Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau

Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white...
Ausführliche Beschreibung

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Autor*in:	Lin, Wen-Lang [verfasserIn] Zehr, Cindy [verfasserIn] Lewis, Jada [verfasserIn] Hutton, Michael [verfasserIn] Yen, Shu-Hui [verfasserIn] Dickson, Dennis W. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2005

Schlagwörter:	Amyotrophic Lateral Sclerosis Myelin Sheath Myelin Debris Axonal Pathology White Matter Pathology

Übergeordnetes Werk:	Enthalten in: Journal of neurocytology - Dordrecht [u.a.] : Springer Science + Business Media B.V., 1972, 34(2005), 6 vom: Dez., Seite 397-410
Übergeordnetes Werk:	volume:34 ; year:2005 ; number:6 ; month:12 ; pages:397-410

Links:	Volltext

DOI / URN:	10.1007/s11068-006-8726-0

Katalog-ID:	SPR016292537

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520			\|a Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation.
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700	1		\|a Dickson, Dennis W. \|e verfasserin \|4 aut
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allfields	10.1007/s11068-006-8726-0 doi (DE-627)SPR016292537 (SPR)s11068-006-8726-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Lin, Wen-Lang verfasserin aut Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Myelin Sheath (dpeaa)DE-He213 Myelin Debris (dpeaa)DE-He213 Axonal Pathology (dpeaa)DE-He213 White Matter Pathology (dpeaa)DE-He213 Zehr, Cindy verfasserin aut Lewis, Jada verfasserin aut Hutton, Michael verfasserin aut Yen, Shu-Hui verfasserin aut Dickson, Dennis W. verfasserin aut Enthalten in Journal of neurocytology Dordrecht [u.a.] : Springer Science + Business Media B.V., 1972 34(2005), 6 vom: Dez., Seite 397-410 (DE-627)320461289 (DE-600)2007301-X 1573-7381 nnns volume:34 year:2005 number:6 month:12 pages:397-410 https://dx.doi.org/10.1007/s11068-006-8726-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_24 GBV_ILN_40 GBV_ILN_63 GBV_ILN_100 GBV_ILN_101 GBV_ILN_285 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2005 GBV_ILN_2027 GBV_ILN_2048 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 44.90 ASE AR 34 2005 6 12 397-410
spelling	10.1007/s11068-006-8726-0 doi (DE-627)SPR016292537 (SPR)s11068-006-8726-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Lin, Wen-Lang verfasserin aut Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Myelin Sheath (dpeaa)DE-He213 Myelin Debris (dpeaa)DE-He213 Axonal Pathology (dpeaa)DE-He213 White Matter Pathology (dpeaa)DE-He213 Zehr, Cindy verfasserin aut Lewis, Jada verfasserin aut Hutton, Michael verfasserin aut Yen, Shu-Hui verfasserin aut Dickson, Dennis W. verfasserin aut Enthalten in Journal of neurocytology Dordrecht [u.a.] : Springer Science + Business Media B.V., 1972 34(2005), 6 vom: Dez., Seite 397-410 (DE-627)320461289 (DE-600)2007301-X 1573-7381 nnns volume:34 year:2005 number:6 month:12 pages:397-410 https://dx.doi.org/10.1007/s11068-006-8726-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_24 GBV_ILN_40 GBV_ILN_63 GBV_ILN_100 GBV_ILN_101 GBV_ILN_285 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2005 GBV_ILN_2027 GBV_ILN_2048 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 44.90 ASE AR 34 2005 6 12 397-410
allfields_unstemmed	10.1007/s11068-006-8726-0 doi (DE-627)SPR016292537 (SPR)s11068-006-8726-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Lin, Wen-Lang verfasserin aut Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Myelin Sheath (dpeaa)DE-He213 Myelin Debris (dpeaa)DE-He213 Axonal Pathology (dpeaa)DE-He213 White Matter Pathology (dpeaa)DE-He213 Zehr, Cindy verfasserin aut Lewis, Jada verfasserin aut Hutton, Michael verfasserin aut Yen, Shu-Hui verfasserin aut Dickson, Dennis W. verfasserin aut Enthalten in Journal of neurocytology Dordrecht [u.a.] : Springer Science + Business Media B.V., 1972 34(2005), 6 vom: Dez., Seite 397-410 (DE-627)320461289 (DE-600)2007301-X 1573-7381 nnns volume:34 year:2005 number:6 month:12 pages:397-410 https://dx.doi.org/10.1007/s11068-006-8726-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_24 GBV_ILN_40 GBV_ILN_63 GBV_ILN_100 GBV_ILN_101 GBV_ILN_285 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2005 GBV_ILN_2027 GBV_ILN_2048 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 44.90 ASE AR 34 2005 6 12 397-410
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allfieldsSound	10.1007/s11068-006-8726-0 doi (DE-627)SPR016292537 (SPR)s11068-006-8726-0-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Lin, Wen-Lang verfasserin aut Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau 2005 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation. Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Myelin Sheath (dpeaa)DE-He213 Myelin Debris (dpeaa)DE-He213 Axonal Pathology (dpeaa)DE-He213 White Matter Pathology (dpeaa)DE-He213 Zehr, Cindy verfasserin aut Lewis, Jada verfasserin aut Hutton, Michael verfasserin aut Yen, Shu-Hui verfasserin aut Dickson, Dennis W. verfasserin aut Enthalten in Journal of neurocytology Dordrecht [u.a.] : Springer Science + Business Media B.V., 1972 34(2005), 6 vom: Dez., Seite 397-410 (DE-627)320461289 (DE-600)2007301-X 1573-7381 nnns volume:34 year:2005 number:6 month:12 pages:397-410 https://dx.doi.org/10.1007/s11068-006-8726-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_24 GBV_ILN_40 GBV_ILN_63 GBV_ILN_100 GBV_ILN_101 GBV_ILN_285 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2005 GBV_ILN_2027 GBV_ILN_2048 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4325 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4338 44.90 ASE AR 34 2005 6 12 397-410
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source	Enthalten in Journal of neurocytology 34(2005), 6 vom: Dez., Seite 397-410 volume:34 year:2005 number:6 month:12 pages:397-410
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topic_facet	Amyotrophic Lateral Sclerosis Myelin Sheath Myelin Debris Axonal Pathology White Matter Pathology
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authorswithroles_txt_mv	Lin, Wen-Lang @@aut@@ Zehr, Cindy @@aut@@ Lewis, Jada @@aut@@ Hutton, Michael @@aut@@ Yen, Shu-Hui @@aut@@ Dickson, Dennis W. @@aut@@
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author	Lin, Wen-Lang
spellingShingle	Lin, Wen-Lang ddc 610 bkl 44.90 misc Amyotrophic Lateral Sclerosis misc Myelin Sheath misc Myelin Debris misc Axonal Pathology misc White Matter Pathology Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau
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topic_title	610 ASE 44.90 bkl Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau Amyotrophic Lateral Sclerosis (dpeaa)DE-He213 Myelin Sheath (dpeaa)DE-He213 Myelin Debris (dpeaa)DE-He213 Axonal Pathology (dpeaa)DE-He213 White Matter Pathology (dpeaa)DE-He213
topic	ddc 610 bkl 44.90 misc Amyotrophic Lateral Sclerosis misc Myelin Sheath misc Myelin Debris misc Axonal Pathology misc White Matter Pathology
topic_unstemmed	ddc 610 bkl 44.90 misc Amyotrophic Lateral Sclerosis misc Myelin Sheath misc Myelin Debris misc Axonal Pathology misc White Matter Pathology
topic_browse	ddc 610 bkl 44.90 misc Amyotrophic Lateral Sclerosis misc Myelin Sheath misc Myelin Debris misc Axonal Pathology misc White Matter Pathology
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title	Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau
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title_full	Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau
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author_browse	Lin, Wen-Lang Zehr, Cindy Lewis, Jada Hutton, Michael Yen, Shu-Hui Dickson, Dennis W.
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title_sort	progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (p301l) human tau
title_auth	Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau
abstract	Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation.
abstractGer	Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation.
abstract_unstemmed	Abstract Transgenic mice expressing mutant (P301L) tau develop paresis, neurofibrillary tangles and neuronal loss in spinal motor neurons beginning at 4 to 6 months of age. Astrocytes and oligodendrocytes acquire filamentous tau inclusions at later ages. Here we report pathology in the spinal white matter of these animals. Progressive white matter pathology, detected as early as 2 months of age, was most marked in lateral and anterior columns, with sparing of posterior columns until late in the disease. Early changes in Luxol fast blue/periodic acid Schiff (LFB/PAS) and toluidine blue stained sections were vacuolation of myelin followed by accumulation of myelin figures within previous axonal tubes and finally influx of PAS-positive macrophages. Myelin debris and vacuoles were found in macrophages. At the ultrastructural level, myelinated axons showed extensive vacuolation of myelin sheaths formed by splitting of myelin lamellae at the intra-period line, while axons were atrophic and contained densely packed neurofilaments. Other axons were lost completely, resulting in collapse and phagocytosis of myelin sheaths. Also present were spheroids derived from swollen axons with thin myelin sheaths containing neurofilaments, tau filaments and degenerating organelles. Many oligodendrocytes had membrane-bound cytoplasmic bodies composed of tightly stacked lamellae capped by dense material. The vacuolar myelopathy in this model to some extent resembles that reported in acquired immune deficiency syndrome and vitamin B12 deficiency. The progressive axonal pathology is most consistent with a dying-back process caused by abnormal accumulation of tau in upstream neurons, while vacuolar myelinopathy may be a secondary manifestation of neuroinflammation.
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title_short	Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau
url	https://dx.doi.org/10.1007/s11068-006-8726-0
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author2	Zehr, Cindy Lewis, Jada Hutton, Michael Yen, Shu-Hui Dickson, Dennis W.
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Progressive white matter pathology in the spinal cord of transgenic mice expressing mutant (P301L) human tau

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Zugang & Verfügbarkeit

Vorhandene Bände

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