Premium
[IC‐P‐055]: EFFECT OF APOE‐ε2 ON REGIONAL GRAY MATTER ATROPHY AND CLINICAL PHENOTYPE IN ALZHEIMER's DISEASE
Author(s) -
Groot Colin,
Weijden Chris W.J.,
Flier Wiesje M.,
Loenhoud Anita C.,
Berckel Bart N.M.,
Barkhof Frederik,
Koene Teddy,
Teunissen Charlotte E.,
Scheltens Philip,
Ossenkoppele Rik
Publication year - 2017
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.2017.06.2328
Subject(s) - atrophy , dementia , apolipoprotein e , neuropsychology , pittsburgh compound b , medicine , psychology , alzheimer's disease , oncology , cognition , disease , pathology , audiology , psychiatry
average EYO of -4.2. While this three-stage pattern was common across regions of the brain, it was not ubiquitous (Figure 1). Most prominently a subset of regions demonstrated elevated PiB PET accumulation and structural declines, but not abnormal glucose utilization. Further, the regional timing within a modality (e.g. PiB PET) was highly variable across brain regions (Figure 2). Conclusions:Our study presents both the longitudinal temporal trajectories of and spatial patterns of Alzheimer pathology in ADAD cohorts. Our results are consistent with prior theoretical models and crosssectional work suggesting that initial increases in amyloid accumulation are followed by hypometabolism, and finally by structural atrophy. We demonstrated that there is not one temporal relationship, but that the emergence of pathology varies across the brain.