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Altered deactivation in individuals with genetic risk for Alzheimer's disease
Abstract
Regions that show task-induced deactivations may be part of a default-mode network related to processes that are more engaged during passive than active task conditions. Alteration of task-induced deactivations with age and dementia is indicated by atypical engagement of default-mode network regions. Genetic studies show a relation between the apolipoprotein E4 (APOE4) allele and the common form of Alzheimer's disease (AD), and altered functional brain activation has been observed in non-demented APOE4 carriers compared to non-carriers. Here we investigate the hypothesis of altered default-mode network brain responses in individuals with genetic risk for AD. Functional MRI was used to assess task-induced deactivation in 60 subjects of which 30 carried at least one copy of the APOE4 allele, and 30 non-carriers. Subjects were scanned while performing a semantic categorization task shown to promote episodic memory encoding. The results show patterns of deactivation consistent with the default-mode network. We also found reduced deactivation in non-demented APOE4 carriers compared to non-carriers, suggesting alterations in the default-mode network in the absence of dementia. These results implicate possibilities for investigating altered properties of task-induced deactivations in individuals with genetic risk for AD, and may prove useful for pre-clinical identification of individuals susceptible to memory problems and AD.
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Cognitively normal apoE4 carriers show reduced task-induced deactivation of the default mode network (DMN).
“First, cognitively normal apoE4 carriers show reduced task-induced deactivation of the default mode network (DMN) [162–164].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [162]
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“Individuals at genetic risk for Alzheimer’s disease (14) and schizophrenia (15) have abnormal default-mode connectivity.”
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“Indeed, deactivation deficits are already present in cognitively normal APOE ε4 carriers (Persson et al. 2008, Pihlajamäki et al. 2010) as well as in subjects with Aβ plaques but without cognitive impairment (Sperling et al. 2009).”
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“…carriers in regions such as the medial prefrontal cortex, the hippocampus, and the posterior cingulate (Reiman et al., 1996; Small et al., 2000; Persson et al., 2008; Pihlajamaki and Sperling, 2009; Adamson et al., 2011), but enhanced activities were also found in these regions (Bookheimer et…”
BackgroundSemantic memory activation in amnestic mild cognitive impairment
Woodard, J. L., Seidenberg, M., Nielson, K. A., Antuono, P., Guidotti, L. M., Durgerian, S., Zhang, Q., Lancaster, M. A., Hantke, N. C., Butts, A. M., et al. (2009) · Brain · doi:10.1093/brain/awp157 · Cited by 124
“In addition, carriers of the ApoE e4 allele show diminished task-induced deactivation relative to non-carriers in brain regions associated with the default network during a semantic categorization task (Persson et al., 2008).”
Interaction of Age and APOE Genotype on Cerebral Blood Flow at Rest
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“Furthermore, high FADE was associated with a failure to deactivate a set of regions, including medial and lateral parietal cortices, often referred to as components of the ‘‘default mode network’’ (Raichle et al., 2001; Andrews-Hanna et al., 2007; Persson et al., 2008; Grady et al., 2010).”
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“2009) as well as old (Persson et al. 2008) APOE4 carriers revealed changes in the default network.”
BackgroundLongitudinal assessment of default-mode brain function in aging
Persson, J., Pudas, S., Nilsson, L., & Nyberg, L. H. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.03.012 · Cited by 114
“This finding nicely replicates previous demonstrations of reduced deactivation in asymptomatic APOE4-carriers compared with noncarriers (Persson et al., 2008; Pihlajamäki et al., 2010).”
ResultSelf-citationThe effects of APOE-ε4 on the BOLD response
Trachtenberg, A. J., Filippini, N., & Mackay, C. E. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.03.009 · Cited by 97
Hyperactivity Induced by Soluble Amyloid-β Oligomers in the Early Stages of Alzheimer's Disease
Hector, A., & Brouillette, J. (2021) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.600084 · Cited by 97
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“the DMN in elderly subjects carrying a genetic risk for AD [67, 68].”
BackgroundAge and amyloid-related alterations in default network habituation to stimulus repetition
Vannini, P., Hedden, T., Becker, J. A., Sullivan, C., Putcha, D., Rentz, D. M., Johnson, K. A., & Sperling, R. A. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.01.003 · Cited by 86
“…encoding (Miller et al., 2008; Duverne et al., 2009), during memory tasks in AD patients (Lustig et al., 2003) and individuals with risk factors for AD (Celone et al., 2006; Petrella et al., 2007; Persson et al., 2008; Pihlajamäki et al., 2008; Fleisher et al., 2009; Pihlajamäki et al., 2009).”
BackgroundImpact of changed positive and negative task-related brain activity on word-retrieval in aging
Meinzer, M., Seeds, L., Flaisch, T., Harnish, S. M., Cohen, M. L., McGregor, K., Conway, T. W., Benjamin, M., & Crosson, B. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.06.020 · Cited by 82
“In line with task difficulty accounting for some of our findings, left inferior frontal areas have been implicated with the controlled selection and retrieval of items from memory stores across a variety of tasks in younger adults, and increased task demands result in more pronounced activity (Persson et al., 2008; Th…”
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Evidence of Altered Posteromedial Cortical fMRI Activity in Subjects at Risk for Alzheimer Disease
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Differential effects of the ApoE4 genotype on brain structure and function
Matura, S., Prvulovic, D., Jurcoane, A., Hartmann, D., Miller, J., Scheibe, M., O’Dwyer, L., Oertel‐Knöchel, V., Knöchel, C., Reinke, B., et al. (2013) · NeuroImage · doi:10.1016/j.neuroimage.2013.11.042 · Cited by 63
“Consistent with our findings, Persson et al. (2008) have also showndecreased task-induced deactivations in ε4 carriers during incidental encoding.”
ResultTask-Induced Brain Activity Patterns in Type 2 Diabetes: A Potential Biomarker for Cognitive Decline
Marder, T. J., Flores, V. L., Bolo, N. R., Hoogenboom, W. S., Simonson, D. C., Jacobson, A. M., Foote, S., Shenton, M. E., Sperling, R. A., & Musen, G. (2014) · Diabetes · doi:10.2337/db13-1783 · Cited by 60
“Differences between our finding and those of others who have observed effects of APOE4 in the medial temporal lobe (23) may stem from particulars about the memory task and ages of the participants.”
Hayes, J. M., Tang, L., Viviano, R. P., van Rooden, S., Ofen, N., & Damoiseaux, J. S. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.08.015 · Cited by 54
“Nevertheless, our fi ndings are consistent with previous studies showing functional changes in DMN regions among individuals at risk for development of AD.”
BackgroundMethodInfluentialThe Influence of Rest Period Instructions on the Default Mode Network
Benjamin, C. F. A., Lieberman, D. A., Chang, M., Ofen, N., Whitfield-Gabrieli, S., Gabrieli, J. D. E., & Gaab, N. (2010) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2010.00218 · Cited by 51
McDonough, I. M., Festini, S. B., & Wood, M. M. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101133 · Cited by 52
Gordon, B. A., Zacks, J. M., Blazey, T., Benzinger, T. L. S., Morris, J. C., Fagan, A. M., Holtzman, D. M., & Balota, D. A. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.01.019 · Cited by 49
Heritability of the Effective Connectivity in the Resting-State Default Mode Network
Xu, J., Yin, X., Ge, H., Han, Y., Pang, Z., Liu, B., Liu, S., & Friston, K. J. (2016) · Cerebral Cortex · doi:10.1093/cercor/bhw332 · Cited by 43
“, 2010) , and subjects with psychiatric disorders, such as Alzheimer’s disease (Persson et al., 2008), schizophrenia (Whitfield-Gabrieli et al.”
BackgroundHansen, N. L., Lauritzen, M., Mortensen, E. L., Osler, M., Avlund, K., Fagerlund, B., & Rostrup, E. (2014) · Human Brain Mapping · doi:10.1002/hbm.22489 · Cited by 48
“Across a wide range of tasks, TID has been consistently demonstrated in brain regions corresponding to the DMN [Lustig et al., 2003; Persson et al., 2008; Rombouts et al., 2005; Shulman et al., 1997].”
BackgroundAge-related changes in neural functional connectivity and its behavioral relevance
Schlee, W., Leirer, V. M., Kolassa, I., Weisz, N., & Elbert, T. R. (2012) · BMC Neuroscience · doi:10.1186/1471-2202-13-16 · Cited by 45
“people with Alzheimer’s disease [3,4] or corresponding genetic risk [36], mild cognitive impairment [5,37], and normal aging [3,17,38].”
BackgroundTok, S., Ahnaou, A., & Drinkenburg, W. H. I. M. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210397 · Cited by 45
“tion might reflect underlying hyperexcitability in the 417 earlier stages of the disease [72, 105].”
BackgroundHsu, C. L., Voss, M. W., Handy, T. C., Davis, J. C., Nagamatsu, L. S., Chan, A., Bolandzadeh, N., & Liu-Ambrose, T. Y. L. (2014) · PLoS ONE · doi:10.1371/journal.pone.0093673 · Cited by 47
“Changes within the DMN have been observed in healthy aging [22,94,95], Alzheimer’s disease [34,95,96], individuals with amnestic mild cognitive impairment [97], and in APOE-e4 carriers [98,99].”
BackgroundBeason‐Held, L. L. (2011) · Current Alzheimer Research · doi:10.2174/156720511795745294 · Cited by 43
Le réseau cérébral par défaut : rôle cognitif et perturbations dans la pathologie
Mevel, K., Grassiot, B., Chételat, G., Defer, G. L., Desgranges, B., & Eustache, F. (2010) · Revue Neurologique · doi:10.1016/j.neurol.2010.01.008 · Cited by 47
Sugarman, M. A., Woodard, J. L., Nielson, K. A., Seidenberg, M., Smith, J. C., Durgerian, S., & Rao, S. M. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.09.016 · Cited by 41
“However, a follow-up report from the same dataset [119] indicated that APOE ε4 carriers had reduced deactivation from baseline due to abnormalities in the default mode (or “resting state”) network.”
Peña-Gómez, C., Solé‐Padullés, C., Clemente, I. C., Junqué, C., Bargalló, N., Bosch, B., Molinuevo, J. L., Valls‐Solé, J., Pascual‐Leone, Á., & Bartrés‐Faz, D. (2012) · PLoS ONE · doi:10.1371/journal.pone.0051833 · Cited by 39
“DMN alterations among APOE e4-bearers have been reported previously, both in resting-state and as attenuated deactivation areas [18,28,54,58,61,62].”
BackgroundSalami, A., Adolfsson, R., Andersson, M., Blennow, K., Lundquist, A., Adolfsson, A. N., Schöll, M., Zetterberg, H., & Nyberg, L. H. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210673 · Cited by 39
“The finding that a longitudinal increase in p-tau levels translated into a reduced hippocampus activity during memory encoding is noteworthy, as several previous cross-sectional studies reported that APOE 4 [13, 39, 40] and higher tau levels [11, 12, 41, 42] are related to higher hippocampal activity and connectivity.”
ResultSelf-citationAdamson, M. M., Hutchinson, J. B., Shelton, A. L., Wagner, A. D., & Taylor, J. L. (2011) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2011.04.022 · Cited by 34
“The DMN is altered in cognitively normal older APOE !4 carriers similar to MCI and AD patients (Filippini et al., 2009; Fleisher et al., 2009; Persson et al., 2008; Pihlajamaki & Sperling, 2009; Pihlajamaki et al., 2010; Rombouts, Barkhof, Goekoop, Stam, & Scheltens, 2005).”
InfluentialChang, L., Ryan, M. C., Liang, H., Zhang, X., Cunningham, E. P., Wang, J. L., Wilson, E. M. P., Herskovits, E. H., Kottilil, S., & Ernst, T. (2023) · Neurology · doi:10.1212/wnl.0000000000207309 · Cited by 32
Tanninen, S. E., Nouriziabari, B., Morrissey, M. D., Bakir, R., Dayton, R. D., Klein, R. L., & Takehara‐Nishiuchi, K. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2017.06.024 · Cited by 32
Failing Compensatory Mechanisms During Working Memory in Older Apolipoprotein E-ε4 Healthy Adults
Filbey, F. M., Chen, G., Sunderland, T., & Cohen, R. M. (2010) · Brain Imaging and Behavior · doi:10.1007/s11682-010-9097-9 · Cited by 34
“Hypofunction in the precuneus/posterior cingulate area, an area that is part of the default network, has also been found with respect to decreases in task-induced deactivations in subjects at risk for Alzheimer’s disease (Pihlajamaki and Sperling 2009; Persson et al. 2008).”
Olfactory ERPs in an odor/visual congruency task differentiate ApoE ε4 carriers from non-carriers
Kowalewski, J., & Murphy, C. (2011) · Brain Research · doi:10.1016/j.brainres.2011.12.030 · Cited by 30
“…well as thinning in areas that developAlzheimer's pathology (Espeseth et al., 2008), particularly entorhinal cortex and subiculum (Burggren et al., 2008) as well as a reduction in fractional anisotropy within the corpus callosum and parahippocampus (Nierenberg et al., 2005; Persson et al., 2008).”
BackgroundADNI, Luo, X., Qiu, T., Jia, Y., Huang, P., Xu, X., Yu, X., Shen, Z., Jiaerken, Y., Guan, X., et al. (2016) · Brain Imaging and Behavior · doi:10.1007/s11682-016-9600-z · Cited by 30
“Meanwhile, our results are consistent with most rsfMRI studies documenting the association between the ε4 allele and decreased functional connectivity or task-related reduced deactivation in MTL regions (Luo et al. 2016; Machulda et al. 2011; Persson et al. 2008; Sheline et al. 2010).”
ResultShine, J. P., Hodgetts, C. J., Postans, M., Lawrence, A. D., & Graham, K. S. (2015) · Scientific Reports · doi:10.1038/srep16322 · Cited by 30
“1038/srep16322 respectively), with greater activity associated with scenes relative to objects and faces; APOE-ε 4 carriers (scenes > faces, t(12) = 8.”
BackgroundInfluentialOurry, V., Binette, A. P., St‐Onge, F., Strikwerda‐Brown, C., Chagnot, A., Poirier, J., Breitner, J. C. S., Arenaza‐Urquijo, E. M., Rabin, J. S., Buckley, R. F., et al. (2023) · Biological Psychiatry · doi:10.1016/j.biopsych.2023.09.003 · Cited by 28
„Default-mode“-Netzwerk des Gehirns
Otti, A., Gündel, H., Wohlschläger, A., Zimmer, C., Sorg, C., & Noll‐Hussong, M. (2011) · Der Nervenarzt · doi:10.1007/s00115-011-3307-6 · Cited by 30
Brain network changes and memory decline in aging
Beason‐Held, L. L., Hohman, T. J., Venkatraman, V. K., An, Y., & Resnick, S. M. (2016) · Brain Imaging and Behavior · doi:10.1007/s11682-016-9560-3 · Cited by 26
“It has also been shown that greater deactivation is associated with better task accuracy (Pihlajamaki & Sperling, 2009), and that the degree of deactivation is less in older individuals who show subsequent cognitive decline (Persson et al., 2008).”
Hojjati, S. H., Feiz, F., Ozoria, S., Razlighi, Q. R., & Initiative, F. T. A. D. N. (2021) · Journal of Alzheimer s Disease · doi:10.3233/jad-210419 · Cited by 22
Targeting Neural Oscillations for Cognitive Enhancement in Alzheimer’s Disease
Palacino, F., Manganotti, P., & Benussi, A. (2025) · Medicina · doi:10.3390/medicina61030547 · Cited by 23
“While hippocampal hypoactivation during memory encoding and persisting DMN deactivation have been observed in the later stages of AD [101,105], the early pattern of hyperactivation may represent a compensatory mechanism in response to emerging cognitive decline, whereas later hypoactivation likely…”
Haase, L., Wang, M., Green, E., & Murphy, C. (2011) · Human Brain Mapping · doi:10.1002/hbm.21451 · Cited by 22
“Recently, BeasonHeld et al. [2009] have shown that the default mode network is relatively stable in normal aging, while studies examining disease processes have found a disruption within the network during task performance [Frings et al., 2009; Persson et al., 2008].”
BackgroundResultNeill, D. (2011) · Ageing Research Reviews · doi:10.1016/j.arr.2011.06.004 · Cited by 22
Ashford, J. W., Salehi, A., Furst, A. J., Bayley, P. J., Frisoni, G. B., Jack, C. R., Sabri, O., Adamson, M. M., Coburn, K. L., Olichney, J., et al. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-0073 · Cited by 20
“In addition, a previous study also reported the pattern of altered task-induced deactivations in ApoE- 4 carriers to be similar with the DMN [134].”
InfluentialFunctional segregation loss over time is moderated by APOE genotype in healthy elderly
Ng, K. K., Qiu, Y., Lo, J. C.-Y., Koay, E. S.-C., Koh, W., Chee, M. W. L., & Zhou, J. H. (2018) · Human Brain Mapping · doi:10.1002/hbm.24036 · Cited by 19
“In parallel, task-based fMRI studies had revealed less deactivation in the DMN in carriers than noncarriers during task performance, implicating a disrupted balance between the DMN and taskpositive networks (Lind et al., 2006; Persson et al., 2008).”
BackgroundInitiative, A. D. N., Luo, X., Li, K., Jia, Y., Zeng, Q., Jiaerken, Y., Qiu, T., Huang, P., Xu, X., Shen, Z., et al. (2018) · Brain Imaging and Behavior · doi:10.1007/s11682-018-9857-5 · Cited by 20
Sala‐Llonch, R., Fortea, J., Bartrés‐Faz, D., Bosch, B., Lladó, A., Peña-Gómez, C., Antonell, A., Castellanos-Pinedo, F., Bargalló, N., Molinuevo, J. L., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130062 · Cited by 21
“Furthermore, studies with cognitively-preserved populations at risk for AD have shown abnormal connectivity in elderly subjects with evidence of amyloid deposition [18–21], as well as in in apolipoprotein (APOE) 4 carriers [22–26].”
BackgroundSpread of activation and deactivation in the brain: does age matter?
Gordon, B. A., Tse, C., Gratton, G., & Fabiani, M. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00288 · Cited by 21
“Reduced levels of deactivation are associated with Alzheimer’s disease (Petrella et al., 2007; Persson et al., 2008; Sperling et al., 2009) further supporting the idea that the task-negative network may be selectively linked to cognitive health.”
BackgroundChoudhury, N., Chen, L., Al‐Harthi, L., & Hu, X. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1194869 · Cited by 15
“In the carriers of late onset/ sporadic AD gene mutation, such as apolipoprotein E (APOE4), dysfunction of neurons in the PFC/HIPP also occurs before fibrillar Aβ deposition and the clinical symptoms of AD (Persson et al., 2008; Sheline et al., 2010).”
BackgroundLuo, X., Qiu, T.-T., Xu, X.-J., Huang, P.-Y., Gu, Q., Shen, Z.-J., Yu, X., Jia, Y.-L., Guan, X.-J., Song, R.-R., et al. (2016) · Journal of Alzheimer's Disease · doi:10.3233/jad-150989 · Cited by 15
“In addition, during memory-encoding tasks, in most functional magnetic resonance imaging (fMRI) studies, the APOE 4 allele was related to a reduction of task-induced deactivations in the default mode network (DMN [17]) [18–20].”
Threlkeld, Z. D., Jicha, G. A., Smith, C. D., & Gold, B. T. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-110206 · Cited by 13
“This issue is of particular importance in light of findings that task deactivation reductions have been reported in cognitive normal seniors at high genetic risk for AD [9, 43], and reduced medial temporal lobe volumes have been reported in normal seniors several years prior to a diagnosis of aMCI [44].”
Fischer, L., Molloy, E. N., Binette, A. P., Vockert, N., Marquardt, J., Pilar, A. P., Kreissl, M. C., Remz, J., Tremblay‐Mercier, J., Poirier, J., et al. (2025) · Journal of Neuroscience · doi:10.1523/jneurosci.1408-24.2024 · Cited by 12
“Further studies have also found associations of the Apolipoprotein-E4 ( APOE4) genotype (Han et al., 2007; Persson et al., 2008; Pihlajamäki et al., 2010) and heightened activity.”
BackgroundImaging early consolidation of perceptual learning with face stimuli during rest
Vilsten, J. S., & Mundy, M. E. (2014) · Brain and Cognition · doi:10.1016/j.bandc.2013.12.005 · Cited by 10
Diaz, J. R., Martá-Ariza, M., Khodadadi‐Jamayran, A., Heguy, A., Tsirigos, A., Pankiewicz, J. E., Sullivan, P. M., & Sadowski, M. J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.845291 · Cited by 11
“This more balanced regulatory effects of apoE2 and apoE3 on excitatory and inhibitory signaling, appears to be essential for neuroprotection and cognition maintenance (Persson et al., 2008; Andrews-Zwilling et al., 2010, 2012; Tong et al., 2016; Nuriel et al., 2017a).”
BackgroundBejanin, A., Viard, A., Chételat, G., Clarys, D., Bernard, F., Pèlerin, A., Sayette, V. D. L., Eustache, F., & Desgranges, B. (2012) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2012.00107 · Cited by 10
“A similar disturbance has also been observed in individuals with genetic risk for AD during incidental encoding (Persson et al., 2008).”
Who's driving? The default mode network in healthy elderly individuals at risk of cognitive decline
González‐López, M., Gonzalez-Moreira, E., Gonzalez, A. A., Paz-Linares, D., & Fernández, T. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.1009574 · Cited by 9
“Moreover, the anatomical regions of the DMN overlap with the typical distribution of depositions of βA, a physiopathological feature of AD, and this βA burden is related to the FC of the DMN (3, 33, 34) and here have been reports of reduced DMNdeactivation during tasks in APOE e4 carriers (35, 36).”
BackgroundShimada, H., Kato, T., Ito, K., Makizako, H., Doi, T., Yoshida, D., Shimokata, H., Washimi, Y., Endo, H., & Suzuki, T. (2012) · European Neurology · doi:10.1159/000334845 · Cited by 8
Subcortical Anatomy of the Default Mode Network: a functional and structural connectivity studyPreprint
Alves, P. N., Foulon, C., Karolis, V. R., Bzdok, D., Margulies, D. S., Emmanuelle Volle, C., & de Schotten, M. T. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/528679 · Cited by 8
“…disease is associated with degeneration of the cholinergic system, including the medial septal nuclei, even in the earliest clinical stages of Mild Cognitive Impairment (Grothe et al., 2010) and apparently related to significant changes of the DMN (He et al., 2007; Persson et al., 2008).”
BackgroundHavlík, M. (2017) · Frontiers in Systems Neuroscience · doi:10.3389/fnsys.2017.00007 · Cited by 7
“The hypothesis is that from a genetic perspective people with the risk of Alzheimer’s diseases have a much lower ability to deactivate the DMN (Persson et al., 2008).”
BackgroundSu, M., Xuan, E., Sun, X., Pan, G., Li, D., Zheng, H., Zhang, Y., & Li, Y. (2024) · Journal of Neurochemistry · doi:10.1111/jnc.16066 · Cited by 7
Functional MRI in Alzheimer’s Disease
Kivistö, J., Soininen, H. S., & Pihlajamaki, M. M. (2014) · InTech eBooks · doi:10.5772/58264 · Cited by 9
“The pat‐ tern of fMRI task-induced deactivation seems to be progressively disrupted along the continuum from normal aging to MCI and to clinical AD and more impaired in ε4 carriers than in non-carriers (Persson et al., 2008; Pihlajamäki et al., 2009).”
BackgroundLifespan brain activity, b-amyloid, and Alzheimer's disease
Jagust, W. J., & Mormino, E. C. (2011) · Cited by 6
Using Magnetic Resonance Imaging in the Early Detection of Alzheimer's Disease
Emily, J., Manus, J., & Ally, B. A. (2013) · InTech eBooks · doi:10.5772/54445 · Cited by 5
“Second, animal models do not develop AD naturally, and genetically engineered models designed to mimic AD do not fully reproduce the human phenotypes [1-3].”
BackgroundCostigan, A. G., Umla‐Runge, K., Evans, J., Raybould, R., Graham, K. S., & Lawrence, A. D. (2021) · Neuroimage Reports · doi:10.1016/j.ynirp.2021.100059 · Cited by 2
“…effect size (Cohen’s d > 1) for the difference in PMC deactivation between APOE E4 carriers and non-carriers, we planned our experiment to detect a conventionally large effect (Cohen’s d = 0.8) while safeguarding against effect size inflation in published studies (Perugini et al., 2014, 2018).”
InfluentialOverlapping but distinct default network functions revealed by independent component analysis
Aso, T., & Fukuyama, H. (2012) · ICME International Conference on Complex Medical Engineering (CME) · doi:10.1109/iccme.2012.6275598 · Cited by 1
Functional and Structural MRI in Alzheimer’s Disease: A Multimodal Approach
Grothe, M. J., Bokde, A. L. W., & Teipel, S. J. (2014) · Springer eBooks · doi:10.1007/978-3-642-54542-9_20 · Cited by 1
„Default-mode“-Netzwerk des Gehirns. Neurobiologie und klinische Bedeutung
Otti, A., Gündel, H., Wohlschläger, A., Zimmer, C., Sorg, C., & Noll‐Hussong, M. (2012) · Der Nervenarzt · Cited by 1
Bosch, B. (2010) · LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) · Cited by 1
Imaging of the Geriatric Brain
Apostolova, L. G., Fleisher, A., Drzezga, A. E., Nair, A. K., & Sabbagh, M. N. (2014) · Wiley eBooks · doi:10.1002/9781118730676.ch7
Apport de l’imagerie par résonance magnétique dans la maladie d’Alzheimer
Lehéricy, S., Boutet, C., de Souza, L. C., Marie Chupin, A., Olivier Colliot, A., Sarazin, M., & Dormont, D. (2013) · Springer eBooks · doi:10.1007/978-2-8178-0443-9_3
Marder, T. J., Flores, V. L., Bolo, N. R., Hoogenboom, W. S., Simonson, D. C., Jacobson, A. M., Foote, S., Shenton, M. E., Reisa, A., Musen, G., et al. (2014)
Functional imaging of Alzheimer's disease
Taler, V., & Saykin, A. J. (2010) · Cambridge University Press eBooks · doi:10.1017/cbo9780511782091.025
Neuromagnetic correlates of aging - evidence from resting state and event-related analyses
Leirer, V. M. (2010) · KOPS (University of Konstanz)
Early Recognition of Alzheimer’s Disease using Brain MRI
Birry, R. A. K. A. G. (2017) · International Journal of Health and Medicine · doi:10.24178/ijhm.2017.2.1.06
Tanninen, S. E. (2018) · TSpace (University of Toronto)
APOE as a Risk Factor for Age‐Related Cognitive Impairment
Korthauer, L. E., & Driscoll, I. F. (2020) · The Wiley Encyclopedia of Health Psychology · doi:10.1002/9781119057840.ch35
Current awareness in geriatric psychiatry
(2008) · International Journal of Geriatric Psychiatry · doi:10.1002/gps.1917
D-sérine : un maillon central de la physiopathologie amyloïde ?
Ploux, E. (2022) · theses.fr (ABES) · doi:10.70675/e7b5bba0z9abcz4325zae71z841a60892f8b
Moore, L., Lund, A. E., & Russell, C. (2026) · BMC Neurology · doi:10.1186/s12883-026-04884-8
“This aligns with research suggesting that episodic memory ability is impacted more greatly by AD due to the degeneration in neural networks implicated in this domain [55].”
Metadata
- Authors
- Persson, J., Lind, J., Larsson, A., Ingvar, M., Sleegers, K., Van Broeckhoven, C., Adolfsson, R., Nilsson, L.-G., & Nyberg, L.
- Affiliations
- Stockholm University (SE)
- Karolinska University Hospital (SE)
- Umeå University (SE)
- University of Antwerp (BE)
- Corresponding author
- Persson, J.
- Venue
- Neuropsychologia
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 46
- Issue
- 6
- Pages
- 1679-1687
- ISSN
- 0028-3932 (ISSN-L)
- OpenAlex
- W2140074909
- Cited by
- 102
- References
- 42
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 7 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 4 · 2016: 6 · 2015: 4 · 2014: 10 · 2013: 6 · 2012: 7
- FWCI
- 8.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropsychologia (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Keywords
- Alzheimer's disease, APOE ε4, default mode network, task-induced deactivation, genetic risk, semantic classification, episodic memory encoding, preclinical Alzheimer's disease, functional brain activation
- MeSH terms
- Aged, Alzheimer Disease, Brain, Brain Mapping, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Memory, Middle Aged, Neuropsychological Tests, Oxygen, Semantics, Apolipoprotein E4
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