Simplification of the modified <scp>G</scp>allyas method

Kuninaka, Nobuo; Kawaguchi, Masahumi; Ogawa, Masaru; Sato, Ayako; Arima, Kunimasa; Murayama, Shigeo; Saito, Yuko

doi:10.1111/neup.12144

Cited by 36 publications

(25 citation statements)

References 14 publications

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“…Assessment of NFTs is generally performed using silver staining techniques such as the Gallyas method . In recent years, sensitive immunochemical methods have been used on routine paraffin sections.…”

Section: Discussionmentioning

confidence: 99%

“…Assessment of NFTs is generally performed using silver staining techniques such as the Gallyas method. 2,3,24 In recent years, sensitive immunochemical methods have been used on routine paraffin sections. The AT8 monoclonal antibody is one of several commercially available specific antibodies that show robust immunoreactivity for phosphotau protein, and can be used even on tissue that has been stored for decades in formaldehyde.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of AT8 immunoreactivity in the locus ceruleus and hippocampus of 154 brains from routine autopsies

Okamoto¹,

Amari²,

Fukuda³

et al. 2017

Neuropathology

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We compared semiquantitatively AT8 immunoreactivity in the locus ceruleus (LC) and hippocampus of 154 brains from routine autopsies to investigate the initial sites of phosphorylated tau (phospho-tau) development. The numbers of AT8-positive neurons and the severity of AT8-positive neuropil threads (NTs) in the LC were strongly associated: there were no cases with AT8-positive neurons that lacked NTs and 20 cases (13%) had only NTs in the LC. Phospho-tau pathologies in the LC were almost equally on both sides, although some cases (7.8%) showed unilateral predominance. The numbers of AT8-positive neurons in the LC and the numbers of AT8-positive neurons and NTs in the hippocampus were also strongly associated. There were only two cases with AT8-positive neurons in the LC that lacked phospho-tau pathology in the hippocampus, and 21 cases (13.6%) with phospho-tau pathology in the hippocampus that lacked AT8-positive neurons in the LC. The numbers of AT8-positive NTs in the LC and AT8-positive neurons and NTs in the hippocampus were also strongly associated. There were seven cases (4.5%) with AT8-positive NTs in the LC that lacked phospho-tau pathology in the hippocampus, and five cases (3.2 %) with phospho-tau pathologies in the hippocampus that lacked AT8-positive NTs in the LC. In this study, we could not confirm that phospho-tau pathologies begin in the LC. We suspect their simultaneous occurrences in both hippocampal regions and in LC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Comparison of AT8 immunoreactivity in the locus ceruleus and hippocampus of 154 brains from routine autopsies

Okamoto¹,

Amari²,

Fukuda³

et al. 2017

Neuropathology

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“…Following hydration through a series of graded ethanol into distilled water (2 × 1 min: 99%, 96%, 70%), sections were stained for neurofibrillary tangles according to the Kuninaka et al 2015 modification [69] of the Gallyas method [70]. Briefly, slides were immersed into an aqueous solution of 0.25% potassium permanganate (20 min), washed in distilled water (1min), and incubated in 1% oxalic acid (2 min).…”

Section: Methodsmentioning

confidence: 99%

An integrated proteomics approach shows synaptic plasticity changes in an APP/PS1 Alzheimer's mouse model

et al. 2016

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The aim of this study was to elucidate the molecular signature of Alzheimer's disease-associated amyloid pathology.We used the double APPswe/PS1ΔE9 mouse, a widely used model of cerebral amyloidosis, to compare changes in proteome, including global phosphorylation and sialylated N-linked glycosylation patterns, pathway-focused transcriptome and neurological disease-associated miRNAome with age-matched controls in neocortex, hippocampus, olfactory bulb and brainstem. We report that signalling pathways related to synaptic functions associated with dendritic spine morphology, neurite outgrowth, long-term potentiation, CREB signalling and cytoskeletal dynamics were altered in 12 month old APPswe/PS1ΔE9 mice, particularly in the neocortex and olfactory bulb. This was associated with cerebral amyloidosis as well as formation of argyrophilic tangle-like structures and microglial clustering in all brain regions, except for brainstem. These responses may be epigenetically modulated by the interaction with a number of miRNAs regulating spine restructuring, Aβ expression and neuroinflammation.We suggest that these changes could be associated with development of cognitive dysfunction in early disease states in patients with Alzheimer's disease.

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“…Formalin-fixed, paraffin-embedded sections of the sciatic nerve (7 mm thick) from 7-and 10-month-old WT and Tg30 mice were stained with a modified Gallyas silver-staining method 10,18 and counterstained with 0.1% Nuclear Fast Red.…”

Section: Gallyas Stainingmentioning

confidence: 99%

Motor Deficit in a Tauopathy Model Is Induced by Disturbances of Axonal Transport Leading to Dying-Back Degeneration and Denervation of Neuromuscular Junctions

Audouard¹,

Hees²,

Suain³

et al. 2015

The American Journal of Pathology

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Several neurodegenerative diseases are characterized by both cognitive and motor deficits associated with accumulation of tau aggregates in brain, brainstem, and spinal cord. The Tg30 murine tauopathy model expresses a human tau protein bearing two frontotemporal dementia with Parkinsonism linked to chromosome 17 pathogenic mutations and develops a severe motor deficit and tau aggregates in brain and spinal cord. To investigate the origin of this motor deficit, we analyzed the age-dependent innervation status of the neuromuscular junctions and mutant tau expression in Tg30 mice. The human transgenic tau was detected from postnatal day 7 onward in motoneurons, axons in the sciatic nerve, and axon terminals of the neuromuscular junctions. The development and maturation of neuromuscular junctions were not disrupted in Tg30 mice, but their maintenance was disturbed in adult Tg30 mice, resulting in a progressive and severe muscle denervation. This muscle denervation was associated with early electrophysiological signs of muscle spontaneous activities and histological signs of muscle degeneration. Early loss of synaptic vesicles in axon terminals preceding motor deficits, accumulation of Gallyas-positive aggregates, and cathepsin-positive vesicular clusters in axons in the sciatic nerve suggest that this denervation results from disturbances of axonal transport. This physiopathological mechanism might be responsible for motor signs observed in some human tauopathies, and for synaptic dysfunction resulting from alterations at the presynaptic level in these diseases. (Am J Pathol 2015 http://dx

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Simplification of the modified Gallyas method

Cited by 36 publications

References 14 publications

Comparison of AT8 immunoreactivity in the locus ceruleus and hippocampus of 154 brains from routine autopsies

Comparison of AT8 immunoreactivity in the locus ceruleus and hippocampus of 154 brains from routine autopsies

An integrated proteomics approach shows synaptic plasticity changes in an APP/PS1 Alzheimer's mouse model

Motor Deficit in a Tauopathy Model Is Induced by Disturbances of Axonal Transport Leading to Dying-Back Degeneration and Denervation of Neuromuscular Junctions

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