title: Alternative neural circuitry that might be impaired in the development of Alzheimer disease.
abstract: It is well established that some individuals with normal cognitive capacity have abundant senile plaques in their brains. It has been proposed that those individuals are resilient or have compensation factors to prevent cognitive decline. In this comment, we explore an alternative mechanism through which cognitive capacity is maintained. This mechanism could involve the impairment of alternative neural circuitry. Also, the proportion of molecules such as Aβ or tau protein present in different areas of the brain could be important.
authors.affiliation: Neurobiology, Centro de Biologia Molecular Severo Ochoa (CSIC-UAM) Madrid, Spain ; Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas Madrid, Spain.
authors.forename: Jesus
authors.initials: J
authors.lastname: Avila
authors.affiliation: College of Sciences, The University of Texas at San Antonio San Antonio, TX, USA.
authors.forename: George
authors.initials: G
authors.lastname: Perry
authors.affiliation: Department of Neuroimaging, Reina Sofia Foundation, Center for Alzheimer Research, FCIEN Madrid, Spain ; Laboratory for Clinical Neuroscience, CTB, Universidad Politecnica de Madrid Madrid, Spain.
authors.forename: Bryan A
authors.initials: BA
authors.lastname: Strange
authors.affiliation: Neurobiology, Centro de Biologia Molecular Severo Ochoa (CSIC-UAM) Madrid, Spain ; Centro de Investigacion Biomedica en Red de Enfermedades Neurodegenerativas Madrid, Spain.
authors.forename: Felix
authors.initials: F
authors.lastname: Hernandez
keywords: Alzheimer disease (AD); abeta; cognitive decline; tau proteins; tauopathies