In Alzheimer disease (AD), which is the most common cause of dementia, the underlying disease pathology most probably precedes the onset of cognitive symptoms by many years. Thus, efforts are underway to find early diagnostic markers as well as disease-modifying treatments for this disorder. PET enables various brain systems to be monitored in living individuals. In patients with AD, PET can be used to investigate changes in cerebral glucose metabolism, various neurotransmitter systems, neuroinflammation, and the protein aggregates that are characteristic of the disease, notably the amyloid deposits. These investigations are helping to further our understanding of the complex pathophysiological mechanisms that underlie AD, as well as aiding the early and differential diagnosis of the disease in the clinic. In the future, PET studies will also be useful for identifying new therapeutic targets and monitoring treatment outcomes. Amyloid imaging could be useful as early diagnostic marker of AD and for selecting patients for anti-amyloid-β therapy, while cerebral glucose metabolism could be a suitable PET marker for monitoring disease progression. For the near future, multitracer PET studies are unlikely to be used routinely in the clinic for AD, being both burdensome and expensive; however, such studies are very informative in a research context.
PET studies facilitate the clinical differentiation between Alzheimer disease (AD) and other types of dementia
Monitoring cerebral glucose metabolism or amyloid deposition by PET could provide diagnostic accuracy in early cognitive impairment
PET amyloid imaging permits the early detection of patients with amnestic mild cognitive impairment—individuals who have a high risk of developing AD
The glucose analog 2-[18F]-fluoro-2-deoxy-D-glucose can be used in PET studies to monitor the clinical progression of AD
PET amyloid imaging has the potential to be used for selecting appropriate patients for future anti-amyloid-β therapies
Multitracer PET studies further our understanding of the underlying pathological disease processes in AD and the relationship between such pathology and the cognitive impairment exhibited by patients
Subscribe to Journal
Get full journal access for 1 year
only $17.75 per issue
All prices are NET prices.
VAT will be added later in the checkout.
Rent or Buy article
Get time limited or full article access on ReadCube.
All prices are NET prices.
Brookmeyer, R., Johnson, E., Ziegler-Graha, K. & Arrighi, H. M. Forecasting the global burden of Alzheimer's disease. Alzheimers Dement. 3, 186–191 (2007).
Thal, D. R., Rub, U., Orantes, M. & Braak, H. Phases of Aβ-deposition in the human brain and its relevance for the development of AD. Neurology 58, 1791–1800 (2002).
Mattson, M. P. Pathways towards and away from Alzheimer's disease. Nature 430, 631–639 (2004).
Dubois, B. et al. Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS–ADRDA criteria. Lancet Neurol. 6, 734–746 (2007).
Herholz, K., Carter, S. F. & Jones, M. Positron emission tomography imaging in dementia. Br. J. Radiol. 80 (Spec. No. 2), S160–S167 (2007).
Small, G. W. et al. Current and future uses of neuroimaging for cognitively impaired patients. Lancet Neurol. 7, 161–172 (2008).
Mosconi, L. et al. FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer's disease. Eur. J. Nucl. Med. Mol. Imaging 36, 811–822 (2009).
Mosconi, L. Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease. FDG-PET studies in MCI and AD. Eur. J. Nucl. Med. Mol. Imaging 32, 486–510 (2005).
Engler, H. et al. Two-year follow-up of amyloid deposition in patients with Alzheimer's disease. Brain 129, 2856–2866 (2006).
Jagust, W., Reed, B., Mungas, D., Ellis, W. & Decarli, C. What does fluorodeoxyglucose PET imaging add to a clinical diagnosis of dementia? Neurology 69, 871–877 (2007).
Drzezga, A. et al. Prediction of individual clinical outcome in MCI by means of genetic assessment and 18F-FDG PET. J. Nucl. Med. 46, 1625–1632 (2005).
Drzezga, A. et al. Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzheimer's disease: a PET follow-up study. Eur. J. Nucl. Med. Mol. Imaging 30, 1104–1113 (2003).
Mosconi, L. et al. Early detection of Alzheimer's disease using neuroimaging. Exp. Gerontol. 42, 129–138 (2007).
Minoshima, S., Foster, N. L. & Kuhl, D. E. Posterior cingulate cortex in Alzheimer's disease. Lancet 344, 895 (1994).
Minoshima, S. et al. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer's disease. Ann. Neurol. 42, 85–94 (1997).
Schöll, M. et al. Glucose metabolism and PIB binding in carriers of a His163Tyr presenilin 1 mutation. Neurobiol. Aging doi:10.1016/j.neurobiolaging.2009.08.016.
Reiman, E. M. et al. Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia. Proc. Natl Acad. Sci. USA 101, 284–289 (2004).
Small, G. W. et al. Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease. JAMA 273, 942–947 (1995).
Reiman, E. M. et al. Declining brain activity in cognitively normal apolipoprotein E ε4 heterozygotes: A foundation for using positron emission tomography to efficiently test treatments to prevent Alzheimer's disease. Proc. Natl Acad. Sci. USA 98, 3334–3339 (2001).
Reiman, E. M. et al. Preclinical evidence of Alzheimer's disease in persons homozygous for the ε4 allele for apolipoprotein E. N. Engl. J. Med. 334, 752–758 (1996).
Pedersen, N. L., Gatz, M., Berg, S. & Johansson, B. How heritable is Alzheimer's disease late in life? Findings from Swedish twins. Ann. Neurol. 55, 180–185 (2004).
Järvenpää, T. et al. Regional cerebral glucose metabolism in monozygotic twins discordant for Alzheimer's disease. Dement. Geriatr. Cogn. Disord. 16, 245–252 (2003).
Virta, J. J. et al. Voxel-based analysis of cerebral glucose metabolism in mono- and dizygotic twins discordant for Alzheimer disease. J. Neurol. Neurosurg. Psychiatry 80, 259–266 (2009).
Mosconi, L. et al. Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism. Proc. Natl Acad. Sci. USA 104, 19067–19072 (2007).
Braak, H., de Vos, R. A., Jansen, E. N., Bratzke, H. & Braak, E. Neuropathological hallmarks of Alzheimer's and Parkinson's diseases. Prog. Brain Res. 117, 267–285 (1998).
Perry, E. K., Perry, R. H., Blessed, G. & Tomlinson, B. E. Changes in brain cholinesterases in senile dementia of Alzheimer type. Neuropathol. Appl. Neurobiol. 4, 273–277 (1978).
Rinne, J. O. et al. Brain acetylcholinesterase activity in mild cognitive impairment and early Alzheimer's disease. J. Neurol. Neurosurg. Psychiatry 74, 113–115 (2003).
Herholz, K., Weisenbach, S., Kalbe, E., Diederich, N. J. & Heiss, W. D. Cerebral acetylcholine esterase activity in mild cognitive impairment. Neuroreport 16, 1431–1434 (2005).
Paterson, D. & Nordberg, A. Neuronal nicotinic receptors in the human brain. Prog. Neurobiol. 61, 75–111 (2000).
Kadir, A., Almkvist, O., Wall, A., Långström, B. & Nordberg, A. PET imaging of cortical 11C-nicotine binding correlates with the cognitive function of attention in Alzheimer's disease. Psychopharmacology (Berl.) 188, 509–520 (2006).
Horti, A. G., Gao, Y., Kuwabara, H. & Dannals, R. F. Development of radioligands with optimized imaging properties for quantification of nicotinic acetylcholine receptors by positron emission tomography. Life Sci. doi:10.1016/j.lfs.2009.02.029.
Sabri, O., Kendziorra, K., Wolf, H., Gertz, H. J. & Brust, P. Acetylcholine receptors in dementia and mild cognitive impairment. Eur. J. Nucl. Med. Mol. Imaging 35 (Suppl. 1), S30–S45 (2008).
Pomper, M. G. et al. Synthesis and biodistribution of radiolabeled α7 nicotinic acetylcholine receptor ligands. J. Nucl. Med. 46, 326–334 (2005).
Toyohara, J. et al. Preclinical and the first clinical studies on [11C]CHIBA-1001 for mapping α7 nicotinic receptors by positron emission tomography. Ann. Nucl. Med. 23, 301–309 (2009).
Zubieta, J. K. et al. Assessment of muscarinic receptor concentrations in aging and Alzheimer disease with [11C]NMPB and PET. Synapse 39, 275–287 (2001).
Cohen, R. M. et al. Higher in vivo muscarinic-2 receptor distribution volumes in aging subjects with an apolipoprotein E-ε4 allele. Synapse 49, 150–156 (2003).
Reinikainen, K. J., Soininen, H. & Riekkinen, P. J. Neurotransmitter changes in Alzheimer's disease: implications to diagnostics and therapy. J. Neurosci. Res. 27, 576–586 (1990).
Rinne, J. O., Sahlberg, N., Ruottinen, H., Nagren, K. & Lehikoinen, P. Striatal uptake of the dopamine reuptake ligand [11C]β-CFT is reduced in Alzheimer's disease assessed by positron emission tomography. Neurology 50, 152–156 (1998).
Walker, Z. et al. Differentiation of dementia with Lewy bodies from Alzheimer's disease using a dopaminergic presynaptic ligand. J. Neurol. Neurosurg. Psychiatry 73, 134–140 (2002).
McKeith, I. et al. Sensitivity and specificity of dopamine transporter imaging with 123I-FP-CIT SPECT in dementia with Lewy bodies: a phase III, multicentre study. Lancet Neurol. 6, 305–313 (2007).
Walker, Z. et al. Dementia with Lewy bodies: a comparison of clinical diagnosis, FP-CIT single photon emission computed tomography imaging and autopsy. J. Neurol. Neurosurg. Psychiatry 78, 1176–1181 (2007).
Kemppainen, N., Ruottinen, H., Någren, K. & Rinne, J. O. PET shows that striatal dopamine D1 and D2 receptors are differentially affected in AD. Neurology 55, 205–209 (2000).
Tanaka, Y. et al. Decreased striatal D2 receptor density associated with severe behavioral abnormality in Alzheimer's disease. Ann. Nucl. Med. 17, 567–573 (2003).
Kemppainen, N. et al. Hippocampal dopamine D2 receptors correlate with memory functions in Alzheimer's disease. Eur. J. Neurosci. 18, 149–154 (2003).
Nordberg, A. Neuroreceptor changes in Alzheimer disease. Cerebrovasc. Brain. Metab. Rev. 4, 303–328 (1992).
Kepe, V. et al. Serotonin 1A receptors in the living brain of Alzheimer's disease patients. Proc. Natl Acad. Sci. USA 103, 702–707 (2006).
Meltzer, C. C. et al. PET imaging of serotonin type 2A receptors in late-life neuropsychiatric disorders. Am. J. Psychiatry 156, 1871–1878 (1999).
Jagust, W. Mapping brain β-amyloid. Curr. Opin. Neurol. 22, 356–361 (2009).
Klunk, W. E. et al. Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B. Ann. Neurol. 55, 306–319 (2004).
Klunk, W. E. et al. Binding of the positron emission tomography tracer Pittsburgh compound-B reflects the amount of amyloid-β in Alzheimer's disease brain but not in transgenic mouse brain. J. Neurosci. 25, 10598–10606 (2005).
Ikonomovic, M. D. et al. Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease. Brain 131, 1630–1645 (2008).
Leinonen, V. et al. Assessment of β-amyloid in a frontal cortical brain biopsy specimen and by positron emission tomography with carbon 11-labeled Pittsburgh Compound B. Arch. Neurol. 65, 1304–1309 (2008).
Svedberg, M. M. et al. [11C]PIB-amyloid binding and levels of Aβ40 and Aβ42 in postmortem brain tissue from Alzheimer patients. Neurochem. Int. 54, 347–357 (2009).
Archer, H. A. et al. Amyloid load and cerebral atrophy in Alzheimer's disease: an 11C-PIB positron emission tomography study. Ann. Neurol. 60, 145–147 (2006).
Kemppainen, N. M. et al. Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease. Neurology 67, 1575–1580 (2006).
Mintun, M. A. et al. [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease. Neurology 67, 446–452 (2006).
Price, J. C. et al. Kinetic modeling of amyloid binding in humans using PET imaging and Pittsburgh Compound-B. J. Cereb. Blood Flow Metab. 25, 1528–1547 (2005).
Rowe, C. C. et al. Imaging β-amyloid burden in aging and dementia. Neurology 68, 1718–1725 (2007).
Forsberg, A. et al. PET imaging of amyloid deposition in patients with mild cognitive impairment. Neurobiol. Aging 29, 1456–1465 (2008).
Jack, C. R. Jr et al. Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer's disease: implications for sequence of pathological events in Alzheimer's disease. Brain 132, 1355–1365 (2009).
Kemppainen, N. M. et al. PET amyloid ligand [11C]PIB uptake is increased in mild cognitive impairment. Neurology 68, 1603–1606 (2007).
Pike, K. E. et al. β-Amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease. Brain 130, 2837–2844 (2007).
Okello, A. et al. Conversion of amyloid positive and negative MCI to AD over 3 years: an 11C-PIB PET study. Neurology 73, 754–760 (2009).
Wolk, D. A. et al. Amyloid imaging in mild cognitive impairment subtypes. Ann. Neurol. 65, 557–568 (2009).
Lowe, V. J. et al. Comparison of 18F-FDG and PiB PET in cognitive impairment. J. Nucl. Med. 50, 878–886 (2009).
Forsberg, A. et al. High PIB retention in Alzheimer's disease is an early event with complex relationship with CSF biomarkers and functional parameters. Curr. Alzheimer Res. doi:10.2174/1567210198607192050.
Fagan, A. M. et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans. Ann. Neurol. 59, 512–519 (2006).
Koivunen, J. et al. PET amyloid ligand [11C]PIB uptake and cerebrospinal fluid beta-amyloid in mild cognitive impairment. Dement. Geriatr. Cogn. Disord. 26, 378–383 (2008).
Edison, P. et al. Amyloid, hypometabolism, and cognition in Alzheimer disease: an [11C]PIB and [18F]FDG PET study. Neurology 68, 501–508 (2007).
Landau, S. M. et al. Associations between cognitive, functional, and FDG-PET measures of decline in AD and MCI. Neurobiol. Aging doi:10.1016/j.neurobiolaging.2009.07.002.
Grimmer, T. et al. Clinical severity of Alzheimer's disease is associated with PIB uptake in PET. Neurobiol. Aging 30, 1902–1909 (2008).
Villemagne, V. L. et al. Aβ deposits in older non-demented individuals with cognitive decline are indicative of preclinical Alzheimer's disease. Neuropsychologia 46, 1688–1697 (2008).
Drzezga, A. et al. Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease. Neurology 72, 1487–1494 (2009).
Reiman, E. M. et al. Fibrillar amyloid-β burden in cognitively normal people at 3 levels of genetic risk for Alzheimer's disease. Proc. Natl Acad. Sci. USA 106, 6820–6825 (2009).
Scheinin, N. M. et al. Follow-up of [11C]PIB uptake and brain volume in patients with Alzheimer disease and controls. Neurology 73, 1186–1192 (2009).
Edison, P. et al. Amyloid load in Parkinson's disease dementia and Lewy body dementia measured with [11C]PIB positron emission tomography. J. Neurol. Neurosurg. Psychiatry 79, 1331–1338 (2008).
Johansson, A. et al. [11C]-PIB imaging in patients with Parkinson's disease: preliminary results. Parkinsonism Relat. Disord. 14, 345–347 (2008).
Maetzler, W. et al. [11C]PIB binding in Parkinson's disease dementia. Neuroimage 39, 1027–1033 (2008).
Drzezga, A. et al. Imaging of amyloid plaques and cerebral glucose metabolism in semantic dementia and Alzheimer's disease. Neuroimage 39, 619–633 (2008).
Engler, H. et al. In vivo amyloid imaging with PET in frontotemporal dementia. Eur. J. Nucl. Med. Mol. Imaging 35, 100–106 (2008).
Gomperts, S. N. et al. Imaging amyloid deposition in Lewy body diseases. Neurology 71, 903–910 (2008).
Johnson, K. A. et al. Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann. Neurol. 62, 229–234 (2007).
Aizenstein, H. J. et al. Frequent amyloid deposition without significant cognitive impairment among the elderly. Arch. Neurol. 65, 1509–1517 (2008).
Small, G. W. et al. PET of brain amyloid and tau in mild cognitive impairment. N. Engl. J. Med. 355, 2652–2663 (2006).
Waragai, M. et al. Comparison study of amyloid PET and voxel-based morphometry analysis in mild cognitive impairment and Alzheimer's disease. J. Neurol. Sci. 285, 100–108 (2009).
Rowe, C. C. et 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).
Tolboom, N. et al. Detection of Alzheimer pathology in vivo using both 11C-PIB and 18F-FDDNP PET. J. Nucl. Med. 50, 191–197 (2009).
Thompson, P. W. et al. Interaction of the amyloid imaging tracer FDDNP with hallmark Alzheimer's disease pathologies. J. Neurochem. 109, 623–630 (2009).
Shoghi-Jadid, K. et al. Localization of neurofibrillary tangles and β-amyloid plaques in the brains of living patients with Alzheimer disease. Am. J. Geriatr. Psychiatry 10, 24–35 (2002).
Walsh, D. M. & Selkoe, D. J. Aβ oligomers—a decade of discovery. J. Neurochem. 101, 1172–1184 (2007).
Cagnin, A. et al. In-vivo measurement of activated microglia in dementia. Lancet 358, 461–467 (2001).
Okello, A. et al. Microglial activation and amyloid deposition in mild cognitive impairment: a PET study. Neurology 72, 56–62 (2009).
Wiley, C. A. et al. Carbon 11-labeled Pittsburgh Compound B and carbon 11-labeled (R)-PK11195 positron emission tomographic imaging in Alzheimer disease. Arch. Neurol. 66, 60–67 (2009).
Hirsch-Reinshagen, V., Burgess, B. L. & Wellington, C. L. Why lipids are important for Alzheimer disease? Mol. Cell Biochem. 326, 121–129 (2009).
Kadir, A. et al. PET imaging of the in vivo brain acetylcholinesterase activity and nicotine binding in galantamine-treated patients with AD. Neurobiol. Aging 29, 1204–1217 (2008).
Bohnen, N. I. et al. Degree of inhibition of cortical acetylcholinesterase activity and cognitive effects by donepezil treatment in Alzheimer's disease. J. Neurol. Neurosurg. Psychiatry 76, 315–319 (2005).
Kuhl, D. E. et al. Limited donepezil inhibition of acetylcholinesterase measured with positron emission tomography in living Alzheimer cerebral cortex. Ann. Neurol. 48, 391–395 (2000).
Kaasinen, V. et al. Regional effects of donepezil and rivastigmine on cortical acetylcholinesterase activity in Alzheimer's disease. J. Clin. Psychopharmacol. 22, 615–620 (2002).
Shinotoh, H. et al. Effect of donepezil on brain acetylcholinesterase activity in patients with AD measured by PET. Neurology 56, 408–410 (2001).
Kadir, A. et al. Changes in brain 11C-nicotine binding sites in patients with mild Alzheimer's disease following rivastigmine treatment as assessed by PET. Psychopharmacology (Berl.) 191, 1005–1014 (2007).
Ellis, J. R. et al. Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer's disease as measured in vivo by 2-[18F]fluoro-A-85380 PET. Psychopharmacology (Berl.) 202, 79–91 (2009).
Diehl-Schmid, J. et al. Longitudinal changes of cerebral glucose metabolism in semantic dementia. Dement. Geriatr. Cogn. Disord. 22, 346–351 (2006).
Diehl-Schmid, J. et al. Decline of cerebral glucose metabolism in frontotemporal dementia: a longitudinal 18F-FDG-PET-study. Neurobiol. Aging 28, 42–50 (2007).
Dickerson, B. C. & Sperling, R. A. Neuroimaging biomarkers for clinical trials of disease-modifying therapies in Alzheimer's disease. NeuroRx 2, 348–360 (2005).
Foster, N. L. et al. Realizing the potential of positron emission tomography with 18F-fluorodeoxyglucose to improve the treatment of Alzheimer's disease. Alzheimers Dement. 4 (Suppl. 1), S29–S36 (2008).
Matthews, B., Siemers, E. R. & Mozley, P. D. Imaging-based measures of disease progression in clinical trials of disease-modifying drugs for Alzheimer disease. Am. J. Geriatr. Psychiatry 11, 146–159 (2003).
Mega, M. S. et al. Cognitive and metabolic responses to metrifonate therapy in Alzheimer disease. Neuropsychiatry Neuropsychol. Behav. Neurol. 14, 63–68 (2001).
Stefanova, E. et al. Longitudinal PET evaluation of cerebral glucose metabolism in rivastigmine treated patients with mild Alzheimer's disease. J. Neural Transm. 113, 205–218 (2006).
Tune, L. et al. Donepezil HCl (E2020) maintains functional brain activity in patients with Alzheimer disease: results of a 24-week, double-blind, placebo-controlled study. Am. J. Geriatr. Psychiatry 11, 169–177 (2003).
Mega, M. S. et al. Metabolic patterns associated with the clinical response to galantamine therapy: a fludeoxyglucose F 18 positron emission tomographic study. Arch. Neurol. 62, 721–728 (2005).
Teipel, S. J. et al. Effects of donepezil on cortical metabolic response to activation during 18FDG-PET in Alzheimer's disease: a double-blind cross-over trial. Psychopharmacology (Berl.) 187, 86–94 (2006).
Kadir, A. et al. Effect of phenserine treatment on brain functional activity and amyloid in Alzheimer's disease. Ann. Neurol. 63, 621–631 (2008).
Smith, G. S. et al. Cholinergic modulation of the cerebral metabolic response to citalopram in Alzheimer's disease. Brain 132, 392–401 (2009).
Tuszynski, M. H. et al. A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease. Nat. Med. 11, 551–555 (2005).
Eriksdotter Jonhagen, M. et al. Intracerebroventricular infusion of nerve growth factor in three patients with Alzheimer's disease. Dement. Geriatr. Cogn. Disord. 9, 246–257 (1998).
Lahiri, D. K. et al. The experimental Alzheimer's disease drug posiphen[(+)-phenserine] lowers amyloid-β peptide levels in cell culture and mice. J. Pharmacol. Exp. Ther. 320, 386–396 (2007).
Marutle, A. et al. Modulation of human neural stem cell differentiation in Alzheimer (APP23) transgenic mice by phenserine. Proc. Natl Acad. Sci. USA 104, 12506–12511 (2007).
Razifar, P. et al. An automated method for delineating a reference region using masked volumewise principal-component analysis in 11C-PIB PET. J. Nucl. Med. Technol. 37, 38–44 (2009).
Razifar, P., Ringheim, A., Engler, H., Hall, H. & Långström, B. Masked-volume-wise PCA and “reference Logan” illustrate similar regional differences in kinetic behavior in human brain PET study using [11C]-PIB. BMC Neurol. 9, 2 (2009).
Nordberg, A. Amyloid imaging in Alzheimer's disease. Curr. Opin. Neurol. 20, 398–402 (2007).
Petersen, R. C. Mild cognitive impairment as a diagnostic entity. J. Intern. Med. 256, 183–194 (2004).
Roivainen, A. et al. Biodistribution and blood metabolism of 1-11C-methyl-4-piperidinyl n-butyrate in humans: an imaging agent for in vivo assessment of butyrylcholinesterase activity with PET. J. Nucl. Med. 45, 2032–2039 (2004).
Nelissen, N. et al. Phase 1 study of the Pittsburgh compound B derivative 18F-flutemetamol in healthy volunteers and patients with probable Alzheimer disease. J. Nucl. Med. 50, 1251–1259 (2009).
Verhoeff, N. P. et al. In-vivo imaging of Alzheimer disease beta-amyloid with [11C]SB-13 PET. Am. J. Geriatr. Psychiatry 12, 584–595 (2004).
Kudo, Y. et al. 2-(2-[2-Dimethylaminothiazol-5-yl]ethenyl)-6- (2-[fluoro]ethoxy)benzoxazole: a novel PET agent for in vivo detection of dense amyloid plaques in Alzheimer's disease patients. J. Nucl. Med. 48, 553–561 (2007).
Choi, S. R. et al. Preclinical properties of 18F-AV-45: a PET agent for Aβ plaques in the brain. J. Nucl. Med. 50, 1887–1894 (2009).
Nyberg, S. et al. Detection of amyloid in Alzheimer's disease with positron emission tomography using [11C]AZD2184. Eur. J. Nucl. Med. Mol. Imaging 36, 1859–1863 (2009).
A. Nordberg gratefully acknowledges the financial support provided by the following: the Swedish Research Council (project 05817), Stockholm County Council–Karolinska Institute (ALF grant), the Foundation for Old Servants, the Stohne's Foundation, the KI Foundations, the Alzheimer Foundation in Sweden, Swedish Brain Power, the EC-FP6 project DiMI (LSHB-CT-2005-512146 and QLK6-CT-2000-00502), and the Swedish Brain Foundation. Anton Forsberg, Michael Schöll (both Karolinska Institute) and Anders Wall (GE Healthcare, Uppsala, Sweden) are thanked for their help in preparing the figures.
The authors declare no competing financial interests.
About this article
Cite this article
Nordberg, A., Rinne, J., Kadir, A. et al. The use of PET in Alzheimer disease. Nat Rev Neurol 6, 78–87 (2010). https://doi.org/10.1038/nrneurol.2009.217
Altered d-glucose in brain parenchyma and cerebrospinal fluid of early Alzheimer’s disease detected by dynamic glucose-enhanced MRI
Science Advances (2020)
Liraglutide Protects Against Brain Amyloid-β1–42 Accumulation in Female Mice with Early Alzheimer’s Disease-Like Pathology by Partially Rescuing Oxidative/Nitrosative Stress and Inflammation
International Journal of Molecular Sciences (2020)
Emphasis Learning, Features Repetition in Width Instead of Length to Improve Classification Performance: Case Study—Alzheimer’s Disease Diagnosis
In situ structural characterization of early amyloid aggregates in Alzheimer’s disease transgenic mice and Octodon degus
Scientific Reports (2020)
Pattern Recognition (2020)