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Larger temporal volume in elderly with high versus low beta-amyloid deposition
Abstract
β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amyloid burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [¹¹C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[¹¹C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[¹¹C]Pittsburgh compound B healthy controls. The same finding was obtained using different [¹¹C]Pittsburgh compound B thresholds, correcting [¹¹C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[¹¹C]Pittsburgh compound B cases compared to low-[¹¹C]Pittsburgh compound B cases, as well as in high-[¹¹C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[¹¹C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[¹¹C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[¹¹C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.
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“A between-group analysis performed by Chetelat et al. indicated that, in participants with SCD, individuals with a higher level of amyloid deposition showed significant gray matter atrophy compared with individuals with a low level of amyloid deposition [180].”
From Neuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer's disease (2020) · cites this paper as [180]
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Self-citationNeuroimaging advances regarding subjective cognitive decline in preclinical Alzheimer's disease
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“…All: n = 133 (75.9±7.0) Aß negative: n = 94 (74.9±7.2) Aß positive: n = 39 (78.4±5.7) Greater SCD relate to increased entorhinal tau burden and Aß burden Chetelat et al. (2010) [180, 181] 1 binary question PiB-PET MRI Cross-sectional NC: n = 45 (74.9±7.1) SCI: n = 49 (73.9±7.2) MCI:n = 34…”
BackgroundInfluentialGlucose metabolism, gray matter structure, and memory decline in subjective memory impairment
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“A similar pattern of enlarged temporopolar cortex was recently reported in cognitively normal elderly individuals with high amyloid burden (Chételat et al., 2010).”
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“However, anatomic differences associated with amyloid burden are of interest and in at least 1 other study (Chetelat et al., 2010) larger volumes (in their case temporal lobe volumes) were reported in controls who were amyloid positive relative to amyloid negative controls.”
BackgroundCortical microstructural changes along the Alzheimer’s disease continuum
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Chételat, G., Villemagne, V. L., Villain, N., Jones, G. R., Ellis, K. A., Ames, D. J., Martins, R. N., Masters, C. L., & Rowe, C. C. (2012) · Neurology · doi:10.1212/wnl.0b013e318246d67a · Cited by 176
Self-citationCognitive reserve and lifestyle: moving towards preclinical Alzheimer’s disease
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Self-citationIncreased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1‐42
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Cholinergic basal forebrain atrophy predicts amyloid burden in Alzheimer's disease
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“…3.8 11.4 3.5 52 42 Buckley et al. (2016) PET 230 58 69 5.9 72 7.2 - - - - 54 50 Chen et al. (2015) PET 88 26 77.7 6.5 77.2 4.6 16.6 3 16 2.5 45 38 Chételat et al. (2010) PET 31 13 73.1 7.1 78.8 5.5 14 3.3 14.3 3 65 31 Chételat et al. (2012) PET 54 20 72.7 7.3 76.6 6.4 14.2 3.2 14.1 3.4 52…”
InfluentialBasal forebrain atrophy and cortical amyloid deposition in nondemented elderly subjects
Grothe, M. J., Ewers, M., Krause, B. J., Heinsen, H., & Teipel, S. J. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2013.09.011 · Cited by 107
Entorhinal cortex tau, amyloid-β, cortical thickness and memory performance in non-demented subjects
Knopman, D. S., Lundt, E. S., Therneau, T. M., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., Machulda, M. M., et al. (2019) · Brain · doi:10.1093/brain/awz025 · Cited by 104
Arenaza‐Urquijo, E. M., Bejanin, A., Gonneaud, J., Wirth, M., Joie, R. L., Mutlu, J., Gaubert, M., Landeau, B., Sayette, V. D. L., Eustache, F., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.06.016 · Cited by 100
Self-citationSubjective cognitive decline: preclinical manifestation of Alzheimer’s disease
Lin, Y., Shan, P., Jiang, W., Sheng, C., & Ma, L. (2018) · Neurological Sciences · doi:10.1007/s10072-018-3620-y · Cited by 95
A review of β-amyloid neuroimaging in Alzheimer's disease
Adlard, P. A., Tran, B. A., Finkelstein, D. I., Desmond, P. M., Johnston, L. A., Bush, A. I., & Egan, G. F. (2014) · Frontiers in Neuroscience · doi:10.3389/fnins.2014.00327 · Cited by 93
“…amyloid burden and various markers of AD, such as cognitive decline (Rowe et al., 2010), functional alterations (Hedden et al., 2009; Rabinovici and Jagust, 2009; Shin et al., 2010, 2011; Mormino et al., 2012) and regional brain atrophy (Jack et al., 2008; Chetelat et al., 2010; Rowe et al., 2010).”
BackgroundIngala, S., de Boer, C., Masselink, L. A., Vergari, I., Lorenzini, L., Blennow, K., Chételat, G., Perri, C. D., Ewers, M., van der Flier, W. M., et al. (2021) · Alzheimer s & Dementia · doi:10.1002/alz.12292 · Cited by 88
Self-citationUnbiased comparison of sample size estimates from longitudinal structural measures in ADNI
Holland, D., McEvoy, L. K., Dale, A. M., & Initiative, T. A. D. N. (2011) · Human Brain Mapping · doi:10.1002/hbm.21386 · Cited by 85
“…for differences in atrophy rates in AD-vulnerable regions between Ab-positive and Ab-negative healthy older adults (or healthy older controls, HCs) [Chetelat et al., 2010; Fjell et al., 2010], though using variants of Boundary Shift Integral (BSI) for whole brain, ventricles, and hippocampus, a…”
MethodA Systematic Review of Longitudinal Studies Which Measure Alzheimer’s Disease Biomarkers
Lawrence, E., Vegvari, C., Ower, A. K., Hadjichrysanthou, C., de Wolf, F., & Anderson, R. M. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170261 · Cited by 89
Association of Gray Matter Atrophy with Age, β-Amyloid, and Cognition in Aging
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“We found a reverse relationship in cognitively intact elderly such that those with A deposition tended to have greater temporal volume (which might reflect brain reserve, see also below) [33].”
Self-citationTosun, D., Veitch, D. P., Aisen, P. S. S., Jack, C. R., Jagust, W. J., Petersen, R. C., Saykin, A. J., Bollinger, J., Ovod, V., Mawuenyega, K. G., et al. (2021) · Brain Communications · doi:10.1093/braincomms/fcab008 · Cited by 86
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de Vries, L. E., Huitinga, I., Kessels, H. W. H. G., Swaab, D. F., & Verhaagen, J. (2024) · Molecular Neurodegeneration · doi:10.1186/s13024-024-00719-7 · Cited by 85
“Using PiB PET imaging to visualize Aβ plaque load, increased temporal volumes in cognitively intact individuals with a higher plaque load compared to those with lower plaque load were demonstrated, while opposite effects were found in AD patients [155].”
ResultUnderstanding the cause of sporadic Alzheimer’s disease
Zetterberg, H., & Mattsson, N. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.915740 · Cited by 73
“Ab load has even been associated with larger volume in temporal regions, perhaps indicating brain reserve mechanisms [24].”
BackgroundEmerging β-amyloid pathology and accelerated cortical atrophy
Mattsson, N., Insel, P. S., Nosheny, R., Tosun, D., Trojanowski, J. Q., Shaw, L. M., Jack, C. R., Donohue, M. C., & Weiner, M. W. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2014.446 · Cited by 71
Distinct effects of beta‐amyloid and tau on cortical thickness in cognitively healthy older adults
Harrison, T. M., Du, R., Klencklen, G., Baker, S. L., & Jagust, W. J. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12249 · Cited by 69
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Self-citationAmyloid Imaging with PET in Early Alzheimer Disease Diagnosis
Rowe, C. C., & Villemagne, V. L. (2013) · Medical Clinics of North America · doi:10.1016/j.mcna.2012.12.017 · Cited by 62
Self-citationTraumatic brain injury and reserve
Bigler, E. D., & Stern, Y. (2015) · Handbook of clinical neurology · doi:10.1016/b978-0-444-63521-1.00043-1 · Cited by 72
“For example, larger temporal lobe volume, including hippocampal volume in the elderly, has been found to potentially mitigate b-amyloid deposition, a key feature in the development of Alzheimer’s disease (Chetelat et al., 2010).”
BackgroundQuejas cognitivas subjetivas: hacia una identificación precoz de la enfermedad de Alzheimer
Ptacek, S. G., Eriksdotter, M., Jelić, V., Porta-Etessam, J., Kåreholt, I., & Palomo, S. M. (2013) · Neurología · doi:10.1016/j.nrl.2013.02.007 · Cited by 73
“A corollary study showed that healthy subjects with high PiB uptake presented higher medial temporal volume than subjects with SCI and high PiB uptake.(72) Healthy subjects with high PiB uptake levels had larger temporal volumes than healthy subjects with low PiB uptake levels; therefore, this finding cannot be explai…”
BackgroundGispert, J. D., Rami, L., Sánchez‐Benavides, G., Falcón, C., Tucholka, A., Rojas, S., & Molinuevo, J. L. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.06.027 · Cited by 56
Biphasic cortical macro‐ and microstructural changes in autosomal dominant Alzheimer's disease
Montal, V., Vilaplana, E., Pegueroles, J., Bejanin, A., Alcolea, D. A., Carmona‐Iragui, M., Clarimón, J., Levin, J., Cruchaga, C., Graff‐Radford, N. R., et al. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.12224 · Cited by 54
“8,40,41 9 The atrophy and increased mean diffusivity found in the youngest mutation carriers might reflect neurodevelopmental abnormalities.”
BackgroundWu, Z., Peng, Y. F., Hong, M., & Zhang, Y. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.593898 · Cited by 54
“Evidence suggests that pathological alteration occurs long before the onset of clinical AD symptoms due to the toxic effects of amyloid-beta plaques (Chetelat et al., 2010; Johnson et al., 2014; Juan et al., 2015).”
BackgroundSong, Z., Insel, P. S., Buckley, S. T., Yohannes, S., Mezher, A. F., Simonson, A., Wilkins, S., Tosun, D., Mueller, S. G., Kramer, J. H., et al. (2015) · Journal of Neuroscience · doi:10.1523/jneurosci.2092-14.2015 · Cited by 55
“Similarly, some studies show that cognitively normal subjects with substantial A load have subtle brain atrophy (Fjell et al., 2010), whereas other studies find no effects on brain structures (Josephs et al., 2008) or even the presence of larger regional brain volumes (Chételat et al., 2010).”
ResultToward a multifactorial model of Alzheimer disease
Storandt, M., Head, D. M., Fagan, A. M., Holtzman, D. M., & Morris, J. C. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.11.029 · Cited by 54
“One study (Chetelat et al., 2010), for example, found no correlation when people with subjective memory complaints were excluded.”
BackgroundLee, G. J., Lu, P. H., Medina, L. D., Rodríguez‐Agudelo, Y., Melchor, S. J., Coppola, G., Braskie, M. N., Hua, X., Apostolova, L. G., Leow, A., et al. (2012) · Journal of Neurology Neurosurgery & Psychiatry · doi:10.1136/jnnp-2011-302087 · Cited by 54
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Self-citationZolochevska, O., & Taglialatela, G. (2016) · Current Pharmaceutical Design · doi:10.2174/1381612822666160518142110 · Cited by 49
“the healthy individuals with high Aβ loads presented larger global and regional grey matter volumes when compared to cognitively impaired subjects with high Aβ [29].”
BackgroundPET imaging of neural activity, β-amyloid, and tau in normal brain aging
Zhang, K., Mizuma, H., Zhang, X., Takahashi, K., Jin, C., Song, F., Gao, Y., Kanayama, Y., Wu, Y., Li, Y., et al. (2021) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-021-05230-5 · Cited by 49
Arenaza‐Urquijo, E. M., Molinuevo, J. L., Sala‐Llonch, R., Solé‐Padullés, C., Balasa, M., Bosch, B., Olives, J., Antonell, A., Lladó, A., Sánchez‐Valle, R., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-121906 · Cited by 50
“It has been suggested [18] that brain A 42 burden is not related to brain atrophy in healthy subjects without memory complaints but only in subjects with memory complaints, thus the inclusion of subjects with memory complaints may have influenced our results.”
BackgroundResultNeuroimaging Results Impose New Views on Alzheimer’s Disease—the Role of Amyloid Revised
Fjell, A. M., & Walhovd, K. B. (2011) · Molecular Neurobiology · doi:10.1007/s12035-011-8228-7 · Cited by 48
“[100] 44 HC, 49 sMCI, 22 aMCI, 34 AD PiB, MRI (VBM) PiB-positive sMCI patients had smaller hippocampal volume; the inverse relationship was observed in controls.”
BackgroundResultInfluentialAmyloid and Tau Biomarkers in Subjective Cognitive Impairment
Colijn, M. A., & Grossberg, G. T. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-150180 · Cited by 51
“[53] found that SCI individuals with high PiB had a significantly higher prevalence of the ApoE allele than those with low PiB, and Verdile et al.”
BackgroundNeuroimaging biomarkers in Alzheimer’s disease and other dementias
Villemagne, V. L., & Chételat, G. (2016) · Ageing Research Reviews · doi:10.1016/j.arr.2016.01.004 · Cited by 55
Self-citationSubjective Cognitive Decline and APOE ɛ4: A Systematic Review
Ali, J. I., Smart, C. M., & Gawryluk, J. R. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180248 · Cited by 48
Salvadó, G., Shekari, M., Falcón, C., Operto, G., Milà‐Alomà, M., Sánchez‐Benavides, G., Cacciaglia, R., Arenaza‐Urquijo, E. M., Niñerola‐Baizán, A., Perissinotti, A., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac134 · Cited by 45
“Previous reports observing increments in these early phases of Alzheimer ’ s disease have suggested multiple non-exclusive biological explanations such as cellular hypertrophy, 5,8,24 oedema or brain swallowing 5 and the buildup of A β plaques.”
Mormino, E. C. (2014) · Neuropsychology Review · doi:10.1007/s11065-014-9267-4 · Cited by 44
“For instance, some studies have reported longitudinal atrophy in the medial temporal lobe (Chetelat et al. 2012; Schott et al. 2010), whereas other work suggest that medial temporal lobe atrophy increases at a similar rate in CNs with and without evidence of Aβ positivity (Fjell et al. 2009, 2014).”
Kok, F. K., van Leerdam, S., & de Lange, E. C. M. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-210607 · Cited by 46
Atrophy Rates in Asymptomatic Amyloidosis: Implications for Alzheimer Prevention Trials
Andrews, K. A., Marc Modat, A., Macdonald, K. E., Yeatman, T., Cardoso, M. J., Leung, K. K., Barnes, J., Villemagne, V. L., Rowe, C. C., Fox, N. C., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0058816 · Cited by 48
“At this level, ,1/3 of this cognitively normal cohort were amyloid-positive, in keeping with previous PET [10,36,39] and CSF [9,40] studies.”
ResultSelf-citationAkinyemi, R., Allan, L. M., Oakley, A. E., & Kalaria, R. N. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00717 · Cited by 43
“Cognitively normal elderly subjects with huge quantities of amyloid pathology but preserved cognitive functioning have been described in the literature (Bennett et al., 2006; Chetelat et al., 2010).”
BackgroundUnderstanding cognitive deficits in Alzheimer's disease based on neuroimaging findings
Braskie, M. N., & Thompson, P. M. (2013) · Trends in Cognitive Sciences · doi:10.1016/j.tics.2013.08.007 · Cited by 48
Sala‐Llonch, R., Idland, A., Borza, T., Watne, L. O., Wyller, T. B., Brækhus, A., Zetterberg, H., Blennow, K., Walhovd, K. B., & Fjell, A. M. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161146 · Cited by 45
“While the role of YKL-40 in normal aging is almost unexplored, previous research on amyloid-related changes in the aging brain are conflicting, with some reporting more atrophy [19–21] in subjects with lower CSF A (cid:2) 42 levels and others larger volumes [22], or non-linear relationships [23].”
Ye, B. S., Kim, Y. J., Kim, Y. J., Jung, N., Lee, J. S., Lee, J., Jang, Y. K., Yang, J., Lee, J. M., Vogel, J. W., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-23676-w · Cited by 41
Evolving brain structural changes in PSEN1 mutation carriers
Sala‐Llonch, R., Lladó, A., Fortea, J., Bosch, B., Antonell, A., Balasa, M., Bargalló, N., Bartrés‐Faz, D., Molinuevo, J. L., & Sánchez‐Valle, R. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.12.022 · Cited by 39
“First, in sporadic AD, some studies have found increased regional volume and thickness in healthy subjects with evidence of initial beta-amyloid deposition (Chételat et al., 2010; Fortea et al., 2011; Johnson et al., 2014).”
Mielke, M. M., Weigand, S. D., Wiste, H. J., Vemuri, P., Machulda, M. M., Knopman, D. S., Lowe, V. J., Roberts, R. O., Kantarci, K., Rocca, W. A., et al. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.09.001 · Cited by 41
“…be interpreted as the proportion of variability in the response accounted for by the regression model. phenomenon is currently unclear but previous studies of cognitively normal individuals counterintuitively have re-ported better cognitive performance in those with high versus low amyloid [36,37].”
ResultTardif, C. L., Devenyi, G. A., Amaral, R. S. C., Pelleïeux, S., Poirier, J., Rosa‐Neto, P., Breitner, J. C. S., & Chakravarty, M. M. (2017) · Human Brain Mapping · doi:10.1002/hbm.23897 · Cited by 36
“, 2009; Storandt, Mintun, Head, & Morris, 2009) and increase (Chetelat et al., 2010).”
BackgroundResultReseco, L., Atienza, M., Fernandez-Alvarez, M., Carro, E., & Cantero, J. L. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00891-8 · Cited by 33
Should We Disclose Amyloid Imaging Results to Cognitively Normal Individuals?
Grill, J. D., Johnson, D. K., & Burns, J. M. (2013) · Neurodegenerative Disease Management · doi:10.2217/nmt.12.75 · Cited by 36
“[21, 22] and the posterior cingulate / precuneus [23-25].”
BackgroundLojo‐Seoane, C., Facal-Mayo, D., & Juncos‐Rabadán, O. (2012) · Revista Española de Geriatría y Gerontología · doi:10.1016/j.regg.2012.02.006 · Cited by 38
Amyloid imaging and memory change for prediction of cognitive impairment
Resnick, S. M., & Sojkova, J. (2011) · Alzheimer s Research & Therapy · doi:10.1186/alzrt62 · Cited by 33
Cai, Y. Q., Shi, D., Lan, G., Chen, L., Jiang, Y., Zhou, L., Guo, T., & Initiative, A. D. N. (2024) · Neurology · doi:10.1212/wnl.0000000000209205 · Cited by 31
Batzu, L., Westman, E., & Pereira, J. B. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.12.012 · Cited by 30
Vaqué‐Alcázar, L., Sala‐Llonch, R., Valls‐Pedret, C., Dídac Vidal-piñeiro, A., Fernández‐Cabello, S., Bargalló, N., Ros, E., & Bartrés‐Faz, D. (2016) · Brain Imaging and Behavior · doi:10.1007/s11682-016-9584-8 · Cited by 30
Ferreira, D., Falahati, F., Linden, C., Buckley, R. F., Ellis, K. A., Savage, G. R., Villemagne, V. L., Rowe, C. C., Ames, D. J., Simmons, A., et al. (2017) · Scientific Reports · doi:10.1038/srep44368 · Cited by 31
Self-citationFalcón, C., Tucholka, A., Monté, G. C., Cacciaglia, R., Operto, G., Rami, L., Gispert, J. D., & Molinuevo, J. L. (2018) · NeuroImage Clinical · doi:10.1016/j.nicl.2018.04.016 · Cited by 29
“, 2011), or even found increased volume in temporal regions including the hippocampus (Chételat et al., 2010) and parahippocampal areas (Gispert et al.”
Neuroanatomical and neurocognitive changes associated with subjective cognitive decline
Rivas‐Fernández, M. Á., Lindı́n, M., Zurrón, M., Dı́az, F., Lojo‐Seoane, C., Pereiro, A. X., & Galdo‐Álvarez, S. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1094799 · Cited by 30
Structural imaging outcomes in subjective cognitive decline: Community vs. clinical-based samples
Pini, L., & Wennberg, A. M. V. (2020) · Experimental Gerontology · doi:10.1016/j.exger.2020.111216 · Cited by 29
Almdahl, I. S., Lauridsen, C., Selnes, P., Kalheim, L. F., Coello, C. S., Gajdzik, B., Møller, I., Wettergreen, M., Grambaitė, R., Bjørnerud, A., et al. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00009 · Cited by 27
Zhan, Y., Initiative, A. D. N., Chen, K., Wu, X., Zhang, D., Zhang, J., Yao, L., & Guo, X. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142820 · Cited by 23
“…showed that A (cid:1) deposition In recent years, many studies suggest that approximately 20–30% of cognitively normal elderly also had A deposition in the brain, mainly in the precuneus temporal lobe, and cingulate cortex accompanied by glucose metabolism reduction and gray matter atrophy [19–22].”
Regional age-related atrophy after screening for preclinical alzheimer disease
Koenig, L. N., LaMontagne, P., Glasser, M. F., Bateman, R. J., Holtzman, D. M., Yakushev, I. Y., Chhatwal, J. P., Day, G. S., Jack, C. R., Mummery, C. J., et al. (2021) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2021.09.010 · Cited by 23
Benvenutto, A., Giusiano, B., Koric, L., Guériot, C., Didic, M., Félician, O., Guye, M., Guedj, É., & Ceccaldi, M. P. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180292 · Cited by 24
Subjective cognitive impairment: Towards early identification of Alzheimer disease
Ptacek, S. G., Eriksdotter, M., Jelić, V., Porta-Etessam, J., Kåreholt, I., & Palomo, S. M. (2016) · Neurología (English Edition) · doi:10.1016/j.nrleng.2013.02.011 · Cited by 26
Teipel, S. J., Cavedo, E., Weschke, S., Grothe, M. J., Rojkova, K., Fontaine, G., Dauphinot, L., Gonzalez-Escamilla, G., Potier, M.-C., Bertin, H., et al. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.05.016 · Cited by 22
“So far, the association between higher amyloid load and gray matter volume was only studied in a sample of 49 people with subjective memory complaints (Chetelat et al., 2010a,b).”
BackgroundResultInfluentialNosheny, R. L., Insel, P. S., Mattsson, N., Tosun, D., Buckley, S. T., Truran, D., Schuff, N. W., Aisen, P. S. S., & Weiner, M. W. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2019.07.005 · Cited by 23
“Unlike previous crosssectional studies (Bakkour et al., 2013; Becker et al., 2011; Bourgeat et al., 2010; Chetelat et al., 2010; Dickerson et al., 2011; Fjell et al., 2010b; Mormino et al., 2009; Oh et al., 2013; Storandt et al., 2009), we did not find areas outside of the temporal lobe with a significant association…”
BackgroundResultParker, A. F., Ohlhauser, L., Scarapicchia, V., Smart, C. M., Szoeke, C., & Gawryluk, J. R. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-215249 · Cited by 23
Self-citationSolé‐Padullés, C., Lladó, A., Bartrés‐Faz, D., Fortea, J., Sánchez‐Valle, R., Bosch, B., Antonell, A., Molinuevo, J. L., & Rami, L. (2011) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2010.12.001 · Cited by 19
Differential effects of sleep on brain structure and metabolism at the preclinical stages of AD
Stankeviciute, L. S., Falcón, C., Operto, G., García-Prat, M., Shekari, M., Iranzo, Á., Niñerola‐Baizán, A., Perissinotti, A., Minguillón, C., Fauria, K., et al. (2023) · Alzheimer s & Dementia · doi:10.1002/alz.13102 · Cited by 18
Brain β-Amyloid and Atrophy in Individuals at Increased Risk of Cognitive Decline
Martikainen, I. K., Kemppainen, N. M., Johansson, J. J., Teuho, J., Helin, S., Liu, Y., Helisalmi, S., Soininen, H. S., Parkkola, R. K., Ngandu, T., et al. (2018) · American Journal of Neuroradiology · doi:10.3174/ajnr.a5891 · Cited by 18
“However, some studies in cognitively healthy subjects have failed to find associations between (11)C PIB uptake and atrophy(8) or have even suggested a positive correlation between (11)C PIB uptake and GM volume.(7) Considering the distinct time scales of brain A accumulation and GM loss, these discrepancies may relat…”
BackgroundCanário, N., Jorge, L., Martins, R., Santana, I. J., & Castelo-Branco, M. S. (2022) · Communications Biology · doi:10.1038/s42003-022-03761-7 · Cited by 21
Self-citationEllis, K. A., Rainey‐Smith, S. R., Rembach, A., Macaulay, S. L., Villemagne, V. L., & Aibl research group (2013) · International Review of Psychiatry · doi:10.3109/09540261.2013.870136 · Cited by 17
“…showed that while global and regional grey matter atrophy were strongly related to global A β burden in cognitively unimpaired participants who were worried about their memory (subjective memory complainers), this relationship was not evident in MCI or AD patients (Ch é telat et al., 2010a).”
BackgroundResultInfluentialSelf-citationMatloff, W. J., Zhao, L., Ning, K., Conti, D. V., & Toga, A. W. (2019) · Alcohol · doi:10.1016/j.alcohol.2019.11.002 · Cited by 20
APOE-ε4-related differences in left thalamic microstructure in cognitively healthy adults
Mole, J. P., Fasano, F., Evans, J., Sims, R., Kidd, E., Aggleton, J. P., & Metzler-Baddeley, C. (2020) · Scientific Reports · doi:10.1038/s41598-020-75992-9 · Cited by 15
Metadata
- Authors
- Chételat, G., Villemagne, V. L., Pike, K. E., Baron, J.-C., Bourgeat, P., Jones, G., Faux, N. G., Ellis, K. A., Salvado, O., Szoeke, C., Martins, R. N., Ames, D., Masters, C. L., & Rowe, C. C.
- Affiliations
- Inserm (FR)
- Mental Health Research Institute (AU)
- University of Cambridge (GB)
- Commonwealth Scientific and Industrial Research Organisation (AU)
- Austin Health (AU)
- The University of Melbourne (AU)
- Edith Cowan University (AU)
- National Ageing Research Institute (AU)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-08-25
- Volume
- 133
- Issue
- 11
- Pages
- 3349-3358
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2075668621
- Cited by
- 159
- References
- 41
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 8 · 2023: 6 · 2022: 5 · 2021: 10 · 2020: 10 · 2019: 11 · 2018: 13 · 2017: 13 · 2016: 8 · 2015: 8 · 2014: 15 · 2013: 17 · 2012: 8
- FWCI
- 8.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Commonwealth Scientific and Industrial Research Organisation
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- amyloid-beta deposition, Alzheimer's disease, hippocampal volume, brain reserve, gray matter atrophy, mild cognitive impairment, subjective cognitive impairment, episodic memory, 11C-Pittsburgh compound B, amyloid PET
- MeSH terms
- Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoproteins E, Female, Heterozygote, Humans, Male, Organ Size, Temporal Lobe, Cohort Studies, Amyloid beta-Peptides
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