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> Disorders > Pathologic Function > Gliosis

Gliosis

Gliosis is a pathological process characterized by the proliferation and hypertrophy of glial cells, typically in response to central nervous system (CNS) injury or disease.
This reactive process involves the activation and changes in morphology of astrocytes, microglia, and oligodendrocytes.
Gliosis can have both beneficial and detrimental effects on neurological function, depending on the severity and duration of the underlying condition.
Understanding the mechanisms and dynamics of gliosis is crucial for developing effective therapies to promote neural repair and regeneration.
PubCompare.ai's AI-driven platform can optimize gliosis research by helping users locate the best protocols and products from literature, pre-prints, and patents, enhancing reproducibility and accuracy to drive your research forward.

Most cited protocols related to «Gliosis»

1
Neuropathological Examination of Aging Brains
Cited 48 times
Brain autopsies were conducted at pre-determined sites across the US, with a mean postmortem interval of 8.3 (SD=8.0) hours. The cerebellar and cerebral hemispheres were cut coronally into 1cm slabs. Slabs not designated for freezing were fixed for at least 48–72 hours. Neuropathologic evaluations were performed at the Rush, blinded to clinical data, and reviewed by a board-certified neuropathologist, as reported elsewhere.16 (link),17 (link) A uniform examination included assessment for common vascular and neurodegenerative conditions in aging. Examination for cerebral infarcts documented age (acute/subacute/chronic), size, and location (side and region) of infarcts visible to the naked eye on fixed slabs.17 (link) All grossly visualized and suspected macroscopic infarcts were dissected for histologic confirmation. For analyses, chronic macroscopic infarcts were characterized as present or absent.17 (link)
A minimum of nine regions in one hemisphere were examined for microinfarcts on 6µm paraffin-embedded sections, stained with hematoxylin/eosin. We examined six cortical regions (midfrontal, middle temporal, entorhinal, hippocampal, inferior parietal, and anterior cingulate cortices), two subcortical regions (anterior basal ganglia, thalamus), and midbrain. Locations of microinfarcts were recorded. Because acute and subacute microinfarcts were unlikely to be related to dementia, we only considered chronic microinfarcts for this study. These included cavitated or incomplete infarcts, with few remaining macrophages and fibrillary gliosis. In primary analyses, each case was classified according to whether any chronic microinfarct was present. We created additional variables for secondary analyses. For quantity, we created a predictor with three levels: no (reference level), one, and multiple microinfarcts. For location, we created two variables: cortical (presence of any microinfarcts in any cortical region; reference = no cortical microinfarcts) and subcortical microinfarcts (presence of any microinfarcts in any subcortical region; reference = no subcortical microinfarcts). To investigate quantity and location simultaneously, we created four variables: one cortical microinfarct and multiple cortical microinfarcts (compared to no cortical microinfarcts), and one subcortical microinfarct and multiple subcortical microinfarcts (compared to no subcortical microinfarcts).
Each brain was examined for pathological markers of other common neurodegenerative conditions associated with dementia. AD pathology was assessed in fixed tissue which was paraffin embedded, cut into 6µm sections, and mounted on slides.17 (link) Using a modified Bielschowsky silver stain, we counted neuritic plaques, diffuse plaques, and neurofibrillary tangles. Counts were scaled separately in each region and averaged across regions to create summary scores of each markers for each subject. For analyses, we created a summary score of global AD pathology, by averaging the summary scores of the three markers.16 (link) Lewy body pathology was identified in 6µm sections of cortex and substantia nigra, using α-synuclein immunohistochemistry (Zymed, 1:100).18 (link) For analyses, Lewy body data was dichotomized as present (if identified in any brain region) vs. absent.
Arvanitakis Z., Leurgans S.E., Barnes L.L., Bennett D.A, & Schneider J.A. (2011). Microinfarct Pathology, Dementia, and Cognitive Systems. Stroke; a journal of cerebral circulation, 42(3), 722-727.
Publication 2011
alpha-Synuclein Autopsy Basal Ganglia Blood Vessel Brain Cerebellum Cerebral Hemispheres Cerebral Infarction Cortex, Cerebral Dementia Eosin Gliosis Gyrus, Anterior Cingulate Immunohistochemistry Infarction Lewy Bodies Macrophage Mesencephalon Neurodegenerative Disorders Neurofibrillary Tangle Neuropathologist Paraffin Paraffin Embedding Pathologic Processes Senile Plaques Silver Stains Substantia Nigra Thalamus
2
Optimizing BIANCA for Vascular WMH Detection
Cited 45 times
This section describes the datasets used to optimise and validate BIANCA for the detection of white matter hyperintensities of presumed vascular origin (Wardlaw et al., 2013 (link)). The datasets are different in terms of populations, were acquired on different scanners and using different imaging protocols (see details below).
Exclusion criteria applied to both cohorts for the purposes of the present study were: presence of intracranial haemorrhage; intracranial space occupying lesion; WMH mimics (multiple sclerosis and irradiation induced gliosis); brain defect due to previous neurosurgery or developmental anomalies; large chronic, subacute or acute infarcts (i.e., > 2 cm on either T1-, T2-weighted or DWI sequences); significant movement artefacts.
For both datasets WMHs were graded on FLAIR images by a trained operator (L.L.) who provided visual ratings according to the following scales: 1) a modified version of the Fazekas scale (Fazekas et al., 1987 (link)), considering periventricular and deep white matter lesions altogether (range total score 0–6); 2) the ARWMC (Age-Related White Matter Changes, (Wahlund et al., 2001 (link))) scale, rating 5 different regions (frontal, parieto-occipital, temporal, basal ganglia, infratentorial) in both hemispheres according to a 0–3 score (range total score 0–30).
Griffanti L., Zamboni G., Khan A., Li L., Bonifacio G., Sundaresan V., Schulz U.G., Kuker W., Battaglini M., Rothwell P.M, & Jenkinson M. (2016). BIANCA (Brain Intensity AbNormality Classification Algorithm): A new tool for automated segmentation of white matter hyperintensities. Neuroimage, 141, 191-205.
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Publication 2016
Basal Ganglia Birth Blood Vessel Brain Gliosis Infarction Intracranial Hemorrhage Movement Multiple Sclerosis Neurosurgical Procedures Population Group Radiotherapy White Matter
3
Neuropathological Evaluation of Hippocampal Sclerosis
Cited 21 times
Completed post-mortem data on HS were available for 1052 subjects. The
frequency of HS in these cases was 7.9%. Due to the low frequency of HS cases,
all HS cases (n=83), and a consecutive series of cases without HS (n=553) but
with complete TDP-43 data analyses were used in this study. The average
post-mortem interval was 8.4 hrs (SD=7.4). A complete neuropathological
evaluation including macroscopic examination of the brain, block selection, and
microscopy was performed as described previously.24 (link),25 (link) The
age, volume, and anatomic location of all macroscopic infarcts were documented.
Sections (6 μm) were stained with hematoxylin and eosin and assessed by a
neuropathologist blinded to age and all clinical data. The location and age of
all microscopic infarcts were documented and only chronic macro and
microinfarcts were included in the analyses as dichotomous variables.
Arteriolosclerosis was assessed in the basal ganglia and atherosclerosis in
vessels at the base of the brain using a semiquantitative grading system from 0
(none) to 6 (severe) as described previously.26 (link) HS was evaluated unilaterally in a coronal
section of the mid-hippocampus at the level of the lateral geniculate body, and
graded as absent or present based on severe neuronal loss and gliosis in
CA1and/or subiculum. Involvement of other sectors was also documented.
AD pathology was defined by the NIA-Reagan criteria 27 (link) with intermediate and high
likelihood cases indicating a pathologic diagnosis of AD as described
previously.25 (link) Modified
Bielschowsky silver stain was used to assess AD pathology and manual counts of
neuritic and diffuse plaques and neurofibrillary tangles were used to create a
summary measure of AD pathology 24 (link) for use in analyses.
Nag S., Yu L., Capuano A.W., Wilson R.S., Leurgans S.E., Bennett D.A, & Schneider J.A. (2015). Hippocampal sclerosis and TDP-43 pathology in aging and Alzheimer’s Disease. Annals of neurology, 77(6), 942-952.
Publication 2015
Arteriolosclerosis Atherosclerosis Autopsy Basal Ganglia Brain Diagnosis Eosin Gliosis Infarction Lateral Geniculate Body Microscopy Neurofibrillary Tangle Neurons protein TDP-43, human Seahorses Senile Plaques Silver Stains Subiculum
4
Differential Gene Expression in Brain Tissue
Cited 14 times

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Publication 2017
Alleles Apolipoproteins E Astrocytes Biological Processes Biopharmaceuticals Blood Vessel Brain Cells Central Nervous System Diagnosis DNA Replication Endothelial Cells ENO2 protein, human Gene Expression Genes Glial Fibrillary Acidic Protein Gliosis Microglia Neurons OLIG2 protein, human Oligodendroglia Temporal Lobe Tissues
5
Immunofluorescence and Neuropathological Analysis Protocols
Cited 12 times

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Publication 2015
alpha-Synuclein Animals Antibodies Avidin Blindness Brain Cell Body Cells Cloning Vectors Fluorescein-5-isothiocyanate Fluorescent Antibody Technique Glial Fibrillary Acidic Protein Gliosis Homo sapiens Infection Lysine matrigel Microscopy Nerve Degeneration paraform Poly A Signal Detection (Psychology) Vision

Most recents protocols related to «Gliosis»

1
Neural Bypass Recording and Stimulation
Neural bypass systems have the ability to perform neural recordings, process data, and deliver neurostimulation. Neural recordings can have varying degrees of spatial and temporal resolution. In order of increasing spatial resolution, recording methods can include: EEG, which typically records on the order of 1,000,000 neurons; ECoG, which typically records on the order of 100,000 neurons; microelectrode arrays, which can record local field potentials from 10,000s of neurons or up to 100 individual neurons within 60 μm, and then single neuron recordings which have the highest spatial and temporal resolution of a single neuron [9 (link)–11 (link)]. One recording system is the Neuroport System which takes a sampling rate of 10 kHz [12 (link)]. Recording methods such as EEG are typically less invasive but carry lower spatial resolution than their more invasive counterparts, such as ECoG [13 (link)]. EEG also greatly varies in the number and location of electrodes, though the sensorimotor cortex has been the most common site of recording. An invasive electrode strategy with stereo encephalography (SEEG) to record fine movement signals in humans has recently been demonstrated and has been highlighted for its potential to provide recording information with low operative risk in a neural bypass [6 (link), 14 (link)]. Chronically implanted recording devices have been prone to signal decay over time due to factors such as gliosis, but multi-unit recording devices have been more resistant to such decay [15 (link)].
Zuccaroli I., Lucke-Wold B., Palla A., Eremiev A., Sorrentino Z., Zakare-Fagbamila R., McNulty J., Christie C., Chandra V, & Mampre D. (2023). Neural Bypasses: Literature Review and Future Directions in Developing Artificial Neural Connections. OBM neurobiology, 7(1), 158.
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Publication 2023
Electrocorticography Gliosis Homo sapiens Medical Devices Microelectrodes Movement Nervousness Neurons Sensorimotor Cortex Systems, Nervous
2
Magnetic Resonance Imaging Protocol for Neurological Emergencies
We used two 3T imagers (Magnetom Skyra, Siemens Healthcare and Achieva, Philips Medical System) in the clinical neuroradiology department. An MRI was performed urgently as soon as the patient's condition allowed, ideally within 72 h of the diagnosis of NOSE and if considered necessary for the care of patients with NISE. A minimum of the following sequences was performed: DWI, ADC mapping, fluid-attenuated inversion recovery (FLAIR), T1 with gadolinium, and gradient-recalled echo T2*. The presence of PMAs in DWI and FLAIR sequences, the volume of PMAs in DWI, the presence and type of old cerebral lesions, and SE etiology were analyzed by a trained neuroradiologist and neurologist (FB and MB). When other lesions (peritumoral edema, gliosis, acute stroke, etc.) could explain the abnormalities in DWI and FLAIR, these were not considered as PMAs.
We semi-automatically quantified the PMA volume in DWI using OLEA software in a one-shot analysis with manual correction [Olea Sphere® version 2.3, cutting thickness of 3 or 4 mm, technique validated for ischemic stroke (44 (link))]. The PMA volume was estimated using the average of three different segmentations for each patient. The standard zones of the magnetic susceptibility artifact were systematically trimmed.
If an MRI control was required, it was scheduled on the same 3T machines within 3 months of the SE.
Benaiteau M., Valton L., Gardy L., Denuelle M., Debs R., Wucher V., Rulquin F., Barbeau E.J., Bonneville F., Pariente J, & Curot J. (2023). Specific profiles of new-onset vs. non-inaugural status epilepticus: From diagnosis to 1-year outcome. Frontiers in Neurology, 14, 1101370.
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Publication 2023
Acute Cerebrovascular Accidents Congenital Abnormality Diagnosis ECHO protocol Edema Gadolinium Gliosis Inversion, Chromosome Neurologists Nose Olea Patients Stroke, Ischemic Susceptibility, Disease
3
Alzheimer's Disease Mouse Model Study
All animal use was approved by the Harvard Medical School Office for Research Subject Protection—Harvard Medical Area Standing Committee on Animals and the Brookhaven National Laboratory Institutional Animal Care and Use Committee. Mice were either APPswe/PS1dE9 transgenic (APP/PS1, Tg) or age- and sex-matched C57BL/6J wildtype (WT) littermates. The APPswe/PS1dE9 mice had the Swedish APPK594N/M595L human transgene as well as the PS1dE9 human transgene, both of which are under a mouse prion promoter. These mice developed AD pathology, including extracellular amyloid deposits in the prefrontal cortex and hippocampus by 5–6 months of age, and by 7–8 months of age, they developed further Aβ plaque deposition, microhemorrhages, gliosis, and cognitive deficits [35 (link),36 (link),37 (link)]. Mice were irradiated at 4 months of age at the Brookhaven National Laboratory (BNL) in Upton, NY, USA. At 11 months of age, they underwent behavioral testing and were euthanized the following month (12 months of age) by CO2 asphyxiation. Mice were housed at a constant temperature on 12 h light/dark cycles with ad libitum access to food (PicoLab Rodent Diet #5053) and water at BWH, HMS, and BNL.
Hinshaw R.G., Schroeder M.K., Ciola J., Varma C., Colletti B., Liu B., Liu G.G., Shi Q., Williams J.P., O’Banion M.K., Caldarone B.J, & Lemere C.A. (2023). High-Energy, Whole-Body Proton Irradiation Differentially Alters Long-Term Brain Pathology and Behavior Dependent on Sex and Alzheimer’s Disease Mutations. International Journal of Molecular Sciences, 24(4), 3615.
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Publication 2023
Animals Animals, Transgenic APP protein, human Asphyxia Diet Disorders, Cognitive Food Gliosis Homo sapiens Institutional Animal Care and Use Committees Mice, Laboratory Prefrontal Cortex Prions Rodent Seahorses Senile Plaques Transgenes
4
Multimodal Characterization of Amyloid and Neuroinflammation
Immunohistochemical methods are described in detail in Liu et al., (2019) [11 (link)]. Briefly, 20 μm, OCT-embedded, frozen mouse brain sections were immunolabeled using the ABC ELITE method (Vector Laboratories, Burlingame, Calif., USA). The R1282 rabbit polyclonal anti-A antibody (1:1000, a gift from Dr. Dennis Selkoe, Brigham and Women’s Hospital, MA, USA) was used to assess Aβ pathology. One percent aqueous Thioflavin S (Thioflavin S; Sigma-Aldrich, St. Louis, MO, USA) was used to visualize fibrillar amyloid in plaques and blood vessels. Gliosis was assessed using anti-TSPO rabbit monoclonal antibody (an activated microglial marker, 1:1000 Abcam, Waltham, MA, USA). Microhemorrhages were detected using 2% ferrocyanide (Sigma, St. Louis, MO, USA) in 2% hydrochloric acid. Immunoreactivity of R1282, Thioflavin S, and TSPO was quantified with a BIOQUANT image analysis (Nashville, TN, USA). The percent area of R1282 and TSPO staining in the entire hippocampus (HC) was calculated for 2 equidistant sagittal sections 300 μm apart per mouse. The threshold of detection was held constant during analyses. Thioflavin S labeling was averaged by 3 consecutive sections in the middle plane of the hemibrain. Microhemorrhages were counted and averaged over 6 sections (3 consecutive sections, 2 planes) of each mouse. To identify synaptic and dendritic markers, immunofluorescence staining was used to identify the density of pre-synaptic marker synaptophysin (SYP; Sigma-Aldrich, St. Louis, MO, USA), post-synaptic marker PSD95 (MilliporeSigma, Burlington, MA, USA), and dendritic marker MAP2 (MilliporeSigma, Burlington, MA, USA) in the CA1 and CA3 regions of the hippocampus.
Hinshaw R.G., Schroeder M.K., Ciola J., Varma C., Colletti B., Liu B., Liu G.G., Shi Q., Williams J.P., O’Banion M.K., Caldarone B.J, & Lemere C.A. (2023). High-Energy, Whole-Body Proton Irradiation Differentially Alters Long-Term Brain Pathology and Behavior Dependent on Sex and Alzheimer’s Disease Mutations. International Journal of Molecular Sciences, 24(4), 3615.
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Publication 2023
Antibodies, Anti-Idiotypic ARID1A protein, human Blood Vessel Brain BZRP protein, human CA3 Field of Hippocampus Cloning Vectors Dendrites Fluorescent Antibody Technique Frozen Sections Gliosis hexacyanoferrate II Hydrochloric acid METAP2 protein, human Mice, House Microglia Monoclonal Antibodies Plaque, Amyloid Rabbits Seahorses Synaptophysin thioflavine thioflavin S Woman
5
Histological Assessment of Brain Damage
Sagittal sections from brain tissue were fixed in paraformaldehyde (4%) and embedded in paraffin blocks. After that, blocks were cut into thin slices (5–6 μm) and stained with hematoxylin and eosin staining [24 ]. Different brain regions were examined in each animal by using an Olympus light microscope (BX43, USA) connected to a DP27 digital camera and CellSens dimensions software. The histological damage score was assessed in each animal according to previous studies [25 (link),26 (link)]. Briefly, variant lesions, including neuronal degeneration, neurophagia, gliosis, and necrosis, were scored in different brain regions according to the severity as follows: 0 = absent, 1 = sporadic neuron (<25%), 2 = distributed neurons (25–50%), 3 = distributed neurons (>75), 4 = multifocal (>75). The final score for each animal was obtained by summation of the total score for multiple lesions (4–5 fields/200×).
Khalil H.M., El Henafy H.M., Khalil I.A., Bakr A.F., Fahmy M.I., Younis N.S, & El-Shiekh R.A. (2023). Hypericum perforatum L. Nanoemulsion Mitigates Cisplatin-Induced Chemobrain via Reducing Neurobehavioral Alterations, Oxidative Stress, Neuroinflammation, and Apoptosis in Adult Rats. Toxics, 11(2), 159.
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Publication 2023
Animals Brain Eosin Fingers Gliosis Light Microscopy Necrosis Nerve Degeneration Neurons Paraffin Embedding paraform Tissues

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1
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Mouse anti-NeuN is a primary antibody that recognizes the neuronal nuclear antigen (NeuN), a protein expressed in the nuclei and cytoplasm of most neuronal cell types. It is commonly used as a marker for identifying and quantifying neurons in various tissues and applications.
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More about "Gliosis"

Gliosis is a pathological process characterized by the proliferation and hypertrophy of glial cells, typically in response to central nervous system (CNS) injury or disease.
This reactive process involves the activation and changes in morphology of astrocytes, microglia, and oligodendrocytes.
Gliosis can have both beneficial and detrimental effects on neurological function, depending on the severity and duration of the underlying condition.
Understanding the mechanisms and dynamics of gliosis is crucial for developing effective therapies to promote neural repair and regeneration.
Glial fibrillary acidic protein (GFAP) is a widely used marker for astrocyte activation and gliosis.
The Z0334 antibody is a specific marker for oligodendrocytes, while the Mouse anti-NeuN antibody is commonly used to identify neuronal nuclei (NeuN).
Magnetic resonance imaging (MRI) using a 1.5-T MRI system can be employed to visualize and monitor gliosis in the brain.
The Rabbit anti-Iba1 antibody is a reliable marker for microglia, and Anti-GFAP is a specific marker for astrocytes.
GraphPad Prism 5 and Prism 8 are statistical software packages that can be utilized for data analysis and visualization in gliosis research.
PubCompare.ai's AI-driven platform can optimize gliosis research by helping users locate the best protocols and products from literature, pre-prints, and patents, enhancing reproducibility and accuracy to drive your research forward.
Experience the power of AI-driven protocol optimization today and take your gliosis research to the next level.