinguishing frontotemporal dementia and Alzheimer‘s disease.Brain130, 2616–2635 (2007).
  • Ishii K , SakamotoS, SasakiMet al.: Cerebral glucose metabolism in patients with frontotemporal dementia.J. Nucl. Med.39, 1875–1878 (1998).
  • Franceschi M , AnchisiD, PelatiOet al.: Glucose metabolism and serotonin receptors in the frontotemporal lobe degeneration.Ann. Neurol.57, 216–225 (2005).
  • Jeong Y , ChoSS, ParkJMet al.: 18F-FDG PET findings in frontotemporal dementia: an SPM analysis of 29 patients.J. Nucl. Med.46, 233–239 (2005).
  • Diehl-Schmid J , GrimmerT, DrzezgaAet al.: Decline of cerebral glucose metabolism in frontotemporal dementia: a longitudinal 18F-FDG-PET-study.Neurobiol. Aging28, 42–50 (2007).
  • Mosconi L , TsuiWH, HerholzKet al.: Multi-center standardized FDG-PET diagnosis of mild cognitive impairment, Alzheimer‘s disease and other dementias.J. Nucl. Med.49, 390–398 (2008).
  • Albin RL , MinoshimaS, D‘AmatoCJ, FreyKA, KuhlDE, SimaAAF: Fluoro-deoxyglucose positron emission tomography in diffuse lewy body disease.Neurol.47, 462–466 (1996).
  • Minoshima S , FosterNL, SimaAA, FreyKA, AlbinRL, KuhlDE: Alzheimer‘s disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmation.Ann. Neurol.50, 358–365 (2001).
  • McKeith IG , GalaskoD, KosakaKet al.: Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the Consortium on DLB International Workshop.Neurology47, 1113–1124 (1996).
  • Gilman S , KoeppeR, LittleRet al.: Differentiation of Alzheimer‘s disease from dementia with Lewy bodies utilizing positron emission tomography with [18F]fluorodeoxyglucose and neuropsychological testing.Exp. Neurol.191, S95–S103 (2005).
  • Lockhart A : Imaging Alzheimer‘s disease pathology: one target, many ligands.Drug Discov. Today11, 1093–1099 (2006).
  • Herholz K : PET studies in dementia.Ann. Nucl. Med.17(2), 79–89 (2003).
  • DeCarli C , AtackJR, BallMJet al.: Post-mortem regional neurofibrillary tangle densities but not senile plaque densities are related to regional cerebral metabolic rates for glucose life in Alzheimer‘s disease patients.Neurodegeneration1, 113–121 (1992).
  • Bradley KM , BydderGM, BudgeMMet al.: Serial brain MRI at 3–6 month intervals as a surrogate marker for Alzheimer‘s disease.Br. J. Radiol.75, 506–513 (2002).
  • Barber R , SnowdenJS, CraufurdD: Frontotemporal dementia and Alzheimer‘s disease: retrospective differentiation using information from informants.J. Neurol. Neurosurg. Psychiatry59, 61–70 (1995).
  • Ishii K , ImamuraT, SasakiMet al.: Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer‘s disease.Neurology51, 125–130 (1998).
  • Santens P , De Bleecker J, Goethals Pet al.: Differential regional cerebral uptake of 18F-fluoro-2-deoxy-D-glucose in Alzheimer‘s disease and frontotemporal dementia at initial diagnosis. Eur. Neurol.45, 19–27 (2001).
  • Higuchi M , TashiroM, AraiHet al.: Glucose hypometabolism and neuropathological correlates in brains of dementia with Lewy bodies.Exp. Neurol.162, 247–256 (2000).
  • Klunk WE , EnglerH, NordbergAet al.: Imaging brain amyloid in Alzheimer‘s disease with Pittsburgh Compound-B.Ann. Neurol.55, 306–319 (2004).
  • Rowe CC , NgS, AckermannUet al.: Imaging β-amyloid burden in aging and dementia.Neurology68, 1718–1725 (2007).
  • Kemppainen N , AaltoS, WilsonIet al.: Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease.Neurology67, 1575–1580 (2006).
  • Pike KE , SavageG, VillemagneVLet al.: β-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer‘s disease.Brain130, 2837–2844 (2007).
  • Mintun MAM , LaRossaGN, ShelineYIMet al.: [11C]PIB in a nondemented population: Potential antecedent marker of Alzheimer disease.Neurology67, 446–452 (2006).
  • Fagan AM , MintunMA, MachRHet al.: Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid.Ann. Neurol.59, 512–519 (2006).
  • Klunk WE , MathisCA, PriceJC, LoprestiBJ, DeKoskyST: Two-year follow-up of amyloid deposition in patients with Alzheimer‘s disease.Brain129, 2805–2807 (2006).
  • Drzezga A , GrimmerT, HenriksenGet al.: Imaging of amyloid plaques and cerebral glucose metabolism in semantic dementia and Alzheimer‘s disease.Neuroimage39, 619–633 (2008).
  • Mathis CA , WangY, KlunkW: Imaging β-amyloid plaques and neurofibrillary tangles in the aging human brain.Curr. Pharm. Des.10, 1469–1492 (2004).
  • Lockhart A , LambJR, OsredkarTet al.: PIB is a non-specific imaging markerof amyloid-β (Aβ) peptide-related cerebral amyloidosis.Brain130, 2607–2615 (2007).
  • Agdeppa ED , KepeV, LiuJet al.: Binding characteristics of radiofluorinated 6-dialkylamino-2-naphthylethylidene derivatives as positron emission tomography imaging probes for β-amyloid plaques in Alzheimer‘s disease.J. Neurosci.21, 1–5 (2001).
  • Small GW , KepeV, ErcoliLMet al.: PET of brain amyloid and tau in mild cognitive impairment.N. Engl. J. Med.355, 2652–2663 (2006).
  • de Leon MJ , MosconiL, LoganJ: Seeing what Alzheimer saw.Nat. Med.13, 129–131 (2007).
  • Powell MR , SmithGE, KnopmanDSet al.: Cognitive measures predict pathologic Alzheimer disease.Arch. Neurol.63, 865–868 (2006).
  • Rowe CC , AckermannU, BrowneWet al.: Imaging of amyloid β in Alzheimer‘s disease with 18F-BAY94–9172, a novel PET tracer: proof of mechanism.Lancet Neurol.7, 129–135 (2008).
  • Mosconi L , BrysM, Glodzik-SobanskaL, De Santi S, Rusinek H, de Leon MJ: Early detection of Alzheimer‘s disease using neuroimaging. Exp. Gerontol.42, 129–138 (2007).
  • Alexander GE , ChenK, PietriniP, RapoportSI, ReimanEM: Longitudinal PET evaluation of cerebral metabolic decline in dementia: a potential outcome measure in Alzheimer‘s disease treatment studies.Am. J. Psychiatry159, 738–745 (2002).

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