Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease

Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. Th...
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Autor*in:	Beauchamp, Leah C. [verfasserIn] Chan, Jacky Hung, Lin W. Padman, Benjamin S. Vella, Laura J. Liu, Xiang M. Coleman, Bradley Bush, Ashley I. Lazarou, Michael Hill, Andrew F. Jacobson, Laura Barnham, Kevin J.

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Tau Parkinson’s disease Olfaction Autophagy Neurodegeneration

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: Acta Neuropathologica Communications - London : Biomed Central, 2013, 6(2018), 1 vom: 05. Juli
Übergeordnetes Werk:	volume:6 ; year:2018 ; number:1 ; day:05 ; month:07

Links:	Volltext

DOI / URN:	10.1186/s40478-018-0560-y

Katalog-ID:	SPR036513431

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allfields	10.1186/s40478-018-0560-y doi (DE-627)SPR036513431 (SPR)s40478-018-0560-y-e DE-627 ger DE-627 rakwb eng Beauchamp, Leah C. verfasserin (orcid)0000-0002-4896-279X aut Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Chan, Jacky aut Hung, Lin W. aut Padman, Benjamin S. aut Vella, Laura J. aut Liu, Xiang M. aut Coleman, Bradley aut Bush, Ashley I. aut Lazarou, Michael aut Hill, Andrew F. aut Jacobson, Laura aut Barnham, Kevin J. aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 05. Juli (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:05 month:07 https://dx.doi.org/10.1186/s40478-018-0560-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 05 07
spelling	10.1186/s40478-018-0560-y doi (DE-627)SPR036513431 (SPR)s40478-018-0560-y-e DE-627 ger DE-627 rakwb eng Beauchamp, Leah C. verfasserin (orcid)0000-0002-4896-279X aut Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Chan, Jacky aut Hung, Lin W. aut Padman, Benjamin S. aut Vella, Laura J. aut Liu, Xiang M. aut Coleman, Bradley aut Bush, Ashley I. aut Lazarou, Michael aut Hill, Andrew F. aut Jacobson, Laura aut Barnham, Kevin J. aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 05. Juli (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:05 month:07 https://dx.doi.org/10.1186/s40478-018-0560-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 05 07
allfields_unstemmed	10.1186/s40478-018-0560-y doi (DE-627)SPR036513431 (SPR)s40478-018-0560-y-e DE-627 ger DE-627 rakwb eng Beauchamp, Leah C. verfasserin (orcid)0000-0002-4896-279X aut Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Chan, Jacky aut Hung, Lin W. aut Padman, Benjamin S. aut Vella, Laura J. aut Liu, Xiang M. aut Coleman, Bradley aut Bush, Ashley I. aut Lazarou, Michael aut Hill, Andrew F. aut Jacobson, Laura aut Barnham, Kevin J. aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 05. Juli (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:05 month:07 https://dx.doi.org/10.1186/s40478-018-0560-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 05 07
allfieldsGer	10.1186/s40478-018-0560-y doi (DE-627)SPR036513431 (SPR)s40478-018-0560-y-e DE-627 ger DE-627 rakwb eng Beauchamp, Leah C. verfasserin (orcid)0000-0002-4896-279X aut Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Chan, Jacky aut Hung, Lin W. aut Padman, Benjamin S. aut Vella, Laura J. aut Liu, Xiang M. aut Coleman, Bradley aut Bush, Ashley I. aut Lazarou, Michael aut Hill, Andrew F. aut Jacobson, Laura aut Barnham, Kevin J. aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 05. Juli (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:05 month:07 https://dx.doi.org/10.1186/s40478-018-0560-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 05 07
allfieldsSound	10.1186/s40478-018-0560-y doi (DE-627)SPR036513431 (SPR)s40478-018-0560-y-e DE-627 ger DE-627 rakwb eng Beauchamp, Leah C. verfasserin (orcid)0000-0002-4896-279X aut Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213 Chan, Jacky aut Hung, Lin W. aut Padman, Benjamin S. aut Vella, Laura J. aut Liu, Xiang M. aut Coleman, Bradley aut Bush, Ashley I. aut Lazarou, Michael aut Hill, Andrew F. aut Jacobson, Laura aut Barnham, Kevin J. aut Enthalten in Acta Neuropathologica Communications London : Biomed Central, 2013 6(2018), 1 vom: 05. Juli (DE-627)746066465 (DE-600)2715589-4 2051-5960 nnns volume:6 year:2018 number:1 day:05 month:07 https://dx.doi.org/10.1186/s40478-018-0560-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2018 1 05 07
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source	Enthalten in Acta Neuropathologica Communications 6(2018), 1 vom: 05. Juli volume:6 year:2018 number:1 day:05 month:07
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authorswithroles_txt_mv	Beauchamp, Leah C. @@aut@@ Chan, Jacky @@aut@@ Hung, Lin W. @@aut@@ Padman, Benjamin S. @@aut@@ Vella, Laura J. @@aut@@ Liu, Xiang M. @@aut@@ Coleman, Bradley @@aut@@ Bush, Ashley I. @@aut@@ Lazarou, Michael @@aut@@ Hill, Andrew F. @@aut@@ Jacobson, Laura @@aut@@ Barnham, Kevin J. @@aut@@
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author	Beauchamp, Leah C.
spellingShingle	Beauchamp, Leah C. misc Tau misc Parkinson’s disease misc Olfaction misc Autophagy misc Neurodegeneration Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease
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topic_title	Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease Tau (dpeaa)DE-He213 Parkinson’s disease (dpeaa)DE-He213 Olfaction (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Neurodegeneration (dpeaa)DE-He213
topic	misc Tau misc Parkinson’s disease misc Olfaction misc Autophagy misc Neurodegeneration
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title	Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease
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title_full	Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease
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title_sort	ablation of tau causes an olfactory deficit in a murine model of parkinson’s disease
title_auth	Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease
abstract	Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. © The Author(s). 2018
abstractGer	Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. © The Author(s). 2018
abstract_unstemmed	Abstract Parkinson’s disease is diagnosed upon the presentation of motor symptoms, resulting from substantial degeneration of dopaminergic neurons in the midbrain. Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. These data implicate a pathological role for tau in early Parkinson’s disease. © The Author(s). 2018
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title_short	Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease
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author2	Chan, Jacky Hung, Lin W. Padman, Benjamin S. Vella, Laura J. Liu, Xiang M. Coleman, Bradley Bush, Ashley I. Lazarou, Michael Hill, Andrew F. Jacobson, Laura Barnham, Kevin J.
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up_date	2024-07-03T18:05:06.029Z
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Prior to diagnosis, there is a lengthy prodromal stage in which non-motor symptoms, including olfactory deficits (hyposmia), develop. There is limited information about non-motor impairments and there is a need for directed research into these early pathogenic cellular pathways that precede extensive dopaminergic death in the midbrain. The protein tau has been identified as a genetic risk factor in the development of sporadic PD. Tau knockout mice have been reported as an age-dependent model of PD, and this study has demonstrated that they develop motor deficits at 15-months-old. We have shown that at 7-month-old tau knockout mice present with an overt hyposmic phenotype. This olfactory deficit correlates with an accumulation of α-synuclein, as well as autophagic impairment, in the olfactory bulb. This pathological feature becomes apparent in the striatum and substantia nigra of 15-month-old tau knockout mice, suggesting the potential for a spread of disease. Initial primary cell culture experiments have demonstrated that ablation of tau results in the release of α-synuclein enriched exosomes, providing a potential mechanism for disease spread. These alterations in α-synuclein level as well as a marked autophagy impairment in the tau knockout primary cells recapitulate results seen in the animal model. 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Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease

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