Affiliations: [a] Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain
| [b] CIBERNED, Madrid, Spain
| [c] Departamento de Anatomía Histología y Neurociencia, Facultad de Medicina UAM, Madrid, Spain
| [d] Departamento de Biología Molecular, Facultad de Medicina, Universidad de Cantabria, Santander, Spain
| [e] Department of Molecular Biology, Faculty of Science, Universidad Autonoma de Madrid, Spain
Correspondence:
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Correspondence to: Jesús Avila, Centro de Biología Molecular Severo Ochoa (CSIC-UAM), 28049 Madrid, Spain. E-mail: javila@cbm.csic.es.
Abstract: Alzheimer’s disease (AD) is characterized by the presence of two aberrant structures: namely senile plaques, composed of amyloid-β peptide (Aβ), and neurofibrillary tangles, composed of tau protein. In this regard, Aβ and tau protein have been widely studied in research efforts aiming to find a therapy for AD. Aβ and tau pathologies do not always overlap. The precursor of Aβ is expressed in peripheral tissues and in the central nervous system (CNS), whereas tau is mainly a neuronal protein. Since AD is a disease of the CNS, it has been proposed that Aβ may initiate the disease process, with tau being the executor. In this review, we will focus on future studies of tau pathology, although we will comment on new beginnings for AD, as other molecules other than Aβ and tau may be involved in the onset of dementia.
Keywords: Extracellular tau, MAPs, tau functions, tauopathies
