Marcel Levy Nogueira1, Olivier Lafitte2, Jean-Marc Steyaert3, Hovagim Bakardjian4, Bruno Dubois5, Harald Hampel6, Laurent Schwartz3. 1. Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France; Institut des Neurosciences Translationnelles de Paris (IHU-A-ICM), Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France; Laboratoire d'informatique (LIX), UMR 7161, Ecole Polytechnique, Université Paris-Saclay, Palaiseau, France. Electronic address: marcel.levy@psl.aphp.fr. 2. LAGA, UMR 7539, Université Paris 13, Sorbonne Paris Cité, Villetaneuse, France. 3. Laboratoire d'informatique (LIX), UMR 7161, Ecole Polytechnique, Université Paris-Saclay, Palaiseau, France. 4. Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France; Institut des Neurosciences Translationnelles de Paris (IHU-A-ICM), Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France. 5. Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France; Institut des Neurosciences Translationnelles de Paris (IHU-A-ICM), Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France; INSERM, CNRS, UMR-S975, Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France. 6. Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Département de Neurologie, Hôpital de la Pitié-Salpêtrière, AP-HP, Paris, France; INSERM, CNRS, UMR-S975, Institut du Cerveau et de la Moelle Epinière (ICM), Paris, France; AXA Research Fund & UPMC Chair, Sorbonne Universités, Université Pierre et Marie Curie, Paris, France.
Abstract
INTRODUCTION: The effects related to endogenous mechanical energy in Alzheimer's disease (AD) pathology have been widely overlooked. With the support of available data from literature and mathematical arguments, we hypothesize that brain atrophy in AD could be co-driven by the cumulative impact of the pressure within brain tissues. METHODS: Brain volumetric and physical data in AD and normal aging (NA) were extracted from the literature. Average brain shrinkage and axial deformations were evaluated mathematically. Mechanical stress equivalents related to brain shrinkage were calculated using a conservation law derived from fluid and solid mechanics. RESULTS: Pressure equivalents of 5.92 and 3.43 mm Hg were estimated in AD and in NA, respectively. DISCUSSION: The calculated increments of brain mechanical stress in AD, which could be impacted by marked dampening of arterial pulse waves, may point to the need to expand the focus on the mechanical processes underpinning pathologic aging of the brain.
INTRODUCTION: The effects related to endogenous mechanical energy in Alzheimer's disease (AD) pathology have been widely overlooked. With the support of available data from literature and mathematical arguments, we hypothesize that brain atrophy in AD could be co-driven by the cumulative impact of the pressure within brain tissues. METHODS: Brain volumetric and physical data in AD and normal aging (NA) were extracted from the literature. Average brain shrinkage and axial deformations were evaluated mathematically. Mechanical stress equivalents related to brain shrinkage were calculated using a conservation law derived from fluid and solid mechanics. RESULTS: Pressure equivalents of 5.92 and 3.43 mm Hg were estimated in AD and in NA, respectively. DISCUSSION: The calculated increments of brain mechanical stress in AD, which could be impacted by marked dampening of arterial pulse waves, may point to the need to expand the focus on the mechanical processes underpinning pathologic aging of the brain.
Authors: Marcel Levy Nogueira; Jorgelindo da Veiga Moreira; Gian Franco Baronzio; Bruno Dubois; Jean-Marc Steyaert; Laurent Schwartz Journal: Front Oncol Date: 2015-09-17 Impact factor: 6.244