Lifespan Changes of the Human Brain In Alzheimer’s Disease.

Pierrick Coupé, José Vicente Manjón, Enrique Lanuza, Gwenaelle Catheline
Sci Rep. 2019-03-08; 9(1):
DOI: 10.1038/s41598-019-39809-8

Lire sur PubMed

1. Sci Rep. 2019 Mar 8;9(1):3998. doi: 10.1038/s41598-019-39809-8.

Lifespan Changes of the Human Brain In Alzheimer’s Disease.

Coupé P(1)(2), Manjón JV(3), Lanuza E(4), Catheline G(5).

Author information:
(1)University Bordeaux, LaBRI, UMR 5800, PICTURA, F-33400, Talence, France.
(2)CNRS, LaBRI, UMR 5800, PICTURA, F-33400, Talence, France.
(3)Instituto Universitario de Tecnologías de la Información y Comunicaciones
(ITACA), Universitat Politècnica de València, Camino de Vera s/n, 46022,
Valencia, Spain.
(4)University Valencia, Department of Cell Biology, Burjassot, 46100, Valencia,
(5)University Bordeaux, CNRS, EPHE, PSL, INCIA, UMR 5283, F-33000, Bordeaux,

Brain imaging studies have shown that slow and progressive cerebral atrophy
characterized the development of Alzheimer’s Disease (AD). Despite a large number
of studies dedicated to AD, key questions about the lifespan evolution of AD
biomarkers remain open. When does the AD model diverge from the normal aging
model? What is the lifespan trajectory of imaging biomarkers for AD? How do the
trajectories of biomarkers in AD differ from normal aging? To answer these
questions, we proposed an innovative way by inferring brain structure model
across the entire lifespan using a massive number of MRI (N = 4329). We compared
the normal model based on 2944 control subjects with the pathological model based
on 3262 patients (AD + Mild cognitive Impaired subjects) older than 55 years and
controls younger than 55 years. Our study provides evidences of early divergence
of the AD models from the normal aging trajectory before 40 years for the
hippocampus, followed by the lateral ventricles and the amygdala around 40 years.
Moreover, our lifespan model reveals the evolution of these biomarkers and
suggests close abnormality evolution for the hippocampus and the amygdala,
whereas trajectory of ventricular enlargement appears to follow an inverted
U-shape. Finally, our models indicate that medial temporal lobe atrophy and
ventricular enlargement are two mid-life physiopathological events characterizing
AD brain.

DOI: 10.1038/s41598-019-39809-8
PMCID: PMC6408544
PMID: 30850617 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus