Articolo in rivista, 2020, ENG, 10.1007/s12640-019-00116-9
Picone P; Nuzzo D; Giacomazza D; Di Carlo M;
Istituto per la Ricerca e l'Innovazione Biomedica (CNR-IRIB), Consiglio Nazionale delle Ricerche, Palermo, 90146, Istituto per la Ricerca e l'Innovazione Biomedica (CNR-IRIB), Consiglio Nazionale delle Ricerche, 90146, Palermo, Italy, , Italy; Istituto di Biofisica (CNR-IBF), Consiglio Nazionale delle Ricerche, Palermo, 90146, Istituto di Biofisica (CNR-IBF), Consiglio Nazionale delle Ricerche, 90146, Palermo, Italy, , Italy
Alzheimer's disease (AD) is the most widespread form of dementia, characterized by memory loss and reduction of cognitive functions that strongly interfere with normal daily life. Numerous evidences show that aggregates of the amyloid beta peptide, formed by 39 to 42 amino acid residues (A?39-43), from soluble small oligomers to large fibrils are characteristic markers of this pathology. However, AD is a complex disease and its neurodegenerative molecular mechanism is not yet fully understood. Growing evidence suggests a link between A? polymorphic nature, oligomers and fibrils, and specific mechanisms of neurodegeneration. The A? variable nature and its multiplicity of interactions with different proteins and organelles reflect the complexity of this pathology. In this review, we analyze the effects of the interaction between A? peptide and different cellular compartments in relation to the different kinds and sizes of amyloid aggregates. In particular, A? interaction with different cell structures such as the plasma membrane, mitochondria, lysosomes, nucleus, and endoplasmic reticulum is discussed. Further, we analyze the A? peptide ability to modify the structure and function of the target organelle, inducing alteration of its physiological role thus contributing to the pathological event. Dysfunction of cellular components terminating with the activation of the cellular death mechanism and subsequent neurodegeneration is also taken into consideration.
Neurotoxicity resarch 37 , pp. 250–263
Alzheimer's disease .A? peptides .Amyloid aggregates . Cellular organelles . Cellular death
Di Carlo Marta, Nuzzo Domenico, Picone Pasquale, Giacomazza Daniela
ID: 433864
Year: 2020
Type: Articolo in rivista
Creation: 2020-10-09 15:26:17.000
Last update: 2021-04-02 14:22:40.000
CNR institutes
External links
OAI-PMH: Dublin Core
OAI-PMH: Mods
OAI-PMH: RDF
DOI: 10.1007/s12640-019-00116-9
URL: http://www.scopus.com/record/display.url?eid=2-s2.0-85076849228&origin=inward
External IDs
CNR OAI-PMH: oai:it.cnr:prodotti:433864
DOI: 10.1007/s12640-019-00116-9
Scopus: 2-s2.0-85076849228