Abstract
Tauopathies represent a vast family of neurodegenerative diseases, the most well-known of which is Alzheimer’s disease. The symptoms observed in patients include cognitive deficits and locomotor problems and can lead ultimately to dementia. The common point found in all these pathologies is the accumulation in neural and/or glial cells of abnormal forms of Tau protein, leading to its aggregation and neurofibrillary tangles. Zebrafish transgenic models have been generated with different overexpression strategies of human Tau protein. These transgenic lines have made it possible to highlight Tau interacting factors or factors which may limit the neurotoxicity induced by mutations and hyperphosphorylation of the Tau protein in neurons. Several studies have tested neuroprotective pharmacological approaches. On few-days-old larvae, modulation of various signaling or degradation pathways reversed the deleterious effects of Tau mutations, mainly hTauP301L and hTauA152T. Live imaging and live tracking techniques as well as behavioral follow-up enable the analysis of the wide range of Tau-related phenotypes from synaptic loss to cognitive functional consequences.
Highlights
Tauopathies are neurodegenerative diseases that all share a common spread of neurotoxicity associated with pathological intracellular deposits of Tau proteins
We will focus on a large group of tauopathies: frontotemporal lobar degeneration (FTLD), which includes frontotemporal dementia linked to chromosome 17 (FTDP-17), progressive supranuclear palsy (PSP), cortico-basal degeneration (CBD), argyrophilic grain disease (AgD), or Pick’s disease
Tauopathies can be classified into two groups: primary tauopathies are characterized by the presence of solely Tau aggregates in brain tissue and secondary tauopathies include on the other hand, other protein aggregates in association with Tau cellular deposits, such as Aβ amyloid in Alzheimer’s disease, for example
Summary
Tauopathies are neurodegenerative diseases that all share a common spread of neurotoxicity associated with pathological intracellular deposits of Tau proteins. The term tauopathy was proposed in 1997 by Spillantini and includes diseases that combine Tau intracellular deposition, which can occurs in neurones, glia, or oligodendrocytes and involved cell degeneration [1]. We will focus on a large group of tauopathies: frontotemporal lobar degeneration (FTLD), which includes frontotemporal dementia linked to chromosome 17 (FTDP-17), progressive supranuclear palsy (PSP), cortico-basal degeneration (CBD), argyrophilic grain disease (AgD), or Pick’s disease. Due to their number and diversity, neuropathologists determine specific characteristics in order to classify these tauopathies [3]
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