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Despite the presence of significant Alzheimer's disease (AD) pathology, characterized by amyloid β (Aβ) plaques and phosphorylated tau (pTau) tangles, some cognitively normal elderly individuals do not inevitably develop dementia. These findings give rise to the notion of cognitive 'resilience', suggesting maintained cognitive function despite the presence of AD neuropathology, highlighting the influence of factors beyond classical pathology. Cortical astroglial inflammation, a ubiquitous feature of symptomatic AD, shows a strong correlation with cognitive impairment severity, potentially contributing to the diversity of clinical presentations.
View Article and Find Full Text PDFCorrespondence of mean apparent propagator MRI metrics with phosphorylated tau and astrogliosis in chronic traumatic encephalopathy.
Brain Commun
October 2023
Center for Neuroscience and Regenerative Medicine, Bethesda, MD 20817, USA.
Chronic traumatic encephalopathy is a neurodegenerative disease that is diagnosed and staged based on the localization and extent of phosphorylated tau pathology. Although its identification remains the primary diagnostic criteria to distinguish chronic traumatic encephalopathy from other tauopathies, the hyperphosphorylated tau that accumulates in neurofibrillary tangles in cortical grey matter and perivascular regions is often accompanied by concomitant pathology such as astrogliosis. Mean apparent propagator MRI is a clinically feasible diffusion MRI method that is suitable to characterize microstructure of complex biological media efficiently and comprehensively.
View Article and Find Full Text PDFAPOE mediated neuroinflammation and neurodegeneration in Alzheimer's disease.
Semin Immunol
January 2022
Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer Disease, Research Center, Washington University, St. Louis, MO, 63110, USA. Electronic address:
Neuroinflammation is a central mechanism involved in neurodegeneration as observed in Alzheimer's disease (AD), the most prevalent form of neurodegenerative disease. Apolipoprotein E4 (APOE4), the strongest genetic risk factor for AD, directly influences disease onset and progression by interacting with the major pathological hallmarks of AD including amyloid-β plaques, neurofibrillary tau tangles, as well as neuroinflammation. Microglia and astrocytes, the two major immune cells in the brain, exist in an immune-vigilant state providing immunological defense as well as housekeeping functions that promote neuronal well-being.
View Article and Find Full Text PDFCyclic multiplex fluorescent immunohistochemistry and machine learning reveal distinct states of astrocytes and microglia in normal aging and Alzheimer's disease.
J Neuroinflammation
February 2022
Department of Neurology, Massachusetts General Hospital, Boston, MA, 02114, USA.
Background: Astrocytes and microglia react to Aβ plaques, neurofibrillary tangles, and neurodegeneration in the Alzheimer's disease (AD) brain. Single-nuclei and single-cell RNA-seq have revealed multiple states or subpopulations of these glial cells but lack spatial information. We have developed a methodology of cyclic multiplex fluorescent immunohistochemistry on human postmortem brains and image analysis that enables a comprehensive morphological quantitative characterization of astrocytes and microglia in the context of their spatial relationships with plaques and tangles.
View Article and Find Full Text PDFSpace-occupying brain lesions, trauma-related tau astrogliopathy, and ARTAG: a report of two cases and a literature review.
Acta Neuropathol Commun
March 2021
Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Astrocytes with intracellular accumulations of misfolded phosphorylated tau protein have been observed in advanced-stage chronic traumatic encephalopathy (CTE) and in other neurodegenerative conditions. There is a growing awareness that astrocytic tau inclusions are also relatively common in the brains of persons over 70 years of age-affecting approximately one-third of autopsied individuals. The pathologic hallmarks of aging-related tau astrogliopathy (ARTAG) include phosphorylated tau protein within thorn-shaped astrocytes (TSA) in subpial, subependymal, perivascular, and white matter regions, whereas granular-fuzzy astrocytes are often seen in gray matter.
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