Open AccessClinical and biomarker trajectories in sporadic Alzheimer's disease: A longitudinal study
Author(s) -
Wang HuiFu,
Shen XueNing,
Li JieQiong,
Suckling John,
Tan ChenChen,
Wang YanJiang,
Feng Lei,
Zhang Can,
Tan Lan,
Dong Qiang,
Touchon Jacques,
Gauthier Serge,
Yu JinTai
Publication year - 2020
Publication title -
alzheimer's and dementia: diagnosis, assessment and disease monitoring
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.497
H-Index - 37
ISSN - 2352-8729
DOI - 10.1002/dad2.12095
Subject(s) - biomarker , dementia , neurodegeneration , cerebrospinal fluid , cognitive decline , atrophy , disease , medicine , alzheimer's disease , hippocampus , amyloid (mycology) , oncology , pathology , neuroscience , psychology , biology , genetics
Amyloid beta (Aβ) deposition was identified to precede tau pathology and neurodegeneration in familial Alzheimer's disease (AD). But the divergence between sporadic and familial AD limits the extension of these findings to sporadic AD. Methods Longitudinal changes of biomarkers among different stages were assessed using linear mixed‐effects models. The slopes of the models were used to estimate rates of change to calculate the biomarker trajectories in sporadic AD. Results Cerebrospinal fluid (CSF) Aβ was estimated to decline 45.2 years (abnormal: 27.8 years) before dementia, and Aβ deposition seemed to increase 31.7 years (abnormal: 26.7 years) before dementia. It was estimated to take 29.0 years (CSF t‐tau), 12.2 years (memory), 11.6 years (hippocampus), 9.3 years (hypometabolism), and 6.1 years (cognition) to move from normal to dementia. Discussion The trajectory in sporadic AD is led by Aβ accumulation, followed by CSF t‐tau increase, memory deficits, brain atrophy, hypometabolism, and cognitive decline.