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13. Preclinical Alzheimer's disease: Definition, natural history, and diagnostic criteria.

Author

Dubois, Bruno, Hampel, Harald, Feldman, Howard H, Scheltens, Philip, Aisen, Paul, Andrieu, Sandrine, Bakardjian, Hovagim, Benali, Habib, Bertram, Lars, Blennow, Kaj, Broich, Karl, Cavedo, Enrica, Crutch, Sebastian, Dartigues, Jean-François, Duyckaerts, Charles, Epelbaum, Stéphane, Frisoni, Giovanni B, Gauthier, Serge, Genthon, Remy, Gouw, Alida A, Habert, Marie-Odile, Holtzman, David M, Kivipelto, Miia, Lista, Simone, Molinuevo, José-Luis, O'Bryant, Sid E, Rabinovici, Gil D, Rowe, Christopher, Salloway, Stephen, Schneider, Lon S, Sperling, Reisa, Teichmann, Marc, Carrillo, Maria C, Cummings, Jeffrey, Jack, Cliff R, Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, and Washington DC, USA

Subjects
Proceedings of the Meeting of the International Working Group (IWG) and the American Alzheimer's Association on “The Preclinical State of AD”, July 23, 2015, Washington DC, USA, Brain, Animals, Humans, Alzheimer Disease, Disease Progression, Alzheimer's disease, Amyloid PET, Asymptomatic, Biomarkers, Blood biomarkers, CSF biomarkers, Diagnostic criteria, Genetics, MRI, Pathophysiology, Preclinical, Tau PET, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Neurodegenerative, Dementia, Alzheimer's Disease, Brain Disorders, Acquired Cognitive Impairment, Human Genome, Neurosciences, Neurological, Clinical Sciences, Geriatrics
Abstract

During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum. Thanks to evolving biomarker research and substantial discoveries, it is now possible to identify the disease even at the preclinical stage before the occurrence of the first clinical symptoms. This preclinical stage of AD has become a major research focus as the field postulates that early intervention may offer the best chance of therapeutic success. To date, very little evidence is established on this "silent" stage of the disease. A clarification is needed about the definitions and lexicon, the limits, the natural history, the markers of progression, and the ethical consequence of detecting the disease at this asymptomatic stage. This article is aimed at addressing all the different issues by providing for each of them an updated review of the literature and evidence, with practical recommendations.

Published
2016

14. In vivo tau pathology is associated with synaptic loss and altered synaptic function

Author

Coomans, Emma M., Schoonhoven, Deborah N., Tuncel, Hayel, Verfaillie, Sander C. J., Wolters, Emma E., Boellaard, Ronald, Ossenkoppele, Rik, den Braber, Anouk, Scheper, Wiep, Schober, Patrick, Sweeney, Steven P., Ryan, J. Michael, Schuit, Robert C., Windhorst, Albert D., Barkhof, Frederik, Scheltens, Philip, Golla, Sandeep S. V., Hillebrand, Arjan, Gouw, Alida A., and van Berckel, Bart N. M.

Published
2021
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19. Hub vulnerability and short path length to entorhinal cortex are associated with tau binding in Alzheimer’s disease: a combined MEG/PET study

Author

Schoonhoven, Deborah N, primary, Millan, Ana P, additional, Coomans, Emma M., additional, Yaqub, Maqsood, additional, van Nifterick, Anne M, additional, Visser, Denise, additional, Ossenkoppele, Rik, additional, Tuncel, Hayel, additional, van der Flier, Wiesje M., additional, de Haan, Willem, additional, Scheltens, Philip, additional, Stam, Cornelis J, additional, van de Giessen, Elsmarieke, additional, Hillebrand, Arjan, additional, and Gouw, Alida A, additional

Published
2023
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29. Tau protein spreads through functionally connected neurons in Alzheimer’s disease: a combined MEG/PET study

Author

Schoonhoven, Deborah N, primary, Coomans, Emma M, additional, Millán, Ana P, additional, van Nifterick, Anne M, additional, Visser, Denise, additional, Ossenkoppele, Rik, additional, Tuncel, Hayel, additional, van der Flier, Wiesje M, additional, Golla, Sandeep S V, additional, Scheltens, Philip, additional, Hillebrand, Arjan, additional, van Berckel, Bart N M, additional, Stam, Cornelis J, additional, and Gouw, Alida A, additional

Published
2023
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34. Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes

Author

van Heusden, Fran C, van Nifterick, Anne M, Souza, Bryan C, França, Arthur S C, Nauta, Ilse M, Stam, Cornelis J, Scheltens, Philip, Smit, August B, Gouw, Alida A, van Kesteren, Ronald E, van Heusden, Fran C, van Nifterick, Anne M, Souza, Bryan C, França, Arthur S C, Nauta, Ilse M, Stam, Cornelis J, Scheltens, Philip, Smit, August B, Gouw, Alida A, and van Kesteren, Ronald E

Abstract

BACKGROUND: Studies in animal models of Alzheimer's disease (AD) have provided valuable insights into the molecular and cellular processes underlying neuronal network dysfunction. Whether and how AD-related neurophysiological alterations translate between mice and humans remains however uncertain.METHODS: We characterized neurophysiological alterations in mice and humans carrying AD mutations in the APP and/or PSEN1 genes, focusing on early pre-symptomatic changes. Longitudinal local field potential recordings were performed in APP/PS1 mice and cross-sectional magnetoencephalography recordings in human APP and/or PSEN1 mutation carriers. All recordings were acquired in the left frontal cortex, parietal cortex, and hippocampus. Spectral power and functional connectivity were analyzed and compared with wildtype control mice and healthy age-matched human subjects.RESULTS: APP/PS1 mice showed increased absolute power, especially at higher frequencies (beta and gamma) and predominantly between 3 and 6 moa. Relative power showed an overall shift from lower to higher frequencies over almost the entire recording period and across all three brain regions. Human mutation carriers, on the other hand, did not show changes in power except for an increase in relative theta power in the hippocampus. Mouse parietal cortex and hippocampal power spectra showed a characteristic peak at around 8 Hz which was not significantly altered in transgenic mice. Human power spectra showed a characteristic peak at around 9 Hz, the frequency of which was significantly reduced in mutation carriers. Significant alterations in functional connectivity were detected in theta, alpha, beta, and gamma frequency bands, but the exact frequency range and direction of change differed for APP/PS1 mice and human mutation carriers.CONCLUSIONS: Both mice and humans carrying APP and/or PSEN1 mutations show abnormal neurophysiological activity, but several measures do not translate one-to-o

Published
2023

35. Tau protein spreads through functionally connected neurons in Alzheimer’s disease: a combined MEG/PET study

Author

Schoonhoven, Deborah N, Coomans, Emma M, Millán, Ana P, van Nifterick, Anne M, Visser, Denise, Ossenkoppele, Rik, Tuncel, Hayel, van der Flier, Wiesje M, Golla, Sandeep S V, Scheltens, Philip, Hillebrand, Arjan, van Berckel, Bart N M, Stam, Cornelis J, Gouw, Alida A, Neurology, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, Amsterdam Neuroscience - Brain Imaging, and Amsterdam Neuroscience - Systems & Network Neuroscience

Abstract

Background: Recent studies on Alzheimer’s disease (AD) suggest that tau proteins spread through the brain following neuronal connections. Several mechanisms could be involved in this process: spreading between brain regions that interact strongly (functional connectivity); through the pattern of anatomical connections (structural connectivity); or simple diffusion. Using magnetoencephalography (MEG), we investigated which spreading pathways influence tau protein spreading by modelling the tau propagation process using an epidemic spreading model. We compared the modelled tau depositions with [18F]flortaucipir PET binding potentials at several stages of the AD continuum. Methods: In this cross-sectional study, we analysed source-reconstructed MEG data and dynamic 100-minutes [18F]flortaucipir PET from 57 subjects positive for amyloid-beta (Aβ)-pathology (preclinical AD (n=16), mild cognitive impairment (MCI) due to AD (n=16) and AD dementia (n=25)). Cognitively healthy subjects without Aβ-pathology were included as controls (n=25). Tau propagation was modelled as an epidemic process (susceptible-infected model) on MEG-based functional networks (in alpha (8-13Hz) and beta (13-30Hz) bands), a structural, or diffusion network, starting from the middle and inferior temporal lobe. The group-level network of the control group was used as input for the model to predict tau deposition in 3 stages of the AD continuum. To assess performance, model output was compared to the group-specific tau deposition patterns as measured with [18F]flortaucipir PET. We repeated the analysis by using networks of the preceding disease stage and/or using regions with most observed tau deposition during the preceding stage as seeds. Results: In the preclinical AD stage, the functional networks predicted most of the modelled tau-PET binding potential, with best correlations between model and tau-PET (AEC-c alpha C=0.584; AEC-c beta C=0.569), followed by the structural network (C=0.451) and simple diffusion (C=0.451). Prediction accuracy declined for the MCI and AD dementia stages, although the correlation between modelled tau and tau-PET binding remained highest for the functional networks (C=0.384; C=0.376). Replacing the control-network with the network from the preceding disease stage and/or alternative seeds improved prediction accuracy in MCI but not in the dementia stage. Conclusion: These results suggest that in addition to structural connections, functional connections play an important role in tau spread, and highlight that neuronal dynamics play a key role in promoting this pathological process. Aberrant neuronal communication patterns should be taken into account when identifying targets for future therapy. Our results also suggest that this process is more important in earlier disease stages (preclinical AD/MCI); possibly, in later stages, other processes may be influential.

Published
2022
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37. Tau protein spreads through functionally connected neurons in Alzheimer’s disease

Author

Schoonhoven, Deborah N, primary, Coomans, Emma M, additional, Millan, Ana P, additional, van Nifterick, Anne M, additional, Visser, Denise, additional, Ossenkoppele, Rik, additional, Tuncel, Hayel, additional, van der Flier, Wiesje M., additional, Golla, Sandeep SV, additional, Scheltens, Philip, additional, Hillebrand, Arjan, additional, van Berckel, Bart NM, additional, Stam, Cornelis J, additional, and Gouw, Alida A, additional

Published
2022
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41. Additional file 1 of A multiscale brain network model links Alzheimer’s disease-mediated neuronal hyperactivity to large-scale oscillatory slowing

Author

van Nifterick, Anne M., Gouw, Alida A., van Kesteren, Ronald E., Scheltens, Philip, Stam, Cornelis J., and de Haan, Willem

Abstract

Additional file 1: The neural mass model. Single neural mass analyses. Parameter range. Table S1. Single neural mass model. Fig. S1. Example traces of simulated MEG signals in control condition and several AD-like (and their contrast) scenarios. Fig. S2. The excitatory and inhibitory post-synaptic potentials (EPSP and IPSP). Fig. S3. Neuronal activity and total power in AD-like and contrast scenarios in a single, uncoupled, neural mass model. Fig. S4. Simulated power spectra for AD-like and contrast scenarios in a single, not-coupled, neural mass model. Fig. S5. Robust changes in outcome measures over a range of values for each relevant model parameter.

Published
2022
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42. EEG slowing in predementia Alzheimer's disease is compatible with neuronal hyperactivity: A multiscale computational modeling study

Author

van Nifterick, Anne M., Gouw, Alida A., de Haan, Willem, Stam, Cornelis J., Scheltens, Philip, Neurology, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Systems & Network Neuroscience, and Amsterdam Neuroscience - Brain Imaging

Abstract

BACKGROUND: Evidence from animal models of Alzheimer's disease (AD) for neuronal hyperactivity and inhibitory dysfunction is accumulating, but the exact mechanism by which these microscale abnormalities lead to large-scale brain dysfunction and cognitive impairment in AD remains unclear. This study investigated empirically informed pathophysiological mechanisms of neuronal hyperactivity in a computational neurophysiological brain model and compared its output to EEG data of predementia AD patients. METHOD: EEG-like oscillations were simulated by a computational brain network model of 78 neural masses, each representing regional activity of a large population of interconnected excitatory and inhibitory neurons, coupled according to human DTI-derived structural topology. Several scenarios of amyloid-β mediated neuronal hyperactivity were investigated, including excitatory hyperexcitability and inhibitory neuronal dysfunction. The model offered a direct readout of neuronal activity by showing excitatory neuron pulse density. Consequently, we performed spectral analysis and analyzed absolute power and relative power in relevant frequency bands and peak frequency on the model output of each simulated AD scenario as well as for resting state EEG of predementia AD patients with positive amyloid biomarkers (n = 196) and elderly controls (n = 180). Similarity in outcome measure changes between the modelled output of each scenario and human EEG resulted in a scenario compatibility score (range 0-6). RESULT: Predementia AD patients showed increased relative theta power and decreased relative higher alpha power. The modeled scenarios involving 'inhibitory neuron hypoexcitability' and 'excessive neuronal excitation' were most compatible with the observed EEG changes in AD (score of 5), providing support for their presumed role. Other scenarios produced improbable physiologically parameter change combinations. Of the two best compatible scenarios, inhibitory hypoexcitability was the only scenario that led to neuronal hyperactivity in the model. CONCLUSION: We found that neuronal hyperactivity scenarios (i.e. increased pulse density) is compatible with large-scale oscillatory slowing of predementia AD patients. This study provides support for amyloid-driven neuronal disinhibition due to inhibitory hypoexcitability as most likely pathophysiological mechanism to explain oscillatory slowing in predementia AD.

Published
2021
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44. Tau pathology is associated with synaptic loss and altered synaptic function: a combined [F-18]flortaucipir, [C-11]UCB-J and magnetoencephalography study

Author

Coomans, Emma M., Schoonhoven, Deborah, Tuncel, Hayel, Verfaillie, Sander C. J., Wolters, Emma E., Boellaard, Ronald, Ossenkoppele, Rik, Scheper, Wiep, Schober, Patrick, Sweeney, Steven P., Ryan, Michael J., Schuit, Robert C., Windhorst, Albert D., Barkhof, Frederik, Scheltens, Philip, Golla, Sandeep S. V., Hillebrand, Arjan, Gouw, Alida, van Berckel, Bart N. M., Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Neurology, Amsterdam Neuroscience - Brain Imaging, IOO, Human genetics, Amsterdam Neuroscience - Cellular & Molecular Mechanisms, Anesthesiology, ACS - Microcirculation, APH - Methodology, APH - Quality of Care, Amsterdam Neuroscience - Neuroinfection & -inflammation, and Amsterdam Neuroscience - Systems & Network Neuroscience

Published
2021

45. Cerebral white matter changes are associated with abnormalities on neurological examination in non-disabled elderly: the LADIS study

Author

Poggesi, Anna, Gouw, Alida, van der Flier, Wiesje, Pracucci, Giovanni, Chabriat, Hugues, Erkinjuntti, Timo, Fazekas, Franz, Ferro, José M., Hennerici, Michael, Langhorne, Peter, O’Brien, John T., Visser, Marieke C., Wahlund, Lars-Olof, Waldemar, Gunhild, Wallin, Anders, Scheltens, Philip, Inzitari, Domenico, and Pantoni, Leonardo

Published
2013
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50. White Matter Lesion Progression in LADIS: Frequency, Clinical Effects, and Sample Size Calculations

Author

Schmidt, Reinhold, Berghold, Andrea, Jokinen, Hanna, Gouw, Alida A., van der Flier, Wiesje M., Barkhof, Frederik, Scheltens, Philip, Petrovic, Katja, Madureira, Sofia, Verdelho, Ana, Ferro, Jose M., Waldemar, Gunhild, Wallin, Anders, Wahlund, Lars-Olof, Poggesi, Anna, Pantoni, Leonardo, Inzitari, Domenico, Fazekas, Franz, and Erkinjuntti, Timo

Published
2012
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