Tau Pathology in Neurons and Glial Cells of Aged Baboons

2001 ◽  
pp. 59-69 ◽  
Author(s):  
Christian Schultz ◽  
Gene B. Hubbard ◽  
Kelly Del Tredici ◽  
Eva Braak ◽  
Heiko Braak
Keyword(s):  
Glial Cells ◽  
Tau Pathology

scholarly journals Critical Molecular and Cellular Contributors to Tau Pathology

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 190
Author(s):  
Liqing Song ◽  
Evan A. Wells ◽  
Anne Skaja Robinson
Keyword(s):  
Signaling Pathways ◽  
Glial Cells ◽  
Early Stage ◽  
Neuronal Loss ◽  
Disease Spread ◽  
Tau Pathology ◽  
Neuroprotective Effects ◽  
Inflammatory Microenvironment ◽  
Mapt Gene ◽  
The Brain

Tauopathies represent a group of neurodegenerative diseases including Alzheimer’s disease (AD) that are characterized by the deposition of filamentous tau aggregates in the brain. The pathogenesis of tauopathies starts from the formation of toxic ‘tau seeds’ from hyperphosphorylated tau monomers. The presence of specific phosphorylation sites and heat shock protein 90 facilitates soluble tau protein aggregation. Transcellular propagation of pathogenic tau into synaptically connected neuronal cells or adjacent glial cells via receptor-mediated endocytosis facilitate disease spread through the brain. While neuroprotective effects of glial cells—including phagocytotic microglial and astroglial phenotypes—have been observed at the early stage of neurodegeneration, dysfunctional neuronal-glial cellular communication results in a series of further pathological consequences as the disease progresses, including abnormal axonal transport, synaptic degeneration, and neuronal loss, accompanied by a pro-inflammatory microenvironment. Additionally, the discovery of microtubule-associated protein tau (MAPT) gene mutations and the strongest genetic risk factor of tauopathies—an increase in the presence of the ε2 allele of apolipoprotein E (ApoE)—provide important clues to understanding tau pathology progression. In this review, we describe the crucial signaling pathways and diverse cellular contributors to the progression of tauopathies. A systematic understanding of disease pathogenesis provides novel insights into therapeutic targets within altered signaling pathways and is of great significance for discovering effective treatments for tauopathies.

scholarly journals Astrocytic Propagation of Tau in the Context of Alzheimer's Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Rebecca M. Fleeman ◽  
Elizabeth A. Proctor
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Significance ◽  
Glial Cells ◽  
Cell Type ◽  
Tau Pathology ◽  
Specific Effects ◽  
Signaling Mechanisms ◽  
Cell Type Specific ◽  
The Brain

More than 6 million Americans are currently living with Alzheimer's disease (AD), and the incidence is growing rapidly with our aging population. Numerous therapeutics have failed to make it to the clinic, potentially due to a focus on presumptive pathogenic proteins instead of cell-type-specific signaling mechanisms. The tau propagation hypothesis that inter-neuronal tau transfer drives AD pathology has recently garnered attention, as accumulation of pathological tau in the brain has high clinical significance in correlating with progression of cognitive AD symptoms. However, studies on tau pathology in AD are classically neuron-centric and have greatly overlooked cell-type specific effects of tau internalization, degradation, and propagation. While the contribution of microglia to tau processing and propagation is beginning to be recognized and understood, astrocytes, glial cells in the brain important for maintaining neuronal metabolic, synaptic, trophic, and immune function which can produce, internalize, degrade, and propagate tau are understudied in their ability to affect AD progression through tau pathology. Here, we showcase evidence for whether tau uptake by astrocytes may be beneficial or detrimental to neuronal health and how astrocytes and their immunometabolic functions may be key targets for future successful AD therapies.

scholarly journals Glial Tau Pathology in Tauopathies: Functional Consequences

2015 ◽  
Vol 9s2 ◽  
pp. JEN.S25515 ◽  
Author(s):  
Martha A. Kahlson ◽  
Kenneth J. Colodner
Keyword(s):  
Neurodegenerative Diseases ◽  
Glial Cells ◽  
Brain Regions ◽  
Model Systems ◽  
Potential Contribution ◽  
Tau Pathology ◽  
Relative Contribution ◽  
Functional Consequences

Tauopathies are a class of neurodegenerative diseases characterized by the presence of hyperphosphorylated and aggregated tau pathology in neuronal and glial cells. Though the ratio of neuronal and glial tau aggregates varies across diseases, glial tau aggregates can populate the same degenerating brain regions as neuronal tau aggregates. While much is known about the deleterious consequences of tau pathology in neurons, the relative contribution of glial tau pathology to these diseases is less clear. Recent studies using a number of model systems implicate glial tau pathology in contributing to tauopathy pathogenesis. This review aims to highlight the functional consequences of tau overexpression in glial cells and explore the potential contribution of glial tau pathology in the pathogenesis of neurodegenerative tauopathies.

Neuron-glia relationship during the early postembryonic development of the nervous system in some oligochaetes

1978 ◽  
Vol 36 (2) ◽  
pp. 600-601
Author(s):  
Wiktor Djaczenko ◽  
Carmen Calenda Cimmino
Keyword(s):  
Nervous System ◽  
Glial Cells ◽  
Early Period ◽  
Postembryonic Development ◽  
Ruthenium Red ◽  
The Body ◽  
Tubifex Tubifex ◽  
Growth Stages ◽  
Cell Processes ◽  
Cytoplasmic Processes

The simplicity of the developing nervous system of oligochaetes makes of it an excellent model for the study of the relationships between glia and neurons. In the present communication we describe the relationships between glia and neurons in the early periods of post-embryonic development in some species of oligochaetes.Tubifex tubifex (Mull. ) and Octolasium complanatum (Dugès) specimens starting from 0. 3 mm of body length were collected from laboratory cultures divided into three groups each group fixed separately by one of the following methods: (a) 4% glutaraldehyde and 1% acrolein fixation followed by osmium tetroxide, (b) TAPO technique, (c) ruthenium red method.Our observations concern the early period of the postembryonic development of the nervous system in oligochaetes. During this period neurons occupy fixed positions in the body the only observable change being the increase in volume of their perikaryons. Perikaryons of glial cells were located at some distance from neurons. Long cytoplasmic processes of glial cells tended to approach the neurons. The superimposed contours of glial cell processes designed from electron micrographs, taken at the same magnification, typical for five successive growth stages of the nervous system of Octolasium complanatum are shown in Fig. 1. Neuron is designed symbolically to facilitate the understanding of the kinetics of the growth process.

High-voltage electron microscopy of subretinal scar formation

1992 ◽  
Vol 50 (1) ◽  
pp. 486-487
Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Retinal Pigment Epithelium ◽  
Glial Cells ◽  
High Voltage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Sodium Iodate ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

Ultrasturcture of cerebellar cells and neuropil in rats subjected to partial global cerebral ischemia

1986 ◽  
Vol 44 ◽  
pp. 126-127
Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros
Keyword(s):  
Purkinje Cells ◽  
Glial Cells ◽  
Granule Cells ◽  
Molecular Layer ◽  
Cell Types ◽  
Primary Objective ◽  
Global Cerebral Ischemia ◽  
Forebrain Ischemia ◽  
Substantial Evidence ◽  
Cerebellar Cells

Although a previous study in this laboratory determined that Purkinje cells of the rat cerebellum did not appear to be damaged following 30 min of forebrain ischemia followed by 30 min of reperfusion, it was suggested that an increase in rough endoplasmic reticulum (RER) and/or polysomes had occurred in these cells. The primary objective of the present study was to morphometrically determine whether or not this increase had occurred. In addition, since there is substantial evidence that glial cells may be affected by ischemia earlier than other cell types, glial cells also were examined. To ascertain possible effects on other cerebellar components, granule cells and neuropil near Purkinje cells as well as neuropil in the molecular layer also were evaluated in this investigation.

Extracellular filaments in the perineurium of the florida lobster, Panulirus argus

1987 ◽  
Vol 45 ◽  
pp. 784-785
Author(s):  
Roy J. Baerwald ◽  
Lura C. Williamson
Keyword(s):  
Blood Brain Barrier ◽  
Glial Cells ◽  
Tannic Acid ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Florida Keys ◽  
Panulirus Argus ◽  
Brain Barrier ◽  
Cacodylate Buffer ◽  
Nerve Cords

In arthropods the perineurium surrounds the neuropile, consists of modified glial cells, and is the morphological basis for the blood-brain barrier. The perineurium is surrounded by an acellular neural lamella, sometimes containing scattered collagen-like fibrils. This perineurial-neural lamellar complex is thought to occur ubiquitously throughout the arthropods. This report describes a SEM and TEM study of the sheath surrounding the ventral nerve cord of Panulirus argus.Juvenile P. argus were collected from the Florida Keys and maintained in marine aquaria. Nerve cords were fixed for TEM in Karnovsky's fixative and saturated tannic acid in 0.1 M Na-cacodylate buffer, pH = 7.4; post-fixed in 1.0% OsO4 in the same buffer; dehydrated through a graded series of ethanols; embedded in Epon-Araldite; and examined in a Philips 200 TEM. Nerve cords were fixed for SEM in a similar manner except that tannic acid was not used.

Amelioration of Tau Pathology by Anle138b Rescues Neuronal Function in a Mouse Model of Human Alzheimer's Disease Tau

2019 ◽  
Author(s):  
M Deussing ◽  
T Blume ◽  
L Kaiser ◽  
F Probst ◽  
F Overhoff ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Neuronal Function ◽  
Tau Pathology
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