title: Expression of Ambra1 in mouse brain during physiological and Alzheimer type aging.
abstract: Autophagy is a major protein degradation pathway, essential for stress-induced and constitutive protein turnover. In nervous tissue, autophagy is constitutively active and crucial to neuronal survival. The efficiency of the autophagic pathway reportedly undergoes age-related decline, and autophagy defects are observed in neurodegenerative diseases. Since Ambra1 plays a fundamental role in regulating the autophagic process in developing nervous tissue, we investigated the expression of this protein in mature mouse brain and during physiological and Alzheimer type aging. The present study accomplished the first complete map of Ambra1 protein distribution in the various brain areas, and highlights differential expression in neuronal/glial cell populations. Differences in Ambra1 content are possibly related to specific neuronal features and properties, particularly concerning susceptibility to neurodegeneration. Furthermore, the analysis of Ambra1 expression in physiological and pathological brain aging supports important, though conflicting, functions of autophagy in neurodegenerative processes. Thus, novel therapeutic approaches, based on autophagy modulation, should also take into account the age-dependent roles of this mechanism in establishing, promoting, or counteracting neurodegeneration.
authors.affiliation: Department of Sciences, University "Roma Tre", Rome, Italy; Department of Genetics, Erasmus Medical Center, Rotterdam, the Netherlands.
authors.forename: Sara
authors.initials: S
authors.lastname: Sepe
authors.forename: Roberta
authors.initials: R
authors.lastname: Nardacci
authors.forename: Francesca
authors.initials: F
authors.lastname: Fanelli
authors.forename: Pamela
authors.initials: P
authors.lastname: Rosso
authors.forename: Cinzia
authors.initials: C
authors.lastname: Bernardi
authors.forename: Francesco
authors.initials: F
authors.lastname: Cecconi
authors.forename: Pier G
authors.initials: PG
authors.lastname: Mastroberardino
authors.forename: Mauro
authors.initials: M
authors.lastname: Piacentini
authors.forename: Sandra
authors.initials: S
authors.lastname: Moreno
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000378:metabolism*; D000375:Aging / Q000235:genetics* / Q000473:pathology / Q000502:physiology; D000544:Alzheimer Disease / Q000235:genetics* / Q000473:pathology; D000818:Animals; D001343:Autophagy / Q000235:genetics* / Q000502:physiology; D001921:Brain / Q000378:metabolism* / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental / Q000235:genetics*; D020022:Genetic Predisposition to Disease / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000473:pathology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C521754:Ambra1 protein, mouse
keywords: Aging; Alzheimer's disease; Ambra1; Autophagy; Brain; Glia; Hippocampus; Neocortex; Neurodegeneration; Neuron; Tg2576