PHF-Core Tau as the Potential Initiating Event for Tau Pathology in Alzheimer's Disease


Por: Luna-Viramontes, Nabil Itzi, Campa-Cordoba, B. Berenice, Ontiveros-Torres, Miguel Angel, Harrington, Charles R., Villanueva-Fierro, Ignacio, Guadarrama-Ortiz, Parmenides, Garces-Ramirez, Linda, de la Cruz, Fidel, Hernandes-Alejandro, Mario, Martinez-Robles, Sandra, Gonzalez-Ballesteros, Erik, Pacheco-Herrero, Mar, Luna-Munoz, Jose

Publicada: 10 sep 2020
Categoría: Cellular and molecular neuroscience

Resumen:
Worldwide, around 50 million people have dementia. Alzheimer's disease (AD) is the most common type of dementia and one of the major causes of disability and dependency among the elderly worldwide. Clinically, AD is characterized by impaired memory accompanied by other deficiencies in the cognitive domain. Neuritic plaques (NPs) and neurofibrillary tangles (NFTs) are histopathological lesions that define brains with AD. NFTs consist of abundant intracellular paired helical filaments (PHFs) whose main constituent is tau protein. Tau undergoes posttranslational changes including hyperphosphorylation and truncation, both of which favor conformational changes in the protein. The sequential pathological processing of tau is illustrated with the following specific markers: pT231, TG3, AT8, AT100, and Alz50. Two proteolysis sites for tau have been described-truncation at glutamate 391 and at aspartate 421-and which can be demonstrated by reactivity with the antibodies 423 and TauC-3, respectively. In this review, we describe the molecular changes in tau protein as pre-NFTs progress to extracellular NFTs and during which the formation of a minimal nucleus of the filament, as the PHF core, occurs. We also analyzed the PHF core as the initiator of PHFs and tau phosphorylation as a protective neuronal mechanism against the assembly of the PHF core.

Filiaciones:
Luna-Viramontes, Nabil Itzi:
 Univ Nacl Autonoma Mexico, Fac Estudios Super, Dept Ciencias Biol, Natl Dementia BioBank, Mexico City, DF, Mexico

 Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Fisiol, Mexico City, DF, Mexico

Campa-Cordoba, B. Berenice:
 Univ Nacl Autonoma Mexico, Fac Estudios Super, Dept Ciencias Biol, Natl Dementia BioBank, Mexico City, DF, Mexico

 Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Fisiol, Mexico City, DF, Mexico

Ontiveros-Torres, Miguel Angel:
 Tecnol Monterrey, Sch Engn & Sci, Toluca, Mexico

Harrington, Charles R.:
 Univ Aberdeen, Sch Med Med Sci & Nutr, Aberdeen, Scotland

Villanueva-Fierro, Ignacio:
 Becario COFAA, Inst Politecn Nacl, CIIDIR, Durango, Mexico

Guadarrama-Ortiz, Parmenides:
 CENNM, Ctr Especializado Neurocirugia & Neurociencias Me, Dept Neurocirugia, Mexico City, DF, Mexico

Garces-Ramirez, Linda:
 Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Fisiol, Mexico City, DF, Mexico

de la Cruz, Fidel:
 Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Fisiol, Mexico City, DF, Mexico

Hernandes-Alejandro, Mario:
 Inst Politecn Nacl UPIBI IPN, Unidad Profes Interdisciplinaria Biotecnol, Dept Bioingn, Mexico City, DF, Mexico

Martinez-Robles, Sandra:
 Univ Nacl Autonoma Mexico, Fac Estudios Super, Dept Ciencias Biol, Natl Dementia BioBank, Mexico City, DF, Mexico

Gonzalez-Ballesteros, Erik:
 Univ Nacl Autonoma Mexico, Fac Estudios Super, Dept Ciencias Biol, Natl Dementia BioBank, Mexico City, DF, Mexico

Pacheco-Herrero, Mar:
 Pontificia Univ Catolica Madre & Maestra, Fac Hlth Sci, Neurosci Res Lab, Santiago De Caballeros, Dominican Rep

Luna-Munoz, Jose:
 Univ Nacl Autonoma Mexico, Fac Estudios Super, Dept Ciencias Biol, Natl Dementia BioBank, Mexico City, DF, Mexico
ISSN: 16625102
Editorial
FRONTIERS RESEARCH FOUNDATION, PO BOX 110, LAUSANNE, 1015, SWITZERLAND, Suiza
Tipo de documento: Article
Volumen: 14 Número:
Páginas:
WOS Id: 000575353100001
ID de PubMed: 33132840