Open AccessAmyloid‐ β , cortical thickness, and subsequent cognitive decline in cognitively normal oldest‐old
Author(s) -
Pelkmans Wiesje,
Legdeur Nienke,
Kate Mara,
Barkhof Frederik,
Yaqub Maqsood M.,
Holstege Henne,
Berckel Bart N. M.,
Scheltens Philip,
Flier Wiesje M.,
Visser Pieter Jelle,
Tijms Betty M.
Publication year - 2021
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.51273
Subject(s) - cognitive decline , atrophy , cognition , medicine , dementia , abnormality , temporal lobe , effects of sleep deprivation on cognitive performance , audiology , neuroscience , psychology , pathology , disease , psychiatry , epilepsy
Objective To investigate the relationship between amyloid‐ β (A β ) deposition and markers of brain structure on cognitive decline in oldest‐old individuals with initial normal cognition. Methods We studied cognitive functioning in four domains at baseline and change over time in fifty‐seven cognitively intact individuals from the EMIF‐AD 90+ study. Predictors were A β status determined by [ 18 F]‐flutemetamol PET (normal = A β − vs. abnormal = A β +), cortical thickness in 34 regions and hippocampal volume. Mediation analyses were performed to test whether effects of A β on cognitive decline were mediated by atrophy of specific anatomical brain areas. Results Subjects had a mean age of 92.7 ± 2.9 years, of whom 19 (33%) were A β +. Compared to A β −, A β + individuals showed steeper decline on memory ( β ± SE = −0.26 ± 0.09), and processing speed ( β ± SE = −0.18 ± 0.08) performance over 1.5 years ( P < 0.05). Furthermore, medial and lateral temporal lobe atrophy was associated with steeper decline in memory and language across individuals. Mediation analyses revealed that part of the memory decline observed in A β + individuals was mediated through parahippocampal atrophy. Interpretation These results show that A β abnormality even in the oldest old with initially normal cognition is not part of normal aging, but is associated with a decline in cognitive functioning. Other pathologies may also contribute to decline in the oldest old as cortical thickness predicted cognitive decline similarly in individuals with and without A β pathology.