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P3‐437: LONGITUDINAL CORTICAL THICKNESS IN SPORADIC YOUNG ONSET ALZHEIMER'S DISEASE
Author(s) -
Keuss Sarah E.,
Slattery Catherine F.,
Parker Thomas D.,
Nicholas Jennifer M.,
Paterson Ross W.,
Foulkes Alexander J.M.,
Malone Ian B.,
Thomas David L.,
Modat Marc,
Cash David M.,
Crutch Sebastian J.,
Yong Keir,
Ourselin Sebastien,
Fox Nick C.,
Schott Jonathan M.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1800
Subject(s) - precuneus , parahippocampal gyrus , middle frontal gyrus , superior frontal gyrus , atrophy , gyrus , early onset alzheimer's disease , cardiology , medicine , posterior cingulate , audiology , nuclear medicine , psychology , alzheimer's disease , temporal lobe , disease , neuroscience , cortex (anatomy) , radiology , magnetic resonance imaging , cognition , epilepsy
MRI from 1713 ADNI subjects; 11593 T1-MRI from 5389 Rotterdam-Study-Scan (Ikram et al, 2015) aging subjects; 244 T1-MRI from 64 PPMS subjects of the Institute of Neurology-UCL; we analyzed 24 T1-MRI and DTI of HCP subjects to estimate an average structural connectome. Results: The mechanistic profile identified by our model (Fig 2) agrees with current results that identify transneuronal spread from and to hubs as the principal mechanism underlying neurodegeneration in AD (Cope et al, 2018). Interestingly, the model points out that we can’t neglect the component of neurodegeneration due to nodal stress – vulnerability of hubs due to increased metabolic demand. The proximity mechanism identified in HA suggests a more uniform brain-loss, while the presence of an un-explained term indicates that the hypothetical mechanisms utilized are not sufficient to fully explain the aging process. In PPMS the profile is a combination of apparently discordant (nodal stress and trophic failure) mechanisms: it is possible that the focal inflammatory component of MS, although not strong in our progressive cohort, plays a role in complicating the patterns of neurodegeneration. Conclusions:Our results suggest that neurodegeneration in AD and PPMS is not simply an acceleration of the aging process: the two diseases have distinct spreading mechanisms underlying neurodegeneration.