Abstract
Astrocytes are of vital importance to neuronal function and the health of the central nervous system (CNS), and astrocytic dysfunction as a primary or secondary event may predispose to neurodegeneration. Until recently, the main astrocytic tauopathies were the frontotemporal lobar degeneration with tau (FTLD-tau) group of disorders; however, aging-related tau astrogliopathy (ARTAG) has now been defined. This condition is a self-describing neuropathology mainly found in individuals over 60 years of age. Astrocytic tau accumulates with a thorny or granular/fuzzy morphology and is commonly found in normal aging as well as coexisting with diverse neurodegenerative disorders. However, there are still many unknown factors associated with ARTAG, including the cause/s, the progression, and the nature of any clinical associations. In addition to FTLD-tau, ARTAG has recently been associated with chronic traumatic encephalopathy (CTE), where it has been proposed as a potential precursor to these conditions, with the different ARTAG morphological subtypes perhaps having separate etiologies. This is an emerging area of exciting research that encompasses complex neurobiological and clinicopathological investigation.
Highlights
Astrocytes play an essential role in maintaining cellular homeostasis in the central nervous system (CNS) and are active contributors to neuronal function [1]
Changes in astrocytic function occur during normal aging and astrocytic pathology underlies a large number of neurodegenerative disorders
Aging-related tau astrogliopathy (ARTAG) has been used to describe tau pathology accumulating in astrocytes in the aged brain [2]
Summary
Astrocytes play an essential role in maintaining cellular homeostasis in the central nervous system (CNS) and are active contributors to neuronal function [1]. Astrocytes are able to communicate with neighboring cells via gap junctions formed by connexins 30 and 43 [7] to allow direct electrical and biochemical coupling [8] Through these mechanisms, astrocytes are able to influence the excitation or inhibition of surrounding neuronal networks and shape neuronal activity [9]. GFAP upregulation is classically used as a marker of astrocyte activation, such as that seen following insult, injury or ischemia This so-called reactive astrogliosis may be mild and involve temporary cellular hypertrophy and restoration of a normal cellular state or it may be more severe resulting in cellular proliferation and permanent remodelling of the cytoarchitecture through glial scar formation. In vitro studies suggest that tau and amyloid-beta protein can switch a healthy astrocyte into one with a senescent phenotype [31,32] and Alzheimer’s disease patients show greater senescence than their age-matched counterparts, indicating that senescent astrocytes accumulate with normal aging and further increase with the onset of AD [31]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
