title: Common key-signals in learning and neurodegeneration: focus on excito-amino acids, beta-amyloid peptides and alpha-synuclein.
abstract: In this paper a hypothesis that some special signals ("key-signals" excito-amino acids, beta-amyloid peptides and alpha-synuclein) are not only involved in information handling by the neuronal circuits, but also trigger out substantial structural and/or functional changes in the Central Nervous System (CNS) is introduced. This forces the neuronal circuits to move from one stable state towards a new state, but in doing so these signals became potentially dangerous. Several mechanisms are put in action to protect neurons and glial cells from these potentially harmful signals. However, in agreement with the Red Queen Theory of Ageing (Agnati et al. in Acta Physiol Scand 145:301-309, 1992), it is proposed that during ageing these neuroprotective processes become less effective while, in the meantime, a shortage of brain plasticity occurs together with an increased need of plasticity for repairing the wear and tear of the CNS. The paper presents findings supporting the concept that such key-signals in instances such as ageing may favour neurodegenerative processes in an attempt of maximizing neuronal plasticity.
authors.affiliation: Department of BioMedical Sciences, University of Modena, Via Campi 287, 41100 Modena, Italy. luigiagnati@tin.it
authors.forename: L F
authors.initials: LF
authors.lastname: Agnati
authors.forename: G
authors.initials: G
authors.lastname: Leo
authors.forename: S
authors.initials: S
authors.lastname: Genedani
authors.forename: L
authors.initials: L
authors.lastname: Piron
authors.forename: A
authors.initials: A
authors.lastname: Rivera
authors.forename: D
authors.initials: D
authors.lastname: Guidolin
authors.forename: K
authors.initials: K
authors.lastname: Fuxe
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000502:physiology / Q000503:physiopathology; D004298:Dopamine / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006710:Homocysteine / Q000378:metabolism; D006801:Humans; D007858:Learning / Q000502:physiology*; D008959:Models, Neurological; D009410:Nerve Degeneration / Q000503:physiopathology*; D019636:Neurodegenerative Diseases / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000502:physiology; D011487:Protein Conformation; D055503:Protein Multimerization; D015398:Signal Transduction; D051844:alpha-Synuclein / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D051844:alpha-Synuclein; D006710:Homocysteine; D018698:Glutamic Acid; D004298:Dopamine