Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain
Tau pathology is known to spread in a hierarchical pattern in Alzheimer’s disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propa...
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| Published in | Nature communications Vol. 6; no. 1; p. 8490 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
13.10.2015
Nature Publishing Group Nature Pub. Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2041-1723 2041-1723 |
| DOI | 10.1038/ncomms9490 |
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| Abstract | Tau pathology is known to spread in a hierarchical pattern in Alzheimer’s disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development.
In Alzheimer's disease, tau spreads throughout the brain, however the nature of the tau species propagating from one neuron to another is not known. Here, Takeda
et al
. identify a rare, high-molecular-weight tau as the primary species taken up and transferred between synaptically connected neurons. |
|---|---|
| AbstractList | Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development.Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development. Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development. In Alzheimer's disease, tau spreads throughout the brain, however the nature of the tau species propagating from one neuron to another is not known. Here, Takeda et al . identify a rare, high-molecular-weight tau as the primary species taken up and transferred between synaptically connected neurons. Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development. |
| ArticleNumber | 8490 |
| Author | Müller, Daniel J. Costantino, Isabel Nobuhara, Chloe K. Commins, Caitlin Nicholls, Samantha B. Roe, Allyson D. Irimia, Daniel Cho, Hansang DeVos, Sarah L. Frosch, Matthew P. Pitstick, Rose Takeda, Shuko Wegmann, Susanne Carlson, George A. Hyman, Bradley T. |
| Author_xml | – sequence: 1 givenname: Shuko surname: Takeda fullname: Takeda, Shuko organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 2 givenname: Susanne surname: Wegmann fullname: Wegmann, Susanne organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 3 givenname: Hansang surname: Cho fullname: Cho, Hansang organization: BioMEMS Resource Center, Massachusetts General Hospital, Harvard Medical School, Department of Mechanical Engineering and Engineering Science, University of North Carolina at Charlotte – sequence: 4 givenname: Sarah L. surname: DeVos fullname: DeVos, Sarah L. organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 5 givenname: Caitlin surname: Commins fullname: Commins, Caitlin organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 6 givenname: Allyson D. surname: Roe fullname: Roe, Allyson D. organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 7 givenname: Samantha B. surname: Nicholls fullname: Nicholls, Samantha B. organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 8 givenname: George A. surname: Carlson fullname: Carlson, George A. organization: McLaughlin Research Institute – sequence: 9 givenname: Rose surname: Pitstick fullname: Pitstick, Rose organization: McLaughlin Research Institute – sequence: 10 givenname: Chloe K. surname: Nobuhara fullname: Nobuhara, Chloe K. organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 11 givenname: Isabel surname: Costantino fullname: Costantino, Isabel organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 12 givenname: Matthew P. surname: Frosch fullname: Frosch, Matthew P. organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School – sequence: 13 givenname: Daniel J. surname: Müller fullname: Müller, Daniel J. organization: Department of Biosystems Science and Engineering, Eidgenössische Technische Hochschule Zürich – sequence: 14 givenname: Daniel surname: Irimia fullname: Irimia, Daniel organization: BioMEMS Resource Center, Massachusetts General Hospital, Harvard Medical School – sequence: 15 givenname: Bradley T. surname: Hyman fullname: Hyman, Bradley T. email: BHYMAN@mgh.harvard.edu organization: Department of Neurology, Alzheimer’s Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26458742$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2015 Copyright Nature Publishing Group Oct 2015 Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. |
| Copyright_xml | – notice: The Author(s) 2015 – notice: Copyright Nature Publishing Group Oct 2015 – notice: Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. |
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| Snippet | Tau pathology is known to spread in a hierarchical pattern in Alzheimer’s disease (AD) brain during disease progression, likely by trans-synaptic tau transfer... Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer... |
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| SubjectTerms | 13 13/1 631/378/1689/1283 631/80/128/1653 64 64/60 82 82/1 82/29 82/51 82/62 Aged Aged, 80 and over Alzheimer Disease - metabolism Alzheimer's disease Animals Biosensors Brain - metabolism Brain research Cell Survival Disease Female HEK293 Cells Humanities and Social Sciences Humans Male Mice, Inbred C57BL Mice, Transgenic Microfluidic Analytical Techniques Molecular weight multidisciplinary Neurons Neurons - metabolism Pathology Phosphorylation Propagation Rare species Science Science (multidisciplinary) tau Proteins - metabolism |
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| Title | Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain |
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