A walk through tau therapeutic strategies
Autor: | Luc Buée, Rohan de Silva, Gabor G. Kovacs, Norbert Zilka, Rostislav Skrabana, Eniko Veronika Kovari, Eva Kontsekova, Michael Schöll, Barbara Malawska, Santosh Jadhav, Jesús Avila, Lewis D. B. Evans |
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Přispěvatelé: | Université de Lille, Centro de Investigación Biomédica en Red Salud Mental (España), Buee, Luc [0000-0002-6261-4230], Apollo - University of Cambridge Repository |
Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Tau vaccines Neurology medicine.medical_treatment PET imaging tau Proteins Review Disease lcsh:RC346-429 Pathology and Forensic Medicine Progressive supranuclear palsy Primary progressive aphasia 03 medical and health sciences Cellular and Molecular Neuroscience ddc:616.89 Aggregation 0302 clinical medicine Therapeutic interventions Alzheimer Disease medicine Animals Humans Gene silencing Protein Kinase Inhibitors lcsh:Neurology. Diseases of the nervous system business.industry Brain Immunotherapy Alzheimer's disease medicine.disease Clinical trial 030104 developmental biology Drug development Tauopathies Supranuclear Palsy Progressive Neurology (clinical) business Neuroscience Alzheimer’s disease 030217 neurology & neurosurgery |
Zdroj: | Digital.CSIC. Repositorio Institucional del CSIC instname Acta Neuropathologica Communications, Vol. 7, No 1 (2019) P. 22 Acta Neuropathologica Communications Acta Neuropathologica Communications, Vol 7, Iss 1, Pp 1-31 (2019) |
ISSN: | 2051-5960 |
Popis: | Tau neuronal and glial pathologies drive the clinical presentation of Alzheimer's disease and related human tauopathies. There is a growing body of evidence indicating that pathological tau species can travel from cell to cell and spread the pathology through the brain. Throughout the last decade, physiological and pathological tau have become attractive targets for AD therapies. Several therapeutic approaches have been proposed, including the inhibition of protein kinases or protein-3-O-(N-acetyl-beta-D-glucosaminyl)-L-serine/threonine Nacetylglucosaminyl hydrolase, the inhibition of tau aggregation, active and passive immunotherapies, and tau silencing by antisense oligonucleotides. New tau therapeutics, across the board, have demonstrated the ability to prevent or reduce tau lesions and improve either cognitive or motor impairment in a variety of animal models developing neurofibrillary pathology. The most advanced strategy for the treatment of human tauopathies remains immunotherapy, which has already reached the clinical stage of drug development. Tau vaccines or humanised antibodies target a variety of tau species either in the intracellular or extracellular spaces. Some of them recognise the amino-terminus or carboxy-terminus, while others display binding abilities to the proline-rich area or microtubule binding domains. The main therapeutic foci in existing clinical trials are on Alzheimer's disease, progressive supranuclear palsy and non-fluent primary progressive aphasia. Tau therapy offers a new hope for the treatment of many fatal brain disorders. First efficacy data from clinical trials will be available by the end of this decade. French and Spanish academic funds from University of Lille, SFR DN2M, LabEx DISTALZ, LiCEND, and Ciberned. |
Databáze: | OpenAIRE |
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