Mesial Temporal Astrocyte Tau Pathology in the MRC-CFAS Ageing Brain Cohort

Lace, G; Ince, Paul G.; Brayne, Carol; Savva, George M.; Matthews, Fiona E.; Silva, R de; Simpson, Julie E.; Wharton, Stephen B.

doi:10.1159/000341581

Cited by 42 publications

(47 citation statements)

References 35 publications

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“…Interestingly, a similar distribution of TSA was reported in aged baboons [55]. A study by the MRC-CFAS group confirmed the findings of Schultz et al and added that the TSA could be less commonly observed in the vicinity of neuronal cell bodies in gray matter areas such as amygdala and dentate gyrus [36]. Also, this study documented the 4R tau nature of TSA [36].…”

Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainsupporting

confidence: 83%

“…A study by the MRC-CFAS group confirmed the findings of Schultz et al and added that the TSA could be less commonly observed in the vicinity of neuronal cell bodies in gray matter areas such as amygdala and dentate gyrus [36]. Also, this study documented the 4R tau nature of TSA [36]. Variable staining for Gallyas and p62 suggest that some of these astrocytes accumulate tau in a fibrillar state [34–36, 38, 46].…”

Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainsupporting

confidence: 72%

“…They found that immunolabeling with AT8 was the most sensitive for demonstrating the TSA, while silver staining was less consistent [57]. They also speculated that the preferential subpial and perivascular location could be a result of exposure to CSF or to extravasated plasma proteins due to defects in blood–brain barrier permeability commonly seen in aging and neurodegeneration [36, 57]. Interestingly, a similar distribution of TSA was reported in aged baboons [55].…”

Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainmentioning

confidence: 99%

“…The introduction of the Gallyas silver stain and particularly diagnostic tau immunohistochemistry led to the identification of astroglial tau pathology in the aging brain in people with or without AD-related changes, cognitive decline or movement disorders [5, 7, 11, 21, 25, 31, 34–36, 38, 46, 57]. There have been attempts to classify these tau astrogliopathies [34], but there is lack of consensus as to how best to describe and categorize them.…”

Section: Introductionmentioning

confidence: 99%

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Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy

et al. 2015

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Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of astroglial tau pathology in the aged brain, facilitating communication among neuropathologists and researchers, and informing interpretation of clinical biomarkers and imaging studies that focus on tau-related indicators.

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Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainsupporting

confidence: 83%

Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainsupporting

confidence: 72%

Section: Overview Of Astrocytic Tau Pathologies In the Aging Brainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy

et al. 2015

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“…Astrocytic PHF-tau pathology in CTE is predominantly 4R tau immunopositive, but more widely distributed than that reported in the medial temporal lobe in aging and AD [103, 114]. Characteristically, the locus coeruleus shows neurofibrillary PHF-tau pathology in early stages of CTE, which can be substantial even in individuals under the age of 30.…”

Section: Adverse Neuropathological Outcomes Associated With Sports Pamentioning

confidence: 89%

The neuropathology of sport

et al. 2013

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The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.

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